prompt stringlengths 2.15k 5.36k | title stringclasses 394 values | abstract stringclasses 394 values | head_entity dict | title_entity dict | candidate_relation_list listlengths 3 7 | label stringclasses 8 values |
|---|---|---|---|---|---|---|
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein Socs3 and a gene or protein EPO in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[Socs3,GeneOrGeneProduct]' and '[EPO,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[Socs3,GeneOrGeneProduct]' and '[EPO,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "Socs3",
"type": "GeneOrGeneProduct"
} | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Lyl1 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Lyl1,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Lyl1,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Lyl1",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein CyclinB1-IP-1 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[CyclinB1-IP-1,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[CyclinB1-IP-1,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "CyclinB1-IP-1",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Cyclin-g2 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Cyclin-g2,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Cyclin-g2,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Cyclin-g2",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein p27-kip1 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[p27-kip1,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[p27-kip1,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "p27-kip1",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Cyclin-d2 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Cyclin-d2,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Cyclin-d2,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Cyclin-d2",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Btg3 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Btg3,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Btg3,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Btg3",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Cdc25a in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Cdc25a,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Cdc25a,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Cdc25a",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Serpina 3g in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Serpina 3g,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Serpina 3g,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Serpina 3g",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Trib3 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Trib3,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Trib3,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Trib3",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Bim in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Bim,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Bim,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Bim",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Pim1 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Pim1,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Pim1,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Pim1",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Pim3 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Pim3,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Pim3,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Pim3",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein Gas5 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[Gas5,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[Gas5,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "Gas5",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPO and a gene or protein EPOR in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPO,GeneOrGeneProduct]' and '[EPOR,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPO,GeneOrGeneProduct]' and '[EPOR,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Bind</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Bind |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein Tnfr-sf13c and a gene or protein EPO in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[Tnfr-sf13c,GeneOrGeneProduct]' and '[EPO,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[Tnfr-sf13c,GeneOrGeneProduct]' and '[EPO,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "Tnfr-sf13c",
"type": "GeneOrGeneProduct"
} | {
"name": "EPO",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a gene or protein p85/PI3K in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[p85/PI3K,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[p85/PI3K,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "p85/PI3K",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a disease polycythemia in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or gene) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[polycythemia,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[polycythemia,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "polycythemia",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a disease anemia in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or gene) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[anemia,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[anemia,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "anemia",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a gene or protein CyclinB1-IP-1 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[CyclinB1-IP-1,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[CyclinB1-IP-1,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "CyclinB1-IP-1",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a gene or protein Cyclin-g2 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[Cyclin-g2,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[Cyclin-g2,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "Cyclin-g2",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a gene or protein p27-kip1 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[p27-kip1,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[p27-kip1,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "p27-kip1",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a gene or protein Cyclin-d2 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[Cyclin-d2,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[Cyclin-d2,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "Cyclin-d2",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a gene or protein Btg3 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[Btg3,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[Btg3,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "Btg3",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a gene or protein Cdc25a in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[Cdc25a,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[Cdc25a,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "Cdc25a",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein EPOR and a gene or protein Tnfr-sf13c in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[EPOR,GeneOrGeneProduct]' and '[Tnfr-sf13c,GeneOrGeneProduct]'.
- Title of the Paper: Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation.
- Abstract of the Paper: [Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.]
Identify how '[EPOR,GeneOrGeneProduct]' and '[Tnfr-sf13c,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. | Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies: Bcl-x levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and Erk1 disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included Lyl1, Gas5, Pim3, Pim1, Bim, Trib3 and Serpina 3g. EPO/EPOR-modulated cell cycle mediators included Cdc25a, Btg3, Cyclin-d2, p27-kip1, Cyclin-g2 and CyclinB1-IP-1. EPO regulation of signal transduction factors was also interestingly complex. For example, not only Socs3 plus Socs2 but also Spred2, Spred1 and Eaf1 were EPO-induced as negative-feedback components. Socs2, plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor Tnfr-sf13c was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation. | {
"name": "EPOR",
"type": "GeneOrGeneProduct"
} | {
"name": "Tnfr-sf13c",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein HOMER1 and a chemical glutamate in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[HOMER1,GeneOrGeneProduct]' and '[glutamate,ChemicalEntity]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[HOMER1,GeneOrGeneProduct]' and '[glutamate,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "HOMER1",
"type": "GeneOrGeneProduct"
} | {
"name": "glutamate",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein HOMER1 and a chemical levodopa in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[HOMER1,GeneOrGeneProduct]' and '[levodopa,ChemicalEntity]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[HOMER1,GeneOrGeneProduct]' and '[levodopa,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "HOMER1",
"type": "GeneOrGeneProduct"
} | {
"name": "levodopa",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein HOMER1 and a disease visual hallucinations in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or gene) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[HOMER1,GeneOrGeneProduct]' and '[visual hallucinations,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[HOMER1,GeneOrGeneProduct]' and '[visual hallucinations,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "HOMER1",
"type": "GeneOrGeneProduct"
} | {
"name": "visual hallucinations",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein HOMER1 and a disease dyskinesia in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or gene) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[HOMER1,GeneOrGeneProduct]' and '[dyskinesia,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[HOMER1,GeneOrGeneProduct]' and '[dyskinesia,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "HOMER1",
"type": "GeneOrGeneProduct"
} | {
"name": "dyskinesia",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical levodopa and a disease Parkinson's disease in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[levodopa,ChemicalEntity]' and '[Parkinson's disease,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[levodopa,ChemicalEntity]' and '[Parkinson's disease,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "levodopa",
"type": "ChemicalEntity"
} | {
"name": "Parkinson's disease",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical Levodopa and a disease visual hallucinations in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[Levodopa,ChemicalEntity]' and '[visual hallucinations,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[Levodopa,ChemicalEntity]' and '[visual hallucinations,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Positive_Correlation</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "Levodopa",
"type": "ChemicalEntity"
} | {
"name": "visual hallucinations",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical Levodopa and a disease dyskinesia in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[Levodopa,ChemicalEntity]' and '[dyskinesia,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[Levodopa,ChemicalEntity]' and '[dyskinesia,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Positive_Correlation</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "Levodopa",
"type": "ChemicalEntity"
} | {
"name": "dyskinesia",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a variant rs4704559 and a chemical levodopa in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' suggests a mutual reinforcement between genetic variations and chemicals. This includes the chemical causing increased gene expression because of the variant, the variant increasing the body's sensitivity to the chemical, the variant causing a stronger reaction to the chemical, or any other type of positive relation between the variant and the chemical.
'Negative_Correlation' means a gene variant weakens the effect of a chemical. Thisinclude when the variant causes less gene activity due to the chemical, makes the body less responsive to the chemical, creates resistance to the chemical, or shows any decrease in interaction between the gene and the chemical.
'Association' indicates that the relation between a chemical and gene variations cannot be clearly defined as either positive or negative correlation.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[rs4704559,SequenceVariant]' and '[levodopa,ChemicalEntity]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[rs4704559,SequenceVariant]' and '[levodopa,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "rs4704559",
"type": "SequenceVariant"
} | {
"name": "levodopa",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a variant rs4704559 and a disease visual hallucinations in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a genetic variant is linked to an increased risk of a disease. This includes cases where the variant is more common in those with the disease, causes abnormal gene expression or non-functionality leading to the disease, results in a disease due to a protein deficiency for which the variant is responsible, contributes to genetic susceptibility to the disease, or has a significant impact on the development of the disease.
'Negative_Correlation' indicates that the variant decreases the risk of the disease.
'Association' means that a genetic variant found in some patients is linked to a lower chance of getting the disease, or it makes them less likely to develop the disease. It also covers relation that don't fit into a positive/negative correlation category or relation that are not clearly defined.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[rs4704559,SequenceVariant]' and '[visual hallucinations,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[rs4704559,SequenceVariant]' and '[visual hallucinations,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "rs4704559",
"type": "SequenceVariant"
} | {
"name": "visual hallucinations",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a variant rs4704559 and a disease dyskinesia in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a genetic variant is linked to an increased risk of a disease. This includes cases where the variant is more common in those with the disease, causes abnormal gene expression or non-functionality leading to the disease, results in a disease due to a protein deficiency for which the variant is responsible, contributes to genetic susceptibility to the disease, or has a significant impact on the development of the disease.
'Negative_Correlation' indicates that the variant decreases the risk of the disease.
'Association' means that a genetic variant found in some patients is linked to a lower chance of getting the disease, or it makes them less likely to develop the disease. It also covers relation that don't fit into a positive/negative correlation category or relation that are not clearly defined.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[rs4704559,SequenceVariant]' and '[dyskinesia,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients.
- Abstract of the Paper: [Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects.]
Identify how '[rs4704559,SequenceVariant]' and '[dyskinesia,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Association of common genetic variants of HOMER1 gene with levodopa adverse effects in Parkinson's disease patients. | Levodopa is the most effective symptomatic therapy for Parkinson's disease, but its chronic use could lead to chronic adverse outcomes, such as motor fluctuations, dyskinesia and visual hallucinations. HOMER1 is a protein with pivotal function in glutamate transmission, which has been related to the pathogenesis of these complications. This study investigates whether polymorphisms in the HOMER1 gene promoter region are associated with the occurrence of the chronic complications of levodopa therapy. A total of 205 patients with idiopathic Parkinson's disease were investigated. Patients were genotyped for rs4704559, rs10942891 and rs4704560 by allelic discrimination with Taqman assays. The rs4704559 G allele was associated with a lower prevalence of dyskinesia (prevalence ratio (PR)=0.615, 95% confidence interval (CI) 0.426-0.887, P=0.009) and visual hallucinations (PR=0.515, 95% CI 0.295-0.899, P=0.020). Our data suggest that HOMER1 rs4704559 G allele has a protective role for the development of levodopa adverse effects. | {
"name": "rs4704559",
"type": "SequenceVariant"
} | {
"name": "dyskinesia",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical methyldopa and a disease hypotensive in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[methyldopa,ChemicalEntity]' and '[hypotensive,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Midline B3 serotonin nerves in rat medulla are involved in hypotensive effect of methyldopa.
- Abstract of the Paper: [Previous experiments in this laboratory have shown that microinjection of methyldopa onto the ventrolateral cells of the B3 serotonin neurons in the medulla elicits a hypotensive response mediated by a projection descending into the spinal cord. The present experiments were designed to investigate the role of the midline cells of the B3 serotonin neurons in the medulla, coinciding with the raphe magnus. In spontaneously hypertensive, stroke-prone rats, microinjection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla caused a potent hypotension of 30-40 mm Hg, which was maximal 2-3 h after administration and was abolished by the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly. However, intraspinal injection of 5,7-DHT to produce a more selective lesion of only descending serotonin projections in the spinal cord did not affect this hypotension. Further, 5,7-DHT lesion of serotonin nerves travelling in the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells, did not affect the fall in blood pressure associated with a midline B3 serotonin methyldopa injection. It is concluded therefore that, unlike the ventrolateral B3 cells which mediate a methyldopa-induced hypotension via descending projections, the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa, either by way of an ascending projection which does not pass through the median forebrain bundle, or through a projection restricted to the caudal brainstem.]
Identify how '[methyldopa,ChemicalEntity]' and '[hypotensive,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Positive_Correlation</s> | Midline B3 serotonin nerves in rat medulla are involved in hypotensive effect of methyldopa. | Previous experiments in this laboratory have shown that microinjection of methyldopa onto the ventrolateral cells of the B3 serotonin neurons in the medulla elicits a hypotensive response mediated by a projection descending into the spinal cord. The present experiments were designed to investigate the role of the midline cells of the B3 serotonin neurons in the medulla, coinciding with the raphe magnus. In spontaneously hypertensive, stroke-prone rats, microinjection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla caused a potent hypotension of 30-40 mm Hg, which was maximal 2-3 h after administration and was abolished by the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly. However, intraspinal injection of 5,7-DHT to produce a more selective lesion of only descending serotonin projections in the spinal cord did not affect this hypotension. Further, 5,7-DHT lesion of serotonin nerves travelling in the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells, did not affect the fall in blood pressure associated with a midline B3 serotonin methyldopa injection. It is concluded therefore that, unlike the ventrolateral B3 cells which mediate a methyldopa-induced hypotension via descending projections, the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa, either by way of an ascending projection which does not pass through the median forebrain bundle, or through a projection restricted to the caudal brainstem. | {
"name": "methyldopa",
"type": "ChemicalEntity"
} | {
"name": "hypotensive",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical serotonin and a chemical 5,7-dihydroxytryptamine in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[serotonin,ChemicalEntity]' and '[5,7-dihydroxytryptamine,ChemicalEntity]'.
- Title of the Paper: Midline B3 serotonin nerves in rat medulla are involved in hypotensive effect of methyldopa.
- Abstract of the Paper: [Previous experiments in this laboratory have shown that microinjection of methyldopa onto the ventrolateral cells of the B3 serotonin neurons in the medulla elicits a hypotensive response mediated by a projection descending into the spinal cord. The present experiments were designed to investigate the role of the midline cells of the B3 serotonin neurons in the medulla, coinciding with the raphe magnus. In spontaneously hypertensive, stroke-prone rats, microinjection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla caused a potent hypotension of 30-40 mm Hg, which was maximal 2-3 h after administration and was abolished by the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly. However, intraspinal injection of 5,7-DHT to produce a more selective lesion of only descending serotonin projections in the spinal cord did not affect this hypotension. Further, 5,7-DHT lesion of serotonin nerves travelling in the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells, did not affect the fall in blood pressure associated with a midline B3 serotonin methyldopa injection. It is concluded therefore that, unlike the ventrolateral B3 cells which mediate a methyldopa-induced hypotension via descending projections, the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa, either by way of an ascending projection which does not pass through the median forebrain bundle, or through a projection restricted to the caudal brainstem.]
Identify how '[serotonin,ChemicalEntity]' and '[5,7-dihydroxytryptamine,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Association</s> | Midline B3 serotonin nerves in rat medulla are involved in hypotensive effect of methyldopa. | Previous experiments in this laboratory have shown that microinjection of methyldopa onto the ventrolateral cells of the B3 serotonin neurons in the medulla elicits a hypotensive response mediated by a projection descending into the spinal cord. The present experiments were designed to investigate the role of the midline cells of the B3 serotonin neurons in the medulla, coinciding with the raphe magnus. In spontaneously hypertensive, stroke-prone rats, microinjection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla caused a potent hypotension of 30-40 mm Hg, which was maximal 2-3 h after administration and was abolished by the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly. However, intraspinal injection of 5,7-DHT to produce a more selective lesion of only descending serotonin projections in the spinal cord did not affect this hypotension. Further, 5,7-DHT lesion of serotonin nerves travelling in the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells, did not affect the fall in blood pressure associated with a midline B3 serotonin methyldopa injection. It is concluded therefore that, unlike the ventrolateral B3 cells which mediate a methyldopa-induced hypotension via descending projections, the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa, either by way of an ascending projection which does not pass through the median forebrain bundle, or through a projection restricted to the caudal brainstem. | {
"name": "serotonin",
"type": "ChemicalEntity"
} | {
"name": "5,7-dihydroxytryptamine",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical serotonin and a chemical methyldopa in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[serotonin,ChemicalEntity]' and '[methyldopa,ChemicalEntity]'.
- Title of the Paper: Midline B3 serotonin nerves in rat medulla are involved in hypotensive effect of methyldopa.
- Abstract of the Paper: [Previous experiments in this laboratory have shown that microinjection of methyldopa onto the ventrolateral cells of the B3 serotonin neurons in the medulla elicits a hypotensive response mediated by a projection descending into the spinal cord. The present experiments were designed to investigate the role of the midline cells of the B3 serotonin neurons in the medulla, coinciding with the raphe magnus. In spontaneously hypertensive, stroke-prone rats, microinjection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla caused a potent hypotension of 30-40 mm Hg, which was maximal 2-3 h after administration and was abolished by the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly. However, intraspinal injection of 5,7-DHT to produce a more selective lesion of only descending serotonin projections in the spinal cord did not affect this hypotension. Further, 5,7-DHT lesion of serotonin nerves travelling in the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells, did not affect the fall in blood pressure associated with a midline B3 serotonin methyldopa injection. It is concluded therefore that, unlike the ventrolateral B3 cells which mediate a methyldopa-induced hypotension via descending projections, the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa, either by way of an ascending projection which does not pass through the median forebrain bundle, or through a projection restricted to the caudal brainstem.]
Identify how '[serotonin,ChemicalEntity]' and '[methyldopa,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Positive_Correlation</s> | Midline B3 serotonin nerves in rat medulla are involved in hypotensive effect of methyldopa. | Previous experiments in this laboratory have shown that microinjection of methyldopa onto the ventrolateral cells of the B3 serotonin neurons in the medulla elicits a hypotensive response mediated by a projection descending into the spinal cord. The present experiments were designed to investigate the role of the midline cells of the B3 serotonin neurons in the medulla, coinciding with the raphe magnus. In spontaneously hypertensive, stroke-prone rats, microinjection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla caused a potent hypotension of 30-40 mm Hg, which was maximal 2-3 h after administration and was abolished by the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly. However, intraspinal injection of 5,7-DHT to produce a more selective lesion of only descending serotonin projections in the spinal cord did not affect this hypotension. Further, 5,7-DHT lesion of serotonin nerves travelling in the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells, did not affect the fall in blood pressure associated with a midline B3 serotonin methyldopa injection. It is concluded therefore that, unlike the ventrolateral B3 cells which mediate a methyldopa-induced hypotension via descending projections, the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa, either by way of an ascending projection which does not pass through the median forebrain bundle, or through a projection restricted to the caudal brainstem. | {
"name": "serotonin",
"type": "ChemicalEntity"
} | {
"name": "methyldopa",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical serotonin and a disease hypotensive in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[serotonin,ChemicalEntity]' and '[hypotensive,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Midline B3 serotonin nerves in rat medulla are involved in hypotensive effect of methyldopa.
- Abstract of the Paper: [Previous experiments in this laboratory have shown that microinjection of methyldopa onto the ventrolateral cells of the B3 serotonin neurons in the medulla elicits a hypotensive response mediated by a projection descending into the spinal cord. The present experiments were designed to investigate the role of the midline cells of the B3 serotonin neurons in the medulla, coinciding with the raphe magnus. In spontaneously hypertensive, stroke-prone rats, microinjection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla caused a potent hypotension of 30-40 mm Hg, which was maximal 2-3 h after administration and was abolished by the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly. However, intraspinal injection of 5,7-DHT to produce a more selective lesion of only descending serotonin projections in the spinal cord did not affect this hypotension. Further, 5,7-DHT lesion of serotonin nerves travelling in the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells, did not affect the fall in blood pressure associated with a midline B3 serotonin methyldopa injection. It is concluded therefore that, unlike the ventrolateral B3 cells which mediate a methyldopa-induced hypotension via descending projections, the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa, either by way of an ascending projection which does not pass through the median forebrain bundle, or through a projection restricted to the caudal brainstem.]
Identify how '[serotonin,ChemicalEntity]' and '[hypotensive,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Positive_Correlation</s> | Midline B3 serotonin nerves in rat medulla are involved in hypotensive effect of methyldopa. | Previous experiments in this laboratory have shown that microinjection of methyldopa onto the ventrolateral cells of the B3 serotonin neurons in the medulla elicits a hypotensive response mediated by a projection descending into the spinal cord. The present experiments were designed to investigate the role of the midline cells of the B3 serotonin neurons in the medulla, coinciding with the raphe magnus. In spontaneously hypertensive, stroke-prone rats, microinjection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla caused a potent hypotension of 30-40 mm Hg, which was maximal 2-3 h after administration and was abolished by the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly. However, intraspinal injection of 5,7-DHT to produce a more selective lesion of only descending serotonin projections in the spinal cord did not affect this hypotension. Further, 5,7-DHT lesion of serotonin nerves travelling in the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells, did not affect the fall in blood pressure associated with a midline B3 serotonin methyldopa injection. It is concluded therefore that, unlike the ventrolateral B3 cells which mediate a methyldopa-induced hypotension via descending projections, the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa, either by way of an ascending projection which does not pass through the median forebrain bundle, or through a projection restricted to the caudal brainstem. | {
"name": "serotonin",
"type": "ChemicalEntity"
} | {
"name": "hypotensive",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein STAT3 and a gene or protein VEGF in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[STAT3,GeneOrGeneProduct]' and '[VEGF,GeneOrGeneProduct]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[STAT3,GeneOrGeneProduct]' and '[VEGF,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "STAT3",
"type": "GeneOrGeneProduct"
} | {
"name": "VEGF",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein VEGF and a gene or protein VEGFR2 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[VEGF,GeneOrGeneProduct]' and '[VEGFR2,GeneOrGeneProduct]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[VEGF,GeneOrGeneProduct]' and '[VEGFR2,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "VEGF",
"type": "GeneOrGeneProduct"
} | {
"name": "VEGFR2",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein VEGF and a chemical ROS in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[VEGF,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[VEGF,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "VEGF",
"type": "GeneOrGeneProduct"
} | {
"name": "ROS",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NOX2 and a chemical ROS in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NOX2,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[NOX2,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "NOX2",
"type": "GeneOrGeneProduct"
} | {
"name": "ROS",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NOX4 and a gene or protein STAT3 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NOX4,GeneOrGeneProduct]' and '[STAT3,GeneOrGeneProduct]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[NOX4,GeneOrGeneProduct]' and '[STAT3,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "NOX4",
"type": "GeneOrGeneProduct"
} | {
"name": "STAT3",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NOX4 and a gene or protein VEGFR2 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NOX4,GeneOrGeneProduct]' and '[VEGFR2,GeneOrGeneProduct]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[NOX4,GeneOrGeneProduct]' and '[VEGFR2,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "NOX4",
"type": "GeneOrGeneProduct"
} | {
"name": "VEGFR2",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NOX4 and a gene or protein VEGF in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NOX4,GeneOrGeneProduct]' and '[VEGF,GeneOrGeneProduct]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[NOX4,GeneOrGeneProduct]' and '[VEGF,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "NOX4",
"type": "GeneOrGeneProduct"
} | {
"name": "VEGF",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NOX4 and a chemical ROS in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NOX4,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[NOX4,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "NOX4",
"type": "GeneOrGeneProduct"
} | {
"name": "ROS",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NOX1 and a chemical ROS in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NOX1,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[NOX1,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "NOX1",
"type": "GeneOrGeneProduct"
} | {
"name": "ROS",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical oxygen and a disease retinopathy in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[oxygen,ChemicalEntity]' and '[retinopathy,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[oxygen,ChemicalEntity]' and '[retinopathy,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "oxygen",
"type": "ChemicalEntity"
} | {
"name": "retinopathy",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NOX4 and a chemical ROS in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NOX4,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[NOX4,GeneOrGeneProduct]' and '[ROS,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "NOX4",
"type": "GeneOrGeneProduct"
} | {
"name": "ROS",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NADPH oxidase 4 and a gene or protein vascular endothelial growth factor receptor 2 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NADPH oxidase 4,GeneOrGeneProduct]' and '[vascular endothelial growth factor receptor 2,GeneOrGeneProduct]'.
- Title of the Paper: Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity.
- Abstract of the Paper: [PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3.]
Identify how '[NADPH oxidase 4,GeneOrGeneProduct]' and '[vascular endothelial growth factor receptor 2,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Endothelial NADPH oxidase 4 mediates vascular endothelial growth factor receptor 2-induced intravitreal neovascularization in a rat model of retinopathy of prematurity. | PURPOSE: NADPH oxidase-generated reactive oxygen species (ROS) are implicated in angiogenesis. Isoforms of NADPH oxidase NOX1, NOX2, and NOX4 are reported to be expressed in endothelial cells (ECs). Of these, NOX1 and NOX2 have been reported to contribute to intravitreal neovascularization (IVNV) in oxygen-induced retinopathy (OIR) models. In this study, we tested the hypothesis that the isoform NOX4 in ECs contributed to vascular endothelial growth factor (VEGF)-induced angiogenesis and IVNV. METHODS: Isoforms of NADPH oxidase MRNA were measured in several types of cultured vascular ecs: human retinal microvascular ECs (hRMVECs), choroidal ECs (CECs), and human umbilical vascular ECs (HUVECs) using real-time PCR. Newborn rat pups and dams were placed into an OIR model that cycled oxygen concentration between 50% and 10% every 24 h for 14 days, and then were placed in room air (RA) for an additional 4 days (rat OIR model). NOX4 expression in retinal lysates from the RA-raised pups at postnatal day 0 (P0), P14, and P18 was determined with western blots. STAT3 activation was determined as the ratio of phosphorylated STAT3 to total STAT3 with western blot analysis of retinal lysates from pups raised in RA or from the rat OIR model at P18. Semiquantitative assessment of the density of NOX4 colabeling with lectin-stained retinal ECs was determined by immunolabeling of retinal cryosections from P18 pups in OIR or in RA. In hRMVECs transfected with NOX4 siRNA and treated with VEGF or control, 1) ROS generation was measured using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate, acetyl ester fluorescence assay and 2) phosphorylated VEGF receptor 2 and STAT3, and total VEGFR2 and STAT3 were measured in western blot analyses. VEGF-stimulated hRMVEC proliferation was measured following transfection with NOX4 siRNA or STAT3 siRNA, or respective controls. RESULTS: NOX4 was the most prevalent isoform of NADPH oxidase in vascular ECs. NOX4 expression in retinal lysates was significantly decreased during development in RA. Compared to RA, the expression of retinal NOX4 increased at P18. At p18 OIR, semiquantitative assessment of the density of lectin and NOX4 colabeling in retinal vascular ECs was greater in retinal cryosections and activated STAT3 was greater in retinal lysates when compared to the RA-raised pups. In cultured hRMVECs, knockdown of NOX4 by siRNA transfection inhibited VEGF-induced ROS generation. VEGF induced a physical interaction of phosphorylated-VEGFR2 and NOX4. Knockdown of NOX4: 1) reduced VEGFR2 activation but did not abolish it and 2) abolished STAT3 activation in response to VEGF. Knockdown of either NOX4 or STAT3 inhibited VEGF-induced EC proliferation. CONCLUSIONS: Our data suggest that in a model representative of human retinopathy of prematurity, NOX4 was increased at a time point when IVNV developed. VEGF-activated NOX4 led to an interaction between VEGF-activated VEGFR2 and NOX4 that mediated EC proliferation via activation of STAT3. Altogether, our results suggest that NOX4 may regulate VEGFR2-mediated IVNV through activated STAT3. | {
"name": "NADPH oxidase 4",
"type": "GeneOrGeneProduct"
} | {
"name": "vascular endothelial growth factor receptor 2",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical tamoxifen and a gene or protein Shh in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[tamoxifen,ChemicalEntity]' and '[Shh,GeneOrGeneProduct]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[tamoxifen,ChemicalEntity]' and '[Shh,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "tamoxifen",
"type": "ChemicalEntity"
} | {
"name": "Shh",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical tamoxifen and a gene or protein b-catenin in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[tamoxifen,ChemicalEntity]' and '[b-catenin,GeneOrGeneProduct]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[tamoxifen,ChemicalEntity]' and '[b-catenin,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "tamoxifen",
"type": "ChemicalEntity"
} | {
"name": "b-catenin",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein Bmp7 and a gene or protein b-catenin in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[Bmp7,GeneOrGeneProduct]' and '[b-catenin,GeneOrGeneProduct]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[Bmp7,GeneOrGeneProduct]' and '[b-catenin,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "Bmp7",
"type": "GeneOrGeneProduct"
} | {
"name": "b-catenin",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein Bmp4 and a gene or protein b-catenin in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[Bmp4,GeneOrGeneProduct]' and '[b-catenin,GeneOrGeneProduct]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[Bmp4,GeneOrGeneProduct]' and '[b-catenin,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "Bmp4",
"type": "GeneOrGeneProduct"
} | {
"name": "b-catenin",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease ARM and a gene or protein Bmp7 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[ARM,DiseaseOrPhenotypicFeature]' and '[Bmp7,GeneOrGeneProduct]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[ARM,DiseaseOrPhenotypicFeature]' and '[Bmp7,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "ARM",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "Bmp7",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease ARM and a gene or protein Bmp4 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[ARM,DiseaseOrPhenotypicFeature]' and '[Bmp4,GeneOrGeneProduct]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[ARM,DiseaseOrPhenotypicFeature]' and '[Bmp4,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "ARM",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "Bmp4",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein b-catenin and a gene or protein Msx2 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[b-catenin,GeneOrGeneProduct]' and '[Msx2,GeneOrGeneProduct]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[b-catenin,GeneOrGeneProduct]' and '[Msx2,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "b-catenin",
"type": "GeneOrGeneProduct"
} | {
"name": "Msx2",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein b-catenin and a disease hypoplastic in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or gene) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[b-catenin,GeneOrGeneProduct]' and '[hypoplastic,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[b-catenin,GeneOrGeneProduct]' and '[hypoplastic,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "b-catenin",
"type": "GeneOrGeneProduct"
} | {
"name": "hypoplastic",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein b-catenin and a gene or protein Shh in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' in genetics refers to a scenario where two genes influence each other in a way that enhances their activity or expression. This includes situations where Gene A is a transcription factor that upregulates Gene B, or any other instance where two genes demonstrate a positive correlation in their function or expression.
'Negative_Correlation' in genetics means that two genes affect each other in a way that reduces their activity or expression. This includes cases where Gene A is a transcription factor for Gene B and downregulates it, or any other situation where two genes show a negative correlation in their function or expression.
'Bind' refers to a physical interaction where two proteins connect with each other, or it can mean Protein A attaching itself to the promoter of Gene B.
'Association' refers to the relation between pairs that either cannot be categorized into any specific type of relation, or is relation that lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[b-catenin,GeneOrGeneProduct]' and '[Shh,GeneOrGeneProduct]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[b-catenin,GeneOrGeneProduct]' and '[Shh,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "b-catenin",
"type": "GeneOrGeneProduct"
} | {
"name": "Shh",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein b-catenin and a disease anorectal malformations in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or gene) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[b-catenin,GeneOrGeneProduct]' and '[anorectal malformations,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations.
- Abstract of the Paper: [The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs.]
Identify how '[b-catenin,GeneOrGeneProduct]' and '[anorectal malformations,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Disruption of the temporally regulated cloaca endodermal b-catenin signaling causes anorectal malformations. | The cloaca is temporally formed and eventually divided by the urorectal septum (URS) during urogenital and anorectal organ development. Although congenital malformations, such as anorectal malformations (ARMs), are frequently observed during this process, the underlying pathogenic mechanisms remain unclear. b-Catenin is a critical component of canonical Wnt signaling and is essential for the regulation of cell differentiation and morphogenesis during embryogenesis. The expression of b-catenin is observed in endodermal epithelia, including URS epithelia. We modulated the b-catenin gene conditionally in endodermal epithelia by utilizing tamoxifen-inducible Cre driver line (Shh(CreERT2)). Both b-catenin loss- and gain-of-function (LOF and GOF) mutants displayed abnormal clefts in the perineal region and hypoplastic elongation of the URS. The mutants also displayed reduced cell proliferation in the URS mesenchyme. In addition, the b-catenin GOF mutants displayed reduced apoptosis and subsequently increased apoptosis in the URS epithelium. This instability possibly resulted in reduced expression levels of differentiation markers, such as keratin 1 and filaggrin, in the perineal epithelia. The expression of bone morphogenetic protein (Bmp) genes, such as Bmp4 and Bmp7, was also ectopically induced in the epithelia of the URS in the b-catenin GOF mutants. The expression of the Msx2 gene and phosphorylated-Smad1/5/8, possible readouts of Bmp signaling, was also increased in the mutants. Moreover, we introduced an additional mutation for a Bmp receptor gene: BmprIA. The Shh(CreERT2/+); b-catenin(flox(ex3)/+); BmprIA(flox/-) mutants displayed partial restoration of URS elongation compared with the b-catenin GOF mutants. These results indicate that some ARM phenotypes in the b-catenin GOF mutants were caused by abnormal Bmp signaling. The current analysis revealed the close relation of endodermal b-catenin signaling to the ARM phenotypes. These results are considered to shed light on the pathogenic mechanisms of human ARMs. | {
"name": "b-catenin",
"type": "GeneOrGeneProduct"
} | {
"name": "anorectal malformations",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical aspartate and a chemical P400 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[aspartate,ChemicalEntity]' and '[P400,ChemicalEntity]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[aspartate,ChemicalEntity]' and '[P400,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "aspartate",
"type": "ChemicalEntity"
} | {
"name": "P400",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical aspartate and a chemical GFC75 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[aspartate,ChemicalEntity]' and '[GFC75,ChemicalEntity]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[aspartate,ChemicalEntity]' and '[GFC75,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "aspartate",
"type": "ChemicalEntity"
} | {
"name": "GFC75",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical pilocarpine and a disease status epilepticus in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[pilocarpine,ChemicalEntity]' and '[status epilepticus,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[pilocarpine,ChemicalEntity]' and '[status epilepticus,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Positive_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "pilocarpine",
"type": "ChemicalEntity"
} | {
"name": "status epilepticus",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical P400 and a gene or protein AChE in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[P400,ChemicalEntity]' and '[AChE,GeneOrGeneProduct]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[P400,ChemicalEntity]' and '[AChE,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "P400",
"type": "ChemicalEntity"
} | {
"name": "AChE",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical pilocarpine and a disease seizures in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[pilocarpine,ChemicalEntity]' and '[seizures,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[pilocarpine,ChemicalEntity]' and '[seizures,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Positive_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "pilocarpine",
"type": "ChemicalEntity"
} | {
"name": "seizures",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical glutamate and a chemical pilocarpine in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[glutamate,ChemicalEntity]' and '[pilocarpine,ChemicalEntity]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[glutamate,ChemicalEntity]' and '[pilocarpine,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "glutamate",
"type": "ChemicalEntity"
} | {
"name": "pilocarpine",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical glutamate and a chemical GFC75 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[glutamate,ChemicalEntity]' and '[GFC75,ChemicalEntity]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[glutamate,ChemicalEntity]' and '[GFC75,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "glutamate",
"type": "ChemicalEntity"
} | {
"name": "GFC75",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical GABA and a chemical pilocarpine in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[GABA,ChemicalEntity]' and '[pilocarpine,ChemicalEntity]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[GABA,ChemicalEntity]' and '[pilocarpine,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Positive_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "GABA",
"type": "ChemicalEntity"
} | {
"name": "pilocarpine",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical r-aminobutyric acid and a chemical GFC in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[r-aminobutyric acid,ChemicalEntity]' and '[GFC,ChemicalEntity]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[r-aminobutyric acid,ChemicalEntity]' and '[GFC,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Positive_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "r-aminobutyric acid",
"type": "ChemicalEntity"
} | {
"name": "GFC",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical GFC and a disease diarrheas in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[GFC,ChemicalEntity]' and '[diarrheas,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[GFC,ChemicalEntity]' and '[diarrheas,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "GFC",
"type": "ChemicalEntity"
} | {
"name": "diarrheas",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical GFC and a disease skin diseases in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[GFC,ChemicalEntity]' and '[skin diseases,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[GFC,ChemicalEntity]' and '[skin diseases,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "GFC",
"type": "ChemicalEntity"
} | {
"name": "skin diseases",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical GFC and a disease status epilepticus in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[GFC,ChemicalEntity]' and '[status epilepticus,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[GFC,ChemicalEntity]' and '[status epilepticus,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "GFC",
"type": "ChemicalEntity"
} | {
"name": "status epilepticus",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical garcinielliptone FC and a chemical pilocarpine in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[garcinielliptone FC,ChemicalEntity]' and '[pilocarpine,ChemicalEntity]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[garcinielliptone FC,ChemicalEntity]' and '[pilocarpine,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Cotreatment</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "garcinielliptone FC",
"type": "ChemicalEntity"
} | {
"name": "pilocarpine",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Cotreatment |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical GFC75 and a gene or protein AChE in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[GFC75,ChemicalEntity]' and '[AChE,GeneOrGeneProduct]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[GFC75,ChemicalEntity]' and '[AChE,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Positive_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "GFC75",
"type": "ChemicalEntity"
} | {
"name": "AChE",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical GFC and a disease inflammatory diseases in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[GFC,ChemicalEntity]' and '[inflammatory diseases,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[GFC,ChemicalEntity]' and '[inflammatory diseases,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "GFC",
"type": "ChemicalEntity"
} | {
"name": "inflammatory diseases",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical Garcinielliptone FC and a disease seizures in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[Garcinielliptone FC,ChemicalEntity]' and '[seizures,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures.
- Abstract of the Paper: [Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent.]
Identify how '[Garcinielliptone FC,ChemicalEntity]' and '[seizures,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Negative_Correlation</s> | Behavioral and neurochemical studies in mice pretreated with garcinielliptone FC in pilocarpine-induced seizures. | Garcinielliptone FC (GFC) isolated from hexanic fraction seed extract of species Platonia insignis Mart. It is widely used in folk medicine to treat skin diseases in both humans and animals as well as the seed decoction has been used to treat diarrheas and inflammatory diseases. However, there is no research on GFC effects in the central nervous system of rodents. The present study aimed to evaluate the GFC effects at doses of 25, 50 or 75 mg/kg on seizure parameters to determine their anticonvulsant activity and its effects on amino acid (r-aminobutyric acid (GABA), glutamine, aspartate and glutathione) levels as well as on acetylcholinesterase (AChE) activity in mice hippocampus after seizures. GFC produced an increased latency to first seizure, at doses 25mg/kg (20.12 + 2.20 min), 50mg/kg (20.95 + 2.21 min) or 75 mg/kg (23.43 + 1.99 min) when compared with seized mice. In addition, GABA content of mice hippocampus treated with GFC75 plus P400 showed an increase of 46.90% when compared with seized mice. In aspartate, glutamine and glutamate levels detected a decrease of 5.21%, 13.55% and 21.80%, respectively in mice hippocampus treated with GFC75 plus P400 when compared with seized mice. Hippocampus mice treated with GFC75 plus P400 showed an increase in AChE activity (63.30%) when compared with seized mice. The results indicate that GFC can exert anticonvulsant activity and reduce the frequency of installation of pilocarpine-induced status epilepticus, as demonstrated by increase in latency to first seizure and decrease in mortality rate of animals. In conclusion, our data suggest that GFC may influence in epileptogenesis and promote anticonvulsant actions in pilocarpine model by modulating the GABA and glutamate contents and of AChE activity in seized mice hippocampus. This compound may be useful to produce neuronal protection and it can be considered as an anticonvulsant agent. | {
"name": "Garcinielliptone FC",
"type": "ChemicalEntity"
} | {
"name": "seizures",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Negative_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NGAL and a disease renal impairment in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or gene) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NGAL,GeneOrGeneProduct]' and '[renal impairment,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[NGAL,GeneOrGeneProduct]' and '[renal impairment,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "NGAL",
"type": "GeneOrGeneProduct"
} | {
"name": "renal impairment",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a gene or protein NGAL and a chemical SRL in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[NGAL,GeneOrGeneProduct]' and '[SRL,ChemicalEntity]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[NGAL,GeneOrGeneProduct]' and '[SRL,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "NGAL",
"type": "GeneOrGeneProduct"
} | {
"name": "SRL",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a chemical TBARs in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' indicates that Chemical A increases the effectiveness of Chemical B. This includes making Chemical B more sensitive, enhancing its ability to treat or induce a disease, or boosting its role in gene activation.
'Negative_Correlation' means that Chemical A reduces the effectiveness and impact of Chemical B. This includes decreasing Chemical B's sensitivity, reducing its ability to treat or induce a disease, diminishing its side effects, and lowering the gene activation it causes.
'Drug_Interaction' is when two different drugs or chemicals affect each other's action in the body, happening when they are used at the same time.
'Cotreatment' means that two different drugs or chemicals are used in combination therapy.
'Conversion' means that one chemical changes into another chemical.
'Comparison' means that two different drugs or chemicals have some differences and similarities in their effects.
'Association' refers to the relation between two chemicals that do not fit into any specific, predefined categories of relations.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[TBARs,ChemicalEntity]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[TBARs,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "TBARs",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Drug_Interaction",
"Cotreatment",
"Conversion",
"Comparison",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a gene or protein IL-7 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[IL-7,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[IL-7,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "IL-7",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a gene or protein NF- kb in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[NF- kb,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[NF- kb,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "NF- kb",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a gene or protein TGF-b in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[TGF-b,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[TGF-b,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "TGF-b",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a gene or protein CTGF in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[CTGF,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[CTGF,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "CTGF",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a gene or protein KIM-1 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[KIM-1,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[KIM-1,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "KIM-1",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a gene or protein TP53 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[TP53,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[TP53,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "TP53",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a gene or protein PCNA in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[PCNA,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[PCNA,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "PCNA",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical CsA and a gene or protein mTOR in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means that a chemical leads to higher gene expression, or higher gene expression increases sensitivity to the chemical, or a gene variant exacerbates the chemical's side effects, or a gene causes an over-response to the chemical, or there is a positive interaction between two genes in any manner.
'Negative_Correlation' indicates that a chemical leads to reduced gene expression, or higher gene expression results in decreased sensitivity or resistance to the chemical, or a gene variant offers protection against the chemical's adverse effects, or a gene contributes to resistance against the chemical, or there exists a negative interaction between two genes in any form.
'Bind' means that a chemical either connects to a gene's promoter region or a protein acts as a receptor for that chemical.
'Association' is used to describe relation that don't clearly fall under categories like positive correlation, negative correlation and bind , or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[CsA,ChemicalEntity]' and '[mTOR,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[CsA,ChemicalEntity]' and '[mTOR,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "CsA",
"type": "ChemicalEntity"
} | {
"name": "mTOR",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Bind",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical cyclosporine and a disease nephropathy in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[cyclosporine,ChemicalEntity]' and '[nephropathy,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[cyclosporine,ChemicalEntity]' and '[nephropathy,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Positive_Correlation</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "cyclosporine",
"type": "ChemicalEntity"
} | {
"name": "nephropathy",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Positive_Correlation |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease renal damage and a chemical TBARs in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[renal damage,DiseaseOrPhenotypicFeature]' and '[TBARs,ChemicalEntity]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[renal damage,DiseaseOrPhenotypicFeature]' and '[TBARs,ChemicalEntity]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "renal damage",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "TBARs",
"type": "ChemicalEntity"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease renal damage and a gene or protein IL-7 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[renal damage,DiseaseOrPhenotypicFeature]' and '[IL-7,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[renal damage,DiseaseOrPhenotypicFeature]' and '[IL-7,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "renal damage",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "IL-7",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease kidney lesions and a gene or protein NF- kb in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[kidney lesions,DiseaseOrPhenotypicFeature]' and '[NF- kb,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[kidney lesions,DiseaseOrPhenotypicFeature]' and '[NF- kb,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "kidney lesions",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "NF- kb",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease kidney lesions and a gene or protein TGF-b in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[kidney lesions,DiseaseOrPhenotypicFeature]' and '[TGF-b,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[kidney lesions,DiseaseOrPhenotypicFeature]' and '[TGF-b,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "kidney lesions",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "TGF-b",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease renal damage and a gene or protein CTGF in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[renal damage,DiseaseOrPhenotypicFeature]' and '[CTGF,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[renal damage,DiseaseOrPhenotypicFeature]' and '[CTGF,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "renal damage",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "CTGF",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease renal damage and a gene or protein KIM-1 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[renal damage,DiseaseOrPhenotypicFeature]' and '[KIM-1,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[renal damage,DiseaseOrPhenotypicFeature]' and '[KIM-1,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "renal damage",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "KIM-1",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease renal damage and a gene or protein TP53 in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[renal damage,DiseaseOrPhenotypicFeature]' and '[TP53,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[renal damage,DiseaseOrPhenotypicFeature]' and '[TP53,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "renal damage",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "TP53",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease kidney lesions and a gene or protein PCNA in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[kidney lesions,DiseaseOrPhenotypicFeature]' and '[PCNA,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[kidney lesions,DiseaseOrPhenotypicFeature]' and '[PCNA,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "kidney lesions",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "PCNA",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a disease kidney lesions and a gene or protein mTOR in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' here means that the relation between a protein or gene and a disease is direct and increases the likelihood of the disease. This includes cases where too much protein causes the disease, removing the gene prevents the disease, or a side effect from the protein or drug results in the disease.
'Negative_Correlation' indicates that when a protein (or drug) is present, it helps to treat or prevent a disease. Conversely, the absence of this protein or the deactivation of its gene can lead to the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[kidney lesions,DiseaseOrPhenotypicFeature]' and '[mTOR,GeneOrGeneProduct]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[kidney lesions,DiseaseOrPhenotypicFeature]' and '[mTOR,GeneOrGeneProduct]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "kidney lesions",
"type": "DiseaseOrPhenotypicFeature"
} | {
"name": "mTOR",
"type": "GeneOrGeneProduct"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
<s>[INST]<<SYS>>
Your task is to determine the relationship between a chemical SRL and a disease proteinuria in a medical text. Choose the correct relation from ['Positive_Correlation', 'Negative_Correlation', 'Association'], based only on the information provided in the text.The meanings of each relation type are as follows: 'Positive_Correlation' means there's a direct link between a chemical and a disease. This includes cases where the chemical causes the disease, higher doses of the chemical increase disease risk, the disease raises the chemical's level in the body, there's a direct positive link between the chemical's level and disease risk, or exposure to the chemical during development affects disease susceptibility later on.
'Negative_Correlation' means there's an inverse relation between a chemical substance and a disease. This includes situations where the chemical or drug is used to treat the disease, the presence of the disease lowers the level of the chemical in the body, or the chemical or drug reduces the likelihood of the disease.
'Association' is used to describe relation that don't clearly fall under categories like positive or negative correlation, or when the nature of the relation lack a clear description.
<</SYS>>
Examine the abstract and title of a medical research paper to determine the relationship between the entities '[SRL,ChemicalEntity]' and '[proteinuria,DiseaseOrPhenotypicFeature]'.
- Title of the Paper: Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers.
- Abstract of the Paper: [Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL.]
Identify how '[SRL,ChemicalEntity]' and '[proteinuria,DiseaseOrPhenotypicFeature]' are related in the text, focusing on their interactions or associations. Then, select the most accurate relationship type from ['Positive_Correlation', 'Negative_Correlation', 'Association']. [/INST]Association</s> | Conversion to sirolimus ameliorates cyclosporine-induced nephropathy in the rat: focus on serum, urine, gene, and protein renal expression biomarkers. | Protocols of conversion from cyclosporin A (CsA) to sirolimus (SRL) have been widely used in immunotherapy after transplantation to prevent CsA-induced nephropathy, but the molecular mechanisms underlying these protocols remain nuclear. This study aimed to identify the molecular pathways and putative biomarkers of CsA-to-SRL conversion in a rat model. Four animal groups (n = 6) were tested during 9 weeks: control, CsA, SRL, and conversion (CsA for 3 weeks followed by SRL for 6 weeks). Classical and emergent serum, urinary, and kidney tissue (gene and protein expression) markers were assessed. Renal lesions were analyzed in hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome stains. SRL-treated rats presented proteinuria and NGAL (serum and urinary) as the best markers of renal impairment. Short CsA treatment presented slight or even absent kidney lesions and TGF-b, NF- kb, mTOR, PCNA, TP53, KIM-1, and CTGF as relevant gene and protein changes. Prolonged CsA exposure aggravated renal damage, without clear changes on the traditional markers, but with changes in serums TGF- b and IL-7, TBARs clearance, and kidney TGF-b and mTOR. Conversion to SRL prevented CsA-induced renal damage evolution (absent/mild grade lesions), while NGAL (serum versus urine) seems to be a feasible biomarker of CsA replacement to SRL. | {
"name": "SRL",
"type": "ChemicalEntity"
} | {
"name": "proteinuria",
"type": "DiseaseOrPhenotypicFeature"
} | [
"Positive_Correlation",
"Negative_Correlation",
"Association"
] | Association |
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