Split (3)

train · 3.83k rows

data stringlengths 1.59k 10.3k
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "metformin" and a gene or protein "TNF-a". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. - Abstract of the article: Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-a and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium. Tips for Analysis: Sentences mentioning a chemical "metformin": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 3. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 4. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. 5. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. 6. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 7. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 8. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). Sentences mentioning a gene or protein "TNF-a": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Similar changes were also seen in the serum levels of TNF-a and IL-6. Sentences mentioning both entities a chemical "metformin" and a gene or protein "TNF-a": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Task: Identify the relationship between a chemical "metformin" and a gene or protein "TNF-a" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "metformin" and a gene or protein "IL-6". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. - Abstract of the article: Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-a and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium. Tips for Analysis: Sentences mentioning a chemical "metformin": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 3. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 4. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. 5. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. 6. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 7. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 8. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). Sentences mentioning a gene or protein "IL-6": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Similar changes were also seen in the serum levels of TNF-a and IL-6. Sentences mentioning both entities a chemical "metformin" and a gene or protein "IL-6": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Task: Identify the relationship between a chemical "metformin" and a gene or protein "IL-6" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "Metfromin" and a gene or protein "myeloid differentiation protein 88". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. - Abstract of the article: Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-a and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium. Tips for Analysis: Sentences mentioning a chemical "Metfromin": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 3. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 4. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. 5. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. 6. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 7. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 8. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). Sentences mentioning a gene or protein "myeloid differentiation protein 88": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Sentences mentioning both entities a chemical "Metfromin" and a gene or protein "myeloid differentiation protein 88": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Task: Identify the relationship between a chemical "Metfromin" and a gene or protein "myeloid differentiation protein 88" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "metformin" and a disease "myocardial infarction". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. - Abstract of the article: Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-a and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium. Tips for Analysis: Sentences mentioning a chemical "metformin": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 3. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 4. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. 5. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. 6. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 7. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 8. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). Sentences mentioning a disease "myocardial infarction": 1. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 2. This mechanism can be considered as a target to protect infarcted myocardium. 3. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 4. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. 5. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 6. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). Sentences mentioning both entities a chemical "metformin" and a disease "myocardial infarction": 1. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 2. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). 3. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 4. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Task: Identify the relationship between a chemical "metformin" and a disease "myocardial infarction" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "metformin" and a chemical "isoproterenol". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. - Abstract of the article: Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-a and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium. Tips for Analysis: Sentences mentioning a chemical "metformin": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 3. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 4. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. 5. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. 6. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 7. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 8. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). Sentences mentioning a chemical "isoproterenol": 1. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. 2. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 3. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. 4. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Sentences mentioning both entities a chemical "metformin" and a chemical "isoproterenol": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Task: Identify the relationship between a chemical "metformin" and a chemical "isoproterenol" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "metformin" and a disease "left ventricular dysfunction". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. - Abstract of the article: Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-a and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium. Tips for Analysis: Sentences mentioning a chemical "metformin": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 3. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 4. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. 5. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. 6. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 7. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 8. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). Sentences mentioning a disease "left ventricular dysfunction": 1. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 2. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. Sentences mentioning both entities a chemical "metformin" and a disease "left ventricular dysfunction": 1. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 2. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. Task: Identify the relationship between a chemical "metformin" and a disease "left ventricular dysfunction" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "metformin" and a gene or protein "toll-like receptor 4". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. - Abstract of the article: Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-a and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium. Tips for Analysis: Sentences mentioning a chemical "metformin": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. 3. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 4. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. 5. Phosphorylated AMPKa (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. 6. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 7. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 8. Acute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). Sentences mentioning a gene or protein "toll-like receptor 4": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 3. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 4. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. Sentences mentioning both entities a chemical "metformin" and a gene or protein "toll-like receptor 4": 1. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-a), and interleukin 6 (IL-6) in the heart tissues. 2. Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction. 3. In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. 4. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. Task: Identify the relationship between a chemical "metformin" and a gene or protein "toll-like receptor 4" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "MYF5" and a disease "diabetic nephropathy". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a gene or protein "MYF5": 1. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning a disease "diabetic nephropathy": 1. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 2. Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning both entities a gene or protein "MYF5" and a disease "diabetic nephropathy": 1. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Task: Identify the relationship between a gene or protein "MYF5" and a disease "diabetic nephropathy" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "MYF5" and a chemical "glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a gene or protein "MYF5": 1. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning a chemical "glucose": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 4. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 5. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 6. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 7. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. Sentences mentioning both entities a gene or protein "MYF5" and a chemical "glucose": 1. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Task: Identify the relationship between a gene or protein "MYF5" and a chemical "glucose" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "MEF2C" and a disease "diabetic nephropathy". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a gene or protein "MEF2C": 1. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning a disease "diabetic nephropathy": 1. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 2. Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning both entities a gene or protein "MEF2C" and a disease "diabetic nephropathy": 1. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Task: Identify the relationship between a gene or protein "MEF2C" and a disease "diabetic nephropathy" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "myocyte-specific enhancer factor 2C" and a chemical "glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a gene or protein "myocyte-specific enhancer factor 2C": 1. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning a chemical "glucose": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 4. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 5. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 6. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 7. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. Sentences mentioning both entities a gene or protein "myocyte-specific enhancer factor 2C" and a chemical "glucose": 1. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Task: Identify the relationship between a gene or protein "myocyte-specific enhancer factor 2C" and a chemical "glucose" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "serine-threonine liver kinase B1" and a chemical "glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a gene or protein "serine-threonine liver kinase B1": 1. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Sentences mentioning a chemical "glucose": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 4. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 5. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 6. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 7. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. Sentences mentioning both entities a gene or protein "serine-threonine liver kinase B1" and a chemical "glucose": 1. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Task: Identify the relationship between a gene or protein "serine-threonine liver kinase B1" and a chemical "glucose" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "AMPK" and a chemical "glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a gene or protein "AMPK": 1. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Sentences mentioning a chemical "glucose": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 4. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 5. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 6. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 7. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. Sentences mentioning both entities a gene or protein "AMPK" and a chemical "glucose": 1. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Task: Identify the relationship between a gene or protein "AMPK" and a chemical "glucose" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PGC-1a" and a disease "diabetic nephropathy". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a gene or protein "PGC-1a": 1. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 2. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning a disease "diabetic nephropathy": 1. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 2. Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning both entities a gene or protein "PGC-1a" and a disease "diabetic nephropathy": 1. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Task: Identify the relationship between a gene or protein "PGC-1a" and a disease "diabetic nephropathy" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "peroxisome proliferator-activated receptor-g coactivator 1a" and a chemical "glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a gene or protein "peroxisome proliferator-activated receptor-g coactivator 1a": 1. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 2. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning a chemical "glucose": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 4. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 5. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 6. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 7. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. Sentences mentioning both entities a gene or protein "peroxisome proliferator-activated receptor-g coactivator 1a" and a chemical "glucose": 1. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 2. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Task: Identify the relationship between a gene or protein "peroxisome proliferator-activated receptor-g coactivator 1a" and a chemical "glucose" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "glucose" and a disease "diabetic nephropathy". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a chemical "glucose": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 4. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 5. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 6. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 7. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. Sentences mentioning a disease "diabetic nephropathy": 1. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 2. Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. 3. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. Sentences mentioning both entities a chemical "glucose" and a disease "diabetic nephropathy": 1. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Task: Identify the relationship between a chemical "glucose" and a disease "diabetic nephropathy" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "glucose" and a disease "lactic acidosis". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. - Abstract of the article: Podocytes play a key role in diabetic nephropathy pathogenesis, but alteration of their metabolism remains unknown in human kidney. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. Accordingly, a reduced expression of MEF2C, MYF5, and PGC-1a was found in kidney tissue sections that were obtained from patients with diabetic nephropathy. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. Tips for Analysis: Sentences mentioning a chemical "glucose": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. 2. Focused transcriptomics revealed that myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expression was inhibited by high glucose levels, and endoribonuclease-prepared small interfering RNA-mediated combined inhibition of those transcription factors phenocopied the glycolytic shift that was observed in high glucose conditions. 3. These findings obtained in human samples demonstrate that MEF2C-MYF5-dependent bioenergetic dedifferentiation occurs in podocytes that are confronted with a high-glucose milieu.-Imasawa, T., Obre, E., Bellance, N., Lavie, J., Imasawa, T., Rigothier, C., Delmas, Y., Combe, C., Lacombe, D., Benard, G., Claverol, S., Bonneu, M., Rossignol, R. 4. In 5 mM glucose medium, we observed a stepwise activation of oxidative metabolism during cell differentiation that was characterized by peroxisome proliferator-activated receptor-g coactivator 1a (PGC-1a)-dependent stimulation of mitochondrial biogenesis and function, with concomitant reduction of the glycolytic enzyme content. 5. High glucose repatterns human podocyte energy metabolism during differentiation and diabetic nephropathy. 6. Expression of the master regulators of oxidative metabolism transcription factor A mitochondrial, PGC-1a, AMPK, and serine-threonine liver kinase B1 was altered by high glucose, as well as their downstream signaling networks. 7. By using a conditionally differentiating human podocyte cell line, we addressed the functional and molecular changes in podocyte energetics during in vitro development or under high glucose conditions. Sentences mentioning a disease "lactic acidosis": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Sentences mentioning both entities a chemical "glucose" and a disease "lactic acidosis": 1. Conversely, when podocytes were cultured in high glucose (20 mM), stepwise oxidative phosphorylation biogenesis was aborted, and a glycolytic switch occurred, with consecutive lactic acidosis. Task: Identify the relationship between a chemical "glucose" and a disease "lactic acidosis" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "EPZ015666" and a gene or protein "AKT". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a chemical "EPZ015666": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 3. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning a gene or protein "AKT": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 2. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning both entities a chemical "EPZ015666" and a gene or protein "AKT": 1. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Task: Identify the relationship between a chemical "EPZ015666" and a gene or protein "AKT" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "EPZ015666" and a gene or protein "p65". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a chemical "EPZ015666": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 3. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning a gene or protein "p65": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 2. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning both entities a chemical "EPZ015666" and a gene or protein "p65": 1. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Task: Identify the relationship between a chemical "EPZ015666" and a gene or protein "p65" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "EPZ015666" and a gene or protein "IkBa". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a chemical "EPZ015666": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 3. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning a gene or protein "IkBa": 1. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning both entities a chemical "EPZ015666" and a gene or protein "IkBa": 1. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Task: Identify the relationship between a chemical "EPZ015666" and a gene or protein "IkBa" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "EPZ015666" and a gene or protein "IkB kinaseb". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a chemical "EPZ015666": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 3. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning a gene or protein "IkB kinaseb": 1. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning both entities a chemical "EPZ015666" and a gene or protein "IkB kinaseb": 1. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Task: Identify the relationship between a chemical "EPZ015666" and a gene or protein "IkB kinaseb" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "EPZ015666" and a gene or protein "IL-8". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a chemical "EPZ015666": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 3. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning a gene or protein "IL-8": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Sentences mentioning both entities a chemical "EPZ015666" and a gene or protein "IL-8": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Task: Identify the relationship between a chemical "EPZ015666" and a gene or protein "IL-8" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "EPZ015666" and a gene or protein "IL-6". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a chemical "EPZ015666": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 3. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning a gene or protein "IL-6": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Sentences mentioning both entities a chemical "EPZ015666" and a gene or protein "IL-6": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Task: Identify the relationship between a chemical "EPZ015666" and a gene or protein "IL-6" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "EPZ015666" and a gene or protein "PRMT5". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a chemical "EPZ015666": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 3. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning a gene or protein "PRMT5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning both entities a chemical "EPZ015666" and a gene or protein "PRMT5": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Task: Identify the relationship between a chemical "EPZ015666" and a gene or protein "PRMT5" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "EPZ015666" and a disease "RA". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a chemical "EPZ015666": 1. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 2. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 3. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning a disease "RA": 1. FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). 2. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning both entities a chemical "EPZ015666" and a disease "RA": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Task: Identify the relationship between a chemical "EPZ015666" and a disease "RA" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PRMT5" and a disease "synovial inflammation". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a gene or protein "PRMT5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a disease "synovial inflammation": 1. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Sentences mentioning both entities a gene or protein "PRMT5" and a disease "synovial inflammation": 1. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Task: Identify the relationship between a gene or protein "PRMT5" and a disease "synovial inflammation" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "protein arginine methyltransferase 5" and a disease "inflammation". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a gene or protein "protein arginine methyltransferase 5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a disease "inflammation": 1. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). 2. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 3. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. Sentences mentioning both entities a gene or protein "protein arginine methyltransferase 5" and a disease "inflammation": 1. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). 2. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 3. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. Task: Identify the relationship between a gene or protein "protein arginine methyltransferase 5" and a disease "inflammation" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PRMT5" and a gene or protein "AKT". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a gene or protein "PRMT5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "AKT": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 2. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning both entities a gene or protein "PRMT5" and a gene or protein "AKT": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Task: Identify the relationship between a gene or protein "PRMT5" and a gene or protein "AKT" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PRMT5" and a gene or protein "p65". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a gene or protein "PRMT5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "p65": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 2. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning both entities a gene or protein "PRMT5" and a gene or protein "p65": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Task: Identify the relationship between a gene or protein "PRMT5" and a gene or protein "p65" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PRMT5" and a gene or protein "IL-8". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a gene or protein "PRMT5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "IL-8": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Sentences mentioning both entities a gene or protein "PRMT5" and a gene or protein "IL-8": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Task: Identify the relationship between a gene or protein "PRMT5" and a gene or protein "IL-8" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PRMT5" and a gene or protein "IL-6". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a gene or protein "PRMT5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "IL-6": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Sentences mentioning both entities a gene or protein "PRMT5" and a gene or protein "IL-6": 1. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. Task: Identify the relationship between a gene or protein "PRMT5" and a gene or protein "IL-6" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PRMT5" and a gene or protein "TNF-a". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a gene or protein "PRMT5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "TNF-a": 1. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Sentences mentioning both entities a gene or protein "PRMT5" and a gene or protein "TNF-a": 1. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Task: Identify the relationship between a gene or protein "PRMT5" and a gene or protein "TNF-a" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PRMT5" and a gene or protein "IL-1b". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a gene or protein "PRMT5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "IL-1b": 1. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Sentences mentioning both entities a gene or protein "PRMT5" and a gene or protein "IL-1b": 1. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Task: Identify the relationship between a gene or protein "PRMT5" and a gene or protein "IL-1b" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "RA" and a gene or protein "AKT". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a disease "RA": 1. FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). 2. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "AKT": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 2. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning both entities a disease "RA" and a gene or protein "AKT": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Task: Identify the relationship between a disease "RA" and a gene or protein "AKT" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "RA" and a gene or protein "NF-kB". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a disease "RA": 1. FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). 2. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "NF-kB": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 2. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. Sentences mentioning both entities a disease "RA" and a gene or protein "NF-kB": 1. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Task: Identify the relationship between a disease "RA" and a gene or protein "NF-kB" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "rheumatoid arthritis" and a gene or protein "protein arginine methyltransferase 5". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. - Abstract of the article: To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. The standard of protein was measured by Western blot or immunofluorescence. The excretion and genetic expression of inflammatory factors were, respectively, estimated by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Migration and invasion in vitro were detected by Boyden chamber assay. FLSs proliferation was detected by BrdU incorporation. Increased PRMT5 was discovered in STs and FLSs from patients with RA. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. Furthermore, EPZ015666 restrained the phosphorylation of IkB kinaseb and IkBa, as well as nucleus transsituation of p65 as well as AKT in FLSs. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. Tips for Analysis: Sentences mentioning a disease "rheumatoid arthritis": 1. FLSs were separated from synovial tissues (STs) from patients with RA and osteoarthritis (OA). 2. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning a gene or protein "protein arginine methyltransferase 5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. An inhibitor of PRMT5 (EPZ015666) and short interference RNA (siRNA) against PRMT5 were used to inhibit PRMT5 expression. 3. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 4. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 5. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 6. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 7. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 8. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 9. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Sentences mentioning both entities a disease "rheumatoid arthritis" and a gene or protein "protein arginine methyltransferase 5": 1. Increased PRMT5 was discovered in STs and FLSs from patients with RA. 2. In RA FLSs, the level of PRMT5 was up-regulated by stimulation with IL-1b and TNF-a. 3. Role of protein arginine methyltransferase 5 in inflammation and migration of fibroblast-like synoviocytes in rheumatoid arthritis. 4. Inhibition of PRMT5 by EPZ015666 and siRNA-mediated knockdown reduced IL-6 and IL-8 production, and proliferation of RA FLSs. 5. PRMT5 regulated the production of inflammatory factors, cell proliferation, migration and invasion of RA FLS, which was mediated by the NF-kB and AKT pathways. 6. Our data suggested that targeting PRMT5 to prevent synovial inflammation and destruction might be a promising therapy for RA. 7. In addition, inhibition of PRMT5 decreased in vitro migration and invasion of RA FLSs. 8. To probe the role of protein arginine methyltransferase 5 (PRMT5) in regulating inflammation, cell proliferation, migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA). Task: Identify the relationship between a disease "rheumatoid arthritis" and a gene or protein "protein arginine methyltransferase 5" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "EGF" and a gene or protein "metalloproteinase". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a gene or protein "EGF": 1. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. Sentences mentioning a gene or protein "metalloproteinase": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 5. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. 6. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. 7. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 8. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 9. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. 10. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 11. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. 12. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 13. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning both entities a gene or protein "EGF" and a gene or protein "metalloproteinase": 1. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. Task: Identify the relationship between a gene or protein "EGF" and a gene or protein "metalloproteinase" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "batimastat" and a gene or protein "EGFR". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a chemical "batimastat": 1. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Sentences mentioning a gene or protein "EGFR": 1. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 2. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Sentences mentioning both entities a chemical "batimastat" and a gene or protein "EGFR": 1. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Task: Identify the relationship between a chemical "batimastat" and a gene or protein "EGFR" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "batimastat" and a gene or protein "metalloproteinase". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a chemical "batimastat": 1. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Sentences mentioning a gene or protein "metalloproteinase": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 5. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. 6. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. 7. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 8. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 9. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. 10. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 11. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. 12. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 13. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning both entities a chemical "batimastat" and a gene or protein "metalloproteinase": 1. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Task: Identify the relationship between a chemical "batimastat" and a gene or protein "metalloproteinase" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "claudin" and a disease "breast cancer". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a gene or protein "claudin": 1. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 2. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 3. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Sentences mentioning a disease "breast cancer": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 3. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 4. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 5. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 6. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning both entities a gene or protein "claudin" and a disease "breast cancer": 1. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 2. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 3. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Task: Identify the relationship between a gene or protein "claudin" and a disease "breast cancer" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "ADAM12" and a gene or protein "estrogen receptor". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a gene or protein "ADAM12": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 5. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. 6. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. 7. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 8. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 9. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. 10. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 11. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. 12. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 13. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning a gene or protein "estrogen receptor": 1. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning both entities a gene or protein "ADAM12" and a gene or protein "estrogen receptor": 1. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Task: Identify the relationship between a gene or protein "ADAM12" and a gene or protein "estrogen receptor" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "ADAM12" and a gene or protein "Epidermal Growth Factor Receptor". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a gene or protein "ADAM12": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 5. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. 6. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. 7. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 8. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 9. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. 10. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 11. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. 12. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 13. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning a gene or protein "Epidermal Growth Factor Receptor": 1. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 2. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Sentences mentioning both entities a gene or protein "ADAM12" and a gene or protein "Epidermal Growth Factor Receptor": 1. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 2. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Task: Identify the relationship between a gene or protein "ADAM12" and a gene or protein "Epidermal Growth Factor Receptor" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "ADAM12" and a disease "tumors". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a gene or protein "ADAM12": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 5. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. 6. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. 7. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 8. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 9. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. 10. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 11. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. 12. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 13. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning a disease "tumors": 1. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 2. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. 3. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 4. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning both entities a gene or protein "ADAM12" and a disease "tumors": 1. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 2. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 3. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Task: Identify the relationship between a gene or protein "ADAM12" and a disease "tumors" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "ADAM12" and a disease "breast cancer". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a gene or protein "ADAM12": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 5. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. 6. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. 7. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 8. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 9. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. 10. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 11. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. 12. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 13. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning a disease "breast cancer": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 3. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 4. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 5. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 6. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning both entities a gene or protein "ADAM12" and a disease "breast cancer": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 3. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 4. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 5. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 6. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Task: Identify the relationship between a gene or protein "ADAM12" and a disease "breast cancer" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "ADAM12" and a gene or protein "claudin". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. - Abstract of the article: BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Cell characteristics commonly associated with the CSC phenotype in vitro (cell migration, invasion, anoikis resistance, mammosphere formation, ALDH activity, and expression of the CD44 and CD24 cell surface markers) and in vivo (tumor formation in mice using limiting dilution transplantation assays) were evaluated. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. Tips for Analysis: Sentences mentioning a gene or protein "ADAM12": 1. It is currently unknown whether ADAM12 plays an active role in promoting the CSC phenotype in breast cancer cells. 2. ADAM12 knockdown also diminished ALDEFLUOR(+) and CD44(hi)/CD24(-/lo) CSC-enriched populations in vitro and reduced tumorigenesis in mice in vivo. 3. Consequently, ADAM12 knockdown lowered the basal activation level of EGFR, and this effect was abolished by batimastat, a metalloproteinase inhibitor. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. 5. RESULTS: We found that sorted SUM159PT cell populations with high ADAM12 levels had elevated expression of CSC markers and an increased ability to form mammospheres. 6. ADAM12 knockdown reduced cell migration and invasion, decreased anoikis resistance, and compromised mammosphere formation. 7. RNA sequencing identified a significant overlap between ADAM12- and Epidermal Growth Factor Receptor (EGFR)-regulated genes. 8. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 9. RNA sequencing was performed to identify global gene expression changes after ADAM12 knockdown. 10. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 11. Furthermore, incubation of cells with exogenously added EGF prevented the downregulation of CD44(hi)/CD24(-/lo) cell population by ADAM12 knockdown. 12. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 13. BACKGROUND: ADAM12 is upregulated in human breast cancers and is a predictor of chemoresistance in estrogen receptor-negative tumors. Sentences mentioning a gene or protein "claudin": 1. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 2. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 3. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Sentences mentioning both entities a gene or protein "ADAM12" and a gene or protein "claudin": 1. Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancer. 2. ADAM12 is induced during epithelial-to-mesenchymal transition, a feature associated with claudin-low breast tumors, which are enriched in cancer stem cell (CSC) markers. 3. CONCLUSIONS: These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR pathway. 4. METHODS: ADAM12 expression was downregulated in representative claudin-low breast cancer cell lines, SUM159PT and Hs578T, using siRNA transfection or inducible shRNA expression. Task: Identify the relationship between a gene or protein "ADAM12" and a gene or protein "claudin" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Bind', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "T" and a chemical "human chorionic gonadotropin". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. - Abstract of the article: The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. A patient of Chinese origin with ambiguous genitalia at 14 months, a 46,XY karyotype, and normal T secretion under human chorionic gonadotropin (hCG) stimulation underwent a gonadectomy at 20 months. Exons 1-8 of the AR gene and exons 1-5 of the SRD5A2 gene were sequenced from peripheral blood DNA. AR gene coding sequences were normal. SRD5A2 gene analysis revealed 2 consecutive mutations in exon 4, each located in a different allele: 1) a T nucleotide deletion, which predicts a frameshift mutation from codon 219, and 2) a missense mutation at codon 227, where the substitution of guanine (CGA) by adenine (CAA) predicts a glutamine replacement of arginine (R227Q). Testes located in the inguinal canal showed a normal morphology for age. The patient was a compound heterozygote for SRD5A2 mutations, carrying 2 mutations in exon 4. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Testis morphology showed that, during early infancy, the 5-alpha-reductase enzyme deficiency may not have affected interstitial or tubular development. Tips for Analysis: Sentences mentioning a chemical "T": 1. The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. 2. A patient of Chinese origin with ambiguous genitalia at 14 months, a 46,XY karyotype, and normal T secretion under human chorionic gonadotropin (hCG) stimulation underwent a gonadectomy at 20 months. Sentences mentioning a chemical "human chorionic gonadotropin": 1. A patient of Chinese origin with ambiguous genitalia at 14 months, a 46,XY karyotype, and normal T secretion under human chorionic gonadotropin (hCG) stimulation underwent a gonadectomy at 20 months. Sentences mentioning both entities a chemical "T" and a chemical "human chorionic gonadotropin": 1. A patient of Chinese origin with ambiguous genitalia at 14 months, a 46,XY karyotype, and normal T secretion under human chorionic gonadotropin (hCG) stimulation underwent a gonadectomy at 20 months. Task: Identify the relationship between a chemical "T" and a chemical "human chorionic gonadotropin" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "Tdel219" and a disease "MPH". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. - Abstract of the article: The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. A patient of Chinese origin with ambiguous genitalia at 14 months, a 46,XY karyotype, and normal T secretion under human chorionic gonadotropin (hCG) stimulation underwent a gonadectomy at 20 months. Exons 1-8 of the AR gene and exons 1-5 of the SRD5A2 gene were sequenced from peripheral blood DNA. AR gene coding sequences were normal. SRD5A2 gene analysis revealed 2 consecutive mutations in exon 4, each located in a different allele: 1) a T nucleotide deletion, which predicts a frameshift mutation from codon 219, and 2) a missense mutation at codon 227, where the substitution of guanine (CGA) by adenine (CAA) predicts a glutamine replacement of arginine (R227Q). Testes located in the inguinal canal showed a normal morphology for age. The patient was a compound heterozygote for SRD5A2 mutations, carrying 2 mutations in exon 4. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Testis morphology showed that, during early infancy, the 5-alpha-reductase enzyme deficiency may not have affected interstitial or tubular development. Tips for Analysis: Sentences mentioning a variant "Tdel219": 1. SRD5A2 gene analysis revealed 2 consecutive mutations in exon 4, each located in a different allele: 1) a T nucleotide deletion, which predicts a frameshift mutation from codon 219, and 2) a missense mutation at codon 227, where the substitution of guanine (CGA) by adenine (CAA) predicts a glutamine replacement of arginine (R227Q). 2. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Sentences mentioning a disease "MPH": 1. The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. 2. Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. 3. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Sentences mentioning both entities a variant "Tdel219" and a disease "MPH": 1. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Task: Identify the relationship between a variant "Tdel219" and a disease "MPH" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "R227Q" and a disease "MPH". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. - Abstract of the article: The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. A patient of Chinese origin with ambiguous genitalia at 14 months, a 46,XY karyotype, and normal T secretion under human chorionic gonadotropin (hCG) stimulation underwent a gonadectomy at 20 months. Exons 1-8 of the AR gene and exons 1-5 of the SRD5A2 gene were sequenced from peripheral blood DNA. AR gene coding sequences were normal. SRD5A2 gene analysis revealed 2 consecutive mutations in exon 4, each located in a different allele: 1) a T nucleotide deletion, which predicts a frameshift mutation from codon 219, and 2) a missense mutation at codon 227, where the substitution of guanine (CGA) by adenine (CAA) predicts a glutamine replacement of arginine (R227Q). Testes located in the inguinal canal showed a normal morphology for age. The patient was a compound heterozygote for SRD5A2 mutations, carrying 2 mutations in exon 4. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Testis morphology showed that, during early infancy, the 5-alpha-reductase enzyme deficiency may not have affected interstitial or tubular development. Tips for Analysis: Sentences mentioning a variant "R227Q": 1. SRD5A2 gene analysis revealed 2 consecutive mutations in exon 4, each located in a different allele: 1) a T nucleotide deletion, which predicts a frameshift mutation from codon 219, and 2) a missense mutation at codon 227, where the substitution of guanine (CGA) by adenine (CAA) predicts a glutamine replacement of arginine (R227Q). 2. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Sentences mentioning a disease "MPH": 1. The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. 2. Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. 3. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Sentences mentioning both entities a variant "R227Q" and a disease "MPH": 1. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Task: Identify the relationship between a variant "R227Q" and a disease "MPH" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "SRD5A2" and a disease "male pseudohermaphrodite". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. - Abstract of the article: The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. A patient of Chinese origin with ambiguous genitalia at 14 months, a 46,XY karyotype, and normal T secretion under human chorionic gonadotropin (hCG) stimulation underwent a gonadectomy at 20 months. Exons 1-8 of the AR gene and exons 1-5 of the SRD5A2 gene were sequenced from peripheral blood DNA. AR gene coding sequences were normal. SRD5A2 gene analysis revealed 2 consecutive mutations in exon 4, each located in a different allele: 1) a T nucleotide deletion, which predicts a frameshift mutation from codon 219, and 2) a missense mutation at codon 227, where the substitution of guanine (CGA) by adenine (CAA) predicts a glutamine replacement of arginine (R227Q). Testes located in the inguinal canal showed a normal morphology for age. The patient was a compound heterozygote for SRD5A2 mutations, carrying 2 mutations in exon 4. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Testis morphology showed that, during early infancy, the 5-alpha-reductase enzyme deficiency may not have affected interstitial or tubular development. Tips for Analysis: Sentences mentioning a gene or protein "SRD5A2": 1. SRD5A2 gene analysis revealed 2 consecutive mutations in exon 4, each located in a different allele: 1) a T nucleotide deletion, which predicts a frameshift mutation from codon 219, and 2) a missense mutation at codon 227, where the substitution of guanine (CGA) by adenine (CAA) predicts a glutamine replacement of arginine (R227Q). 2. Exons 1-8 of the AR gene and exons 1-5 of the SRD5A2 gene were sequenced from peripheral blood DNA. 3. Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. 4. Testis morphology showed that, during early infancy, the 5-alpha-reductase enzyme deficiency may not have affected interstitial or tubular development. 5. The patient was a compound heterozygote for SRD5A2 mutations, carrying 2 mutations in exon 4. 6. The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. Sentences mentioning a disease "male pseudohermaphrodite": 1. The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. 2. Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. 3. The patient showed an R227Q mutation that has been described in an Asian population and MPH patients, along with a novel frameshift mutation, Tdel219. Sentences mentioning both entities a gene or protein "SRD5A2" and a disease "male pseudohermaphrodite": 1. The goal of this study was to perform 5-alpha-reductase type 2 gene (SRD5A2) analysis in a male pseudohermaphrodite (MPH) patient with normal testosterone (T) production and normal androgen receptor (AR) gene coding sequences. 2. Compound heterozygous mutations in the SRD5A2 gene exon 4 in a male pseudohermaphrodite patient of Chinese origin. Task: Identify the relationship between a gene or protein "SRD5A2" and a disease "male pseudohermaphrodite" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "arginine 555-to-tryptophan" and a disease "GCD type I". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a variant "arginine 555-to-tryptophan": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. 3. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. Sentences mentioning a disease "GCD type I": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Sentences mentioning both entities a variant "arginine 555-to-tryptophan" and a disease "GCD type I": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Task: Identify the relationship between a variant "arginine 555-to-tryptophan" and a disease "GCD type I" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "Arg555Trp" and a disease "GCD". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a variant "Arg555Trp": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. 3. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. Sentences mentioning a disease "GCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 3. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 4. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. 5. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 6. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning both entities a variant "Arg555Trp" and a disease "GCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Task: Identify the relationship between a variant "Arg555Trp" and a disease "GCD" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "GCD type I" and a variant "leucine 269 to phenylalanine". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "GCD type I": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Sentences mentioning a variant "leucine 269 to phenylalanine": 1. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. Sentences mentioning both entities a disease "GCD type I" and a variant "leucine 269 to phenylalanine": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "GCD type I" and a variant "leucine 269 to phenylalanine" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "GCD type I" and a gene or protein "TGFBI". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "GCD type I": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Sentences mentioning a gene or protein "TGFBI": 1. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. 2. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. 3. TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. Sentences mentioning both entities a disease "GCD type I" and a gene or protein "TGFBI": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "GCD type I" and a gene or protein "TGFBI" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "Reis-Bucklers dystrophy" and a variant "Arg124Leu". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "Reis-Bucklers dystrophy": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Sentences mentioning a variant "Arg124Leu": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Sentences mentioning both entities a disease "Reis-Bucklers dystrophy" and a variant "Arg124Leu": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Task: Identify the relationship between a disease "Reis-Bucklers dystrophy" and a variant "Arg124Leu" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "GCD type III" and a gene or protein "TGFBI". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "GCD type III": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Sentences mentioning a gene or protein "TGFBI": 1. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. 2. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. 3. TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. Sentences mentioning both entities a disease "GCD type III" and a gene or protein "TGFBI": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "GCD type III" and a gene or protein "TGFBI" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "GCD" and a variant "Leu269Phe". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "GCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 3. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 4. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. 5. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 6. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning a variant "Leu269Phe": 1. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. Sentences mentioning both entities a disease "GCD" and a variant "Leu269Phe": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "GCD" and a variant "Leu269Phe" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "GCD" and a variant "Arg124Leu". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "GCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 3. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 4. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. 5. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 6. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning a variant "Arg124Leu": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Sentences mentioning both entities a disease "GCD" and a variant "Arg124Leu": 1. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Task: Identify the relationship between a disease "GCD" and a variant "Arg124Leu" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "LCD" and a variant "His626Arg". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "LCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. 3. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 4. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 5. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 6. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 7. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning a variant "His626Arg": 1. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Sentences mentioning both entities a disease "LCD" and a variant "His626Arg": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "LCD" and a variant "His626Arg" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "LCD" and a variant "Arg124Cys". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "LCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. 3. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 4. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 5. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 6. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 7. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning a variant "Arg124Cys": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Sentences mentioning both entities a disease "LCD" and a variant "Arg124Cys": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. Task: Identify the relationship between a disease "LCD" and a variant "Arg124Cys" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "LCD" and a variant "Val624-Val625del". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "LCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. 3. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 4. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 5. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 6. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 7. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning a variant "Val624-Val625del": 1. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. Sentences mentioning both entities a disease "LCD" and a variant "Val624-Val625del": 1. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. Task: Identify the relationship between a disease "LCD" and a variant "Val624-Val625del" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "LCD" and a variant "valine-539-aspartic acid". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "LCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. 3. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 4. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 5. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 6. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 7. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning a variant "valine-539-aspartic acid": 1. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. Sentences mentioning both entities a disease "LCD" and a variant "valine-539-aspartic acid": 1. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. Task: Identify the relationship between a disease "LCD" and a variant "valine-539-aspartic acid" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "LCD" and a variant "glycine-594-valine". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a disease "LCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. 3. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 4. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 5. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 6. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 7. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning a variant "glycine-594-valine": 1. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. Sentences mentioning both entities a disease "LCD" and a variant "glycine-594-valine": 1. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. Task: Identify the relationship between a disease "LCD" and a variant "glycine-594-valine" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "TGFBI" and a disease "GCD". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a gene or protein "TGFBI": 1. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. 2. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. 3. TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. Sentences mentioning a disease "GCD": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 3. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 4. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. 5. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 6. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning both entities a gene or protein "TGFBI" and a disease "GCD": 1. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Task: Identify the relationship between a gene or protein "TGFBI" and a disease "GCD" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "TGFBI" and a disease "lattice corneal dystrophy". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. - Abstract of the article: PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. PCR products were screened by the method of single-strand conformation polymorphism followed by sequencing. Mutations were confirmed by screening at least 100 unrelated normal control subjects. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. In addition, mutation of arginine 124-to-cysteine (Arg124Cys) was found in 8 of 18 patients and histidine 626-to-arginine (His626Arg) in 2 of 18 patients. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. In GCD, 18 patients with GCD type I had a mutation of arginine 555-to-tryptophan (Arg555Trp) and 1 patient with GCD type III (Reis-Bucklers dystrophy), had the Arg124Leu mutation. Seven novel single-nucleotide polymorphisms (SNPs) were also found, of which a change of leucine 269 to phenylalanine (Leu269Phe) was found in 12 of 18 patients with the Arg555Trp mutation. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. The novel mutations identified in this study are associated with distinct phenotypes. Tips for Analysis: Sentences mentioning a gene or protein "TGFBI": 1. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. 2. Exons and flanking intron sequences of the TGFBI gene were amplified by PCR with specific primers. 3. TGFBI gene mutations causing lattice and granular corneal dystrophies in Indian patients. Sentences mentioning a disease "lattice corneal dystrophy": 1. CONCLUSIONS: Arg124Cys and Arg555Trp appear to be the predominant mutations causing LCD and GCD, respectively, in the population studied. 2. Atypical clinical features for LCD were noted in patients with the Gly594Val and Val624-Val625del mutations. 3. The diagnosis of LCD or GCD was made on the basis of clinical and/or histopathological evaluation. 4. In LCD, three novel heterozygous mutations found were glycine-594-valine (Gly594Val) in 2 of 18 patients, valine-539-aspartic acid (Val539Asp) in 1 patient, and deletion of valine 624, valine 625 (Val624-Val625del) in 1 patient. 5. METHODS: Thirty-seven unrelated patients were studied, 18 with LCD and 19 with GCD. 6. RESULTS: Mutations were identified in 14 of 18 patients with LCD and in all 19 patients with GCD. 7. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Sentences mentioning both entities a gene or protein "TGFBI" and a disease "lattice corneal dystrophy": 1. PURPOSE: To identify mutations in the TGFBI gene in Indian patients with lattice corneal dystrophy (LCD) or granular corneal dystrophy (GCD) and to look for genotype-phenotype correlations. Task: Identify the relationship between a gene or protein "TGFBI" and a disease "lattice corneal dystrophy" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "c.461_462delAG" and a disease "XLMR". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a variant "c.461_462delAG": 1. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Sentences mentioning a disease "XLMR": 1. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. 2. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. 3. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. 4. X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Sentences mentioning both entities a variant "c.461_462delAG" and a disease "XLMR": There is no sentence that contains both these two entities. Task: Identify the relationship between a variant "c.461_462delAG" and a disease "XLMR" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "c.461_462delAG" and a disease "Hamel cerebropalatocardiac syndrome". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a variant "c.461_462delAG": 1. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Sentences mentioning a disease "Hamel cerebropalatocardiac syndrome": 1. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Sentences mentioning both entities a variant "c.461_462delAG" and a disease "Hamel cerebropalatocardiac syndrome": There is no sentence that contains both these two entities. Task: Identify the relationship between a variant "c.461_462delAG" and a disease "Hamel cerebropalatocardiac syndrome" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "BCOR" and a disease "Lenz microphthalmia syndrome". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a gene or protein "BCOR": 1. However, no mutation in the BCOR gene was found in both patients. 2. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. 3. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. Sentences mentioning a disease "Lenz microphthalmia syndrome": 1. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. Sentences mentioning both entities a gene or protein "BCOR" and a disease "Lenz microphthalmia syndrome": 1. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. Task: Identify the relationship between a gene or protein "BCOR" and a disease "Lenz microphthalmia syndrome" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "microphthalmia" and a variant "c.461_462delAG". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a disease "microphthalmia": 1. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 2. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. 3. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Sentences mentioning a variant "c.461_462delAG": 1. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Sentences mentioning both entities a disease "microphthalmia" and a variant "c.461_462delAG": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "microphthalmia" and a variant "c.461_462delAG" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PQBP1" and a disease "XLMR". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a gene or protein "PQBP1": 1. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. 2. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 3. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. 4. X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Sentences mentioning a disease "XLMR": 1. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. 2. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. 3. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. 4. X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Sentences mentioning both entities a gene or protein "PQBP1" and a disease "XLMR": 1. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. 2. X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Task: Identify the relationship between a gene or protein "PQBP1" and a disease "XLMR" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PQBP1" and a disease "Hamel cerebropalatocardiac syndrome". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a gene or protein "PQBP1": 1. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. 2. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 3. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. 4. X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Sentences mentioning a disease "Hamel cerebropalatocardiac syndrome": 1. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Sentences mentioning both entities a gene or protein "PQBP1" and a disease "Hamel cerebropalatocardiac syndrome": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "PQBP1" and a disease "Hamel cerebropalatocardiac syndrome" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PQBP1" and a disease "mental retardation". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a gene or protein "PQBP1": 1. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. 2. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 3. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. 4. X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Sentences mentioning a disease "mental retardation": 1. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 2. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. Sentences mentioning both entities a gene or protein "PQBP1" and a disease "mental retardation": 1. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. Task: Identify the relationship between a gene or protein "PQBP1" and a disease "mental retardation" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PQBP1" and a disease "microcephaly". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a gene or protein "PQBP1": 1. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. 2. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 3. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. 4. X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Sentences mentioning a disease "microcephaly": 1. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 2. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. Sentences mentioning both entities a gene or protein "PQBP1" and a disease "microcephaly": 1. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. Task: Identify the relationship between a gene or protein "PQBP1" and a disease "microcephaly" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "PQBP1" and a disease "microphthalmia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. - Abstract of the article: X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. By multipoint linkage analysis with markers spanning the entire X-chromosome we mapped the disease locus to a 28-Mb interval between Xp11.4 and Xq12, including the BCOR gene. A missense mutation in BCOR was described in a family with Lenz microphthalmia syndrome, a phenotype showing substantial overlapping features with that described in the two cousins. However, no mutation in the BCOR gene was found in both patients. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. Notably, the same mutation is associated with the Hamel cerebropalatocardiac syndrome, another form of S-XLMR. Haplotype analysis suggests a germline mosaicism of the 2-bp deletion in the maternal grandmother of both affected individuals. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Tips for Analysis: Sentences mentioning a gene or protein "PQBP1": 1. Subsequent mutation analysis of PQBP1, located within the delineated linkage interval in Xp11.23, revealed a 2-bp deletion, c.461_462delAG, that cosegregated with the disease. 2. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 3. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. 4. X-linked mental retardation has been traditionally divided into syndromic (S-XLMR) and non-syndromic forms (NS-XLMR), although the borderlines between these phenotypes begin to vanish and mutations in a single gene, for example PQBP1, can cause S-XLMR as well as NS-XLMR. Sentences mentioning a disease "microphthalmia": 1. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 2. Here, we report two maternal cousins with an apparently X-linked phenotype of mental retardation (MR), microphthalmia, choroid coloboma, microcephaly, renal hypoplasia, and spastic paraplegia. 3. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Sentences mentioning both entities a gene or protein "PQBP1" and a disease "microphthalmia": 1. A two base pair deletion in the PQBP1 gene is associated with microphthalmia, microcephaly, and mental retardation. 2. In summary, our findings demonstrate for the first time that mutations in PQBP1 are associated with an S-XLMR phenotype including microphthalmia, thereby further extending the clinical spectrum of phenotypes associated with PQBP1 mutations. Task: Identify the relationship between a gene or protein "PQBP1" and a disease "microphthalmia" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "levofloxacin" and a chemical "warfarin". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Interaction between warfarin and levofloxacin: case series. - Abstract of the article: Warfarin is the most widely used oral anticoagulant and is indicated for many clinical conditions. Levofloxacin, a fluoroquinolone, is one of the most commonly prescribed antibiotics in clinical practice and is effective against Gram-positive, Gram-negative, and atypical bacteria. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin. Tips for Analysis: Sentences mentioning a chemical "levofloxacin": 1. Levofloxacin, a fluoroquinolone, is one of the most commonly prescribed antibiotics in clinical practice and is effective against Gram-positive, Gram-negative, and atypical bacteria. 2. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. 3. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. 4. Interaction between warfarin and levofloxacin: case series. 5. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin. Sentences mentioning a chemical "warfarin": 1. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. 2. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. 3. Interaction between warfarin and levofloxacin: case series. 4. Warfarin is the most widely used oral anticoagulant and is indicated for many clinical conditions. 5. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin. Sentences mentioning both entities a chemical "levofloxacin" and a chemical "warfarin": 1. Interaction between warfarin and levofloxacin: case series. 2. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. 3. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. 4. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin. Task: Identify the relationship between a chemical "levofloxacin" and a chemical "warfarin" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "bleeding" and a chemical "levofloxacin". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Interaction between warfarin and levofloxacin: case series. - Abstract of the article: Warfarin is the most widely used oral anticoagulant and is indicated for many clinical conditions. Levofloxacin, a fluoroquinolone, is one of the most commonly prescribed antibiotics in clinical practice and is effective against Gram-positive, Gram-negative, and atypical bacteria. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin. Tips for Analysis: Sentences mentioning a disease "bleeding": 1. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Sentences mentioning a chemical "levofloxacin": 1. Levofloxacin, a fluoroquinolone, is one of the most commonly prescribed antibiotics in clinical practice and is effective against Gram-positive, Gram-negative, and atypical bacteria. 2. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. 3. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. 4. Interaction between warfarin and levofloxacin: case series. 5. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin. Sentences mentioning both entities a disease "bleeding" and a chemical "levofloxacin": 1. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Task: Identify the relationship between a disease "bleeding" and a chemical "levofloxacin" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "bleeding" and a chemical "warfarin". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Interaction between warfarin and levofloxacin: case series. - Abstract of the article: Warfarin is the most widely used oral anticoagulant and is indicated for many clinical conditions. Levofloxacin, a fluoroquinolone, is one of the most commonly prescribed antibiotics in clinical practice and is effective against Gram-positive, Gram-negative, and atypical bacteria. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin. Tips for Analysis: Sentences mentioning a disease "bleeding": 1. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Sentences mentioning a chemical "warfarin": 1. While small prospective studies have not revealed any significant drug-drug interaction between warfarin and levofloxacin, several case reports have indicated that levofloxacin may significantly potentiate the anticoagulation effect of warfarin. 2. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. 3. Interaction between warfarin and levofloxacin: case series. 4. Warfarin is the most widely used oral anticoagulant and is indicated for many clinical conditions. 5. Physicians should be aware of this potential interaction and use caution when prescribing levofloxacin to patients taking warfarin. Sentences mentioning both entities a disease "bleeding" and a chemical "warfarin": 1. We report 3 cases of serious bleeding complications that appear to be the result of the interaction between warfarin and levofloxacin. Task: Identify the relationship between a disease "bleeding" and a chemical "warfarin" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "warfarin" and a disease "intracerebral hemorrhage". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. - Abstract of the article: Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. There is no consensus on the optimal treatment for W-ICH. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. Male CD-1 mice were treated with warfarin (2 mg/kg over 24 h), resulting in a mean (+/-s.d.) International Normalized Ratio of 3.5+/-0.9. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. Forty-five minutes later, the animals were randomly treated with PCC (100 U/kg) or saline i.v. (n=12 per group). Twenty-four hours after hemorrhage induction, hemorrhagic blood volume was quantified using a photometric hemoglobin assay. The mean hemorrhagic blood volume was reduced in PCC-treated animals (6.5+/-3.1 microL) compared with saline controls (15.3+/-11.2 microL, P=0.015). In the saline group, 45% of the mice developed large hematomas (i.e., >15 microL). In contrast, such extensive lesions were never found in the PCC group. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. Tips for Analysis: Sentences mentioning a chemical "warfarin": 1. Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. 2. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. 3. There is no consensus on the optimal treatment for W-ICH. 4. Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. 5. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. 6. Male CD-1 mice were treated with warfarin (2 mg/kg over 24 h), resulting in a mean (+/-s.d.) International Normalized Ratio of 3.5+/-0.9. Sentences mentioning a disease "intracerebral hemorrhage": 1. Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. 2. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. 3. There is no consensus on the optimal treatment for W-ICH. 4. Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. 5. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Sentences mentioning both entities a chemical "warfarin" and a disease "intracerebral hemorrhage": 1. Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. 2. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. 3. There is no consensus on the optimal treatment for W-ICH. 4. Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. 5. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Task: Identify the relationship between a chemical "warfarin" and a disease "intracerebral hemorrhage" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "PCC" and a chemical "W". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. - Abstract of the article: Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. There is no consensus on the optimal treatment for W-ICH. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. Male CD-1 mice were treated with warfarin (2 mg/kg over 24 h), resulting in a mean (+/-s.d.) International Normalized Ratio of 3.5+/-0.9. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. Forty-five minutes later, the animals were randomly treated with PCC (100 U/kg) or saline i.v. (n=12 per group). Twenty-four hours after hemorrhage induction, hemorrhagic blood volume was quantified using a photometric hemoglobin assay. The mean hemorrhagic blood volume was reduced in PCC-treated animals (6.5+/-3.1 microL) compared with saline controls (15.3+/-11.2 microL, P=0.015). In the saline group, 45% of the mice developed large hematomas (i.e., >15 microL). In contrast, such extensive lesions were never found in the PCC group. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. Tips for Analysis: Sentences mentioning a chemical "PCC": 1. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. 2. In contrast, such extensive lesions were never found in the PCC group. 3. The mean hemorrhagic blood volume was reduced in PCC-treated animals (6.5+/-3.1 microL) compared with saline controls (15.3+/-11.2 microL, P=0.015). 4. Forty-five minutes later, the animals were randomly treated with PCC (100 U/kg) or saline i.v. 5. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. 6. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Sentences mentioning a chemical "W": 1. Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. 2. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. 3. There is no consensus on the optimal treatment for W-ICH. 4. Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. 5. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. 6. Male CD-1 mice were treated with warfarin (2 mg/kg over 24 h), resulting in a mean (+/-s.d.) International Normalized Ratio of 3.5+/-0.9. Sentences mentioning both entities a chemical "PCC" and a chemical "W": 1. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Task: Identify the relationship between a chemical "PCC" and a chemical "W" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Drug_Interaction', 'Cotreatment', 'Conversion', 'Comparison', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "PCC" and a disease "ICH". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. - Abstract of the article: Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. There is no consensus on the optimal treatment for W-ICH. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. Male CD-1 mice were treated with warfarin (2 mg/kg over 24 h), resulting in a mean (+/-s.d.) International Normalized Ratio of 3.5+/-0.9. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. Forty-five minutes later, the animals were randomly treated with PCC (100 U/kg) or saline i.v. (n=12 per group). Twenty-four hours after hemorrhage induction, hemorrhagic blood volume was quantified using a photometric hemoglobin assay. The mean hemorrhagic blood volume was reduced in PCC-treated animals (6.5+/-3.1 microL) compared with saline controls (15.3+/-11.2 microL, P=0.015). In the saline group, 45% of the mice developed large hematomas (i.e., >15 microL). In contrast, such extensive lesions were never found in the PCC group. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. Tips for Analysis: Sentences mentioning a chemical "PCC": 1. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. 2. In contrast, such extensive lesions were never found in the PCC group. 3. The mean hemorrhagic blood volume was reduced in PCC-treated animals (6.5+/-3.1 microL) compared with saline controls (15.3+/-11.2 microL, P=0.015). 4. Forty-five minutes later, the animals were randomly treated with PCC (100 U/kg) or saline i.v. 5. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. 6. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Sentences mentioning a disease "ICH": 1. Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. 2. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. 3. There is no consensus on the optimal treatment for W-ICH. 4. Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. 5. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Sentences mentioning both entities a chemical "PCC" and a disease "ICH": 1. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Task: Identify the relationship between a chemical "PCC" and a disease "ICH" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "hemorrhage" and a chemical "PCC". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. - Abstract of the article: Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. There is no consensus on the optimal treatment for W-ICH. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. Male CD-1 mice were treated with warfarin (2 mg/kg over 24 h), resulting in a mean (+/-s.d.) International Normalized Ratio of 3.5+/-0.9. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. Forty-five minutes later, the animals were randomly treated with PCC (100 U/kg) or saline i.v. (n=12 per group). Twenty-four hours after hemorrhage induction, hemorrhagic blood volume was quantified using a photometric hemoglobin assay. The mean hemorrhagic blood volume was reduced in PCC-treated animals (6.5+/-3.1 microL) compared with saline controls (15.3+/-11.2 microL, P=0.015). In the saline group, 45% of the mice developed large hematomas (i.e., >15 microL). In contrast, such extensive lesions were never found in the PCC group. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. Tips for Analysis: Sentences mentioning a disease "hemorrhage": 1. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. 2. Twenty-four hours after hemorrhage induction, hemorrhagic blood volume was quantified using a photometric hemoglobin assay. 3. Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. Sentences mentioning a chemical "PCC": 1. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. 2. In contrast, such extensive lesions were never found in the PCC group. 3. The mean hemorrhagic blood volume was reduced in PCC-treated animals (6.5+/-3.1 microL) compared with saline controls (15.3+/-11.2 microL, P=0.015). 4. Forty-five minutes later, the animals were randomly treated with PCC (100 U/kg) or saline i.v. 5. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. 6. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Sentences mentioning both entities a disease "hemorrhage" and a chemical "PCC": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "hemorrhage" and a chemical "PCC" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "collagenase" and a disease "hemorrhage". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. - Abstract of the article: Warfarin-associated intracerebral hemorrhage (W-ICH) is a severe type of stroke. There is no consensus on the optimal treatment for W-ICH. Using a mouse model, we tested whether the rapid reversal of anticoagulation using human prothrombin complex concentrate (PCC) can reduce hemorrhagic blood volume. Male CD-1 mice were treated with warfarin (2 mg/kg over 24 h), resulting in a mean (+/-s.d.) International Normalized Ratio of 3.5+/-0.9. First, we showed that an intravenous administration of human PCC rapidly reversed anticoagulation in mice. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. Forty-five minutes later, the animals were randomly treated with PCC (100 U/kg) or saline i.v. (n=12 per group). Twenty-four hours after hemorrhage induction, hemorrhagic blood volume was quantified using a photometric hemoglobin assay. The mean hemorrhagic blood volume was reduced in PCC-treated animals (6.5+/-3.1 microL) compared with saline controls (15.3+/-11.2 microL, P=0.015). In the saline group, 45% of the mice developed large hematomas (i.e., >15 microL). In contrast, such extensive lesions were never found in the PCC group. We provide experimental data suggesting PCC to be an effective acute treatment for W-ICH in terms of reducing hemorrhagic blood volume. Future studies are needed to assess the therapeutic potential emerging from our finding for human W-ICH. Tips for Analysis: Sentences mentioning a chemical "collagenase": 1. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. Sentences mentioning a disease "hemorrhage": 1. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. 2. Twenty-four hours after hemorrhage induction, hemorrhagic blood volume was quantified using a photometric hemoglobin assay. 3. Rapid reversal of anticoagulation reduces hemorrhage volume in a mouse model of warfarin-associated intracerebral hemorrhage. Sentences mentioning both entities a chemical "collagenase" and a disease "hemorrhage": 1. Second, a stereotactic injection of collagenase was administered to induce hemorrhage in the right striatum. Task: Identify the relationship between a chemical "collagenase" and a disease "hemorrhage" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "Gly388Arg" and a disease "prostate cancer". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: FGFR4 Gly388Arg polymorphism and prostate cancer risk in Scottish men. - Abstract of the article: Fibroblast growth factor receptor 4 (FGFR4), a member of the fibroblast growth receptor family, was recently reported to be more abundantly expressed in malignant than benign prostate cells. A single nucleotide polymorphism at position 388 of the FGFR4 amino-acid sequence results in the substitution of glycine (Gly) with arginine (Arg) and higher frequency of the ArgArg genotype was previously found in prostate cancer patients. DNA was extracted from the blood drawn from 399 prostate cancer patients, 150 BPH patients and 294 healthy community controls. Polymerase chain reaction was carried out and single nucleotide polymorphisms of FGFR4 were identified by restriction enzyme digestion. No overall association is detectable between the Arg allele and increased prostate cancer risk. Subgroup analysis shows a higher incidence of the heterozygous ArgGly genotype in cancer cases than in the combined group of BPH and controls (P<0.05); this difference is statistically significant between cancer and BPH patients but not between cancer cases and community controls. The single nucleotide polymorphism Gly(388)Arg in FGFR4 is not associated with increased risk of prostate cancer in Scottish men. This observation is in contrast with results from two previous studies conducted in the USA and Japan. Tips for Analysis: Sentences mentioning a variant "Gly388Arg": 1. The single nucleotide polymorphism Gly(388)Arg in FGFR4 is not associated with increased risk of prostate cancer in Scottish men. 2. FGFR4 Gly388Arg polymorphism and prostate cancer risk in Scottish men. 3. A single nucleotide polymorphism at position 388 of the FGFR4 amino-acid sequence results in the substitution of glycine (Gly) with arginine (Arg) and higher frequency of the ArgArg genotype was previously found in prostate cancer patients. Sentences mentioning a disease "prostate cancer": 1. The single nucleotide polymorphism Gly(388)Arg in FGFR4 is not associated with increased risk of prostate cancer in Scottish men. 2. A single nucleotide polymorphism at position 388 of the FGFR4 amino-acid sequence results in the substitution of glycine (Gly) with arginine (Arg) and higher frequency of the ArgArg genotype was previously found in prostate cancer patients. 3. DNA was extracted from the blood drawn from 399 prostate cancer patients, 150 BPH patients and 294 healthy community controls. 4. No overall association is detectable between the Arg allele and increased prostate cancer risk. 5. FGFR4 Gly388Arg polymorphism and prostate cancer risk in Scottish men. Sentences mentioning both entities a variant "Gly388Arg" and a disease "prostate cancer": 1. The single nucleotide polymorphism Gly(388)Arg in FGFR4 is not associated with increased risk of prostate cancer in Scottish men. 2. FGFR4 Gly388Arg polymorphism and prostate cancer risk in Scottish men. 3. A single nucleotide polymorphism at position 388 of the FGFR4 amino-acid sequence results in the substitution of glycine (Gly) with arginine (Arg) and higher frequency of the ArgArg genotype was previously found in prostate cancer patients. Task: Identify the relationship between a variant "Gly388Arg" and a disease "prostate cancer" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "FGFR4" and a disease "prostate cancer". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: FGFR4 Gly388Arg polymorphism and prostate cancer risk in Scottish men. - Abstract of the article: Fibroblast growth factor receptor 4 (FGFR4), a member of the fibroblast growth receptor family, was recently reported to be more abundantly expressed in malignant than benign prostate cells. A single nucleotide polymorphism at position 388 of the FGFR4 amino-acid sequence results in the substitution of glycine (Gly) with arginine (Arg) and higher frequency of the ArgArg genotype was previously found in prostate cancer patients. DNA was extracted from the blood drawn from 399 prostate cancer patients, 150 BPH patients and 294 healthy community controls. Polymerase chain reaction was carried out and single nucleotide polymorphisms of FGFR4 were identified by restriction enzyme digestion. No overall association is detectable between the Arg allele and increased prostate cancer risk. Subgroup analysis shows a higher incidence of the heterozygous ArgGly genotype in cancer cases than in the combined group of BPH and controls (P<0.05); this difference is statistically significant between cancer and BPH patients but not between cancer cases and community controls. The single nucleotide polymorphism Gly(388)Arg in FGFR4 is not associated with increased risk of prostate cancer in Scottish men. This observation is in contrast with results from two previous studies conducted in the USA and Japan. Tips for Analysis: Sentences mentioning a gene or protein "FGFR4": 1. The single nucleotide polymorphism Gly(388)Arg in FGFR4 is not associated with increased risk of prostate cancer in Scottish men. 2. Polymerase chain reaction was carried out and single nucleotide polymorphisms of FGFR4 were identified by restriction enzyme digestion. 3. A single nucleotide polymorphism at position 388 of the FGFR4 amino-acid sequence results in the substitution of glycine (Gly) with arginine (Arg) and higher frequency of the ArgArg genotype was previously found in prostate cancer patients. 4. Fibroblast growth factor receptor 4 (FGFR4), a member of the fibroblast growth receptor family, was recently reported to be more abundantly expressed in malignant than benign prostate cells. 5. FGFR4 Gly388Arg polymorphism and prostate cancer risk in Scottish men. Sentences mentioning a disease "prostate cancer": 1. The single nucleotide polymorphism Gly(388)Arg in FGFR4 is not associated with increased risk of prostate cancer in Scottish men. 2. A single nucleotide polymorphism at position 388 of the FGFR4 amino-acid sequence results in the substitution of glycine (Gly) with arginine (Arg) and higher frequency of the ArgArg genotype was previously found in prostate cancer patients. 3. DNA was extracted from the blood drawn from 399 prostate cancer patients, 150 BPH patients and 294 healthy community controls. 4. No overall association is detectable between the Arg allele and increased prostate cancer risk. 5. FGFR4 Gly388Arg polymorphism and prostate cancer risk in Scottish men. Sentences mentioning both entities a gene or protein "FGFR4" and a disease "prostate cancer": 1. The single nucleotide polymorphism Gly(388)Arg in FGFR4 is not associated with increased risk of prostate cancer in Scottish men. 2. FGFR4 Gly388Arg polymorphism and prostate cancer risk in Scottish men. 3. A single nucleotide polymorphism at position 388 of the FGFR4 amino-acid sequence results in the substitution of glycine (Gly) with arginine (Arg) and higher frequency of the ArgArg genotype was previously found in prostate cancer patients. Task: Identify the relationship between a gene or protein "FGFR4" and a disease "prostate cancer" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "arginine 714" and a disease "hypokalemia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a variant "arginine 714": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a disease "hypokalemia": 1. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a variant "arginine 714" and a disease "hypokalemia": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a variant "arginine 714" and a disease "hypokalemia" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "arginine 714" and a disease "hypoglycemia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a variant "arginine 714": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a disease "hypoglycemia": 1. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a variant "arginine 714" and a disease "hypoglycemia": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a variant "arginine 714" and a disease "hypoglycemia" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "arginine 714" and a disease "hypertension". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a variant "arginine 714": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a disease "hypertension": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a variant "arginine 714" and a disease "hypertension": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a variant "arginine 714" and a disease "hypertension" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a variant "arginine 714" and a disease "glucocorticoid resistance". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a variant "arginine 714": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a disease "glucocorticoid resistance": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. 2. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. 3. A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. Sentences mentioning both entities a variant "arginine 714" and a disease "glucocorticoid resistance": There is no sentence that contains both these two entities. Task: Identify the relationship between a variant "arginine 714" and a disease "glucocorticoid resistance" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "premature pubarche" and a variant "arginine 714". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a disease "premature pubarche": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a variant "arginine 714": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a disease "premature pubarche" and a variant "arginine 714": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a disease "premature pubarche" and a variant "arginine 714" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "premature pubarche" and a chemical "dexamethasone". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a disease "premature pubarche": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a chemical "dexamethasone": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a disease "premature pubarche" and a chemical "dexamethasone": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a disease "premature pubarche" and a chemical "dexamethasone" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "premature pubarche" and a gene or protein "GR". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a disease "premature pubarche": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a gene or protein "GR": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. 2. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. 3. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. 4. A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. Sentences mentioning both entities a disease "premature pubarche" and a gene or protein "GR": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a disease "premature pubarche" and a gene or protein "GR" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "dexamethasone" and a disease "hypokalemia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a chemical "dexamethasone": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a disease "hypokalemia": 1. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a chemical "dexamethasone" and a disease "hypokalemia": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a chemical "dexamethasone" and a disease "hypokalemia" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "Dexamethasone" and a disease "hypoglycemia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a chemical "Dexamethasone": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a disease "hypoglycemia": 1. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a chemical "Dexamethasone" and a disease "hypoglycemia": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a chemical "Dexamethasone" and a disease "hypoglycemia" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a chemical "dexamethasone" and a disease "seizure". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a chemical "dexamethasone": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a disease "seizure": 1. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. Sentences mentioning both entities a chemical "dexamethasone" and a disease "seizure": There is no sentence that contains both these two entities. Task: Identify the relationship between a chemical "dexamethasone" and a disease "seizure" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "hypertension" and a chemical "dexamethasone". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a disease "hypertension": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning a chemical "dexamethasone": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a disease "hypertension" and a chemical "dexamethasone": 1. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a disease "hypertension" and a chemical "dexamethasone" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "glucocorticoid resistance" and a chemical "glucocorticoids". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a disease "glucocorticoid resistance": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. 2. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. 3. A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. Sentences mentioning a chemical "glucocorticoids": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Sentences mentioning both entities a disease "glucocorticoid resistance" and a chemical "glucocorticoids": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Task: Identify the relationship between a disease "glucocorticoid resistance" and a chemical "glucocorticoids" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Negative_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "glucocorticoid resistance" and a variant "arginine by glutamine at amino acid position 714". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a disease "glucocorticoid resistance": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. 2. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. 3. A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. Sentences mentioning a variant "arginine by glutamine at amino acid position 714": 1. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. 2. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. Sentences mentioning both entities a disease "glucocorticoid resistance" and a variant "arginine by glutamine at amino acid position 714": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "glucocorticoid resistance" and a variant "arginine by glutamine at amino acid position 714" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a disease "glucocorticoid resistance" and a variant "(G-->A) at nucleotide position 2141". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a disease "glucocorticoid resistance": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. 2. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. 3. A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. Sentences mentioning a variant "(G-->A) at nucleotide position 2141": 1. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Sentences mentioning both entities a disease "glucocorticoid resistance" and a variant "(G-->A) at nucleotide position 2141": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "glucocorticoid resistance" and a variant "(G-->A) at nucleotide position 2141" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Positive_Correlation</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "GR alpha" and a disease "hypokalemia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a gene or protein "GR alpha": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. 2. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. 3. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. 4. A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. Sentences mentioning a disease "hypokalemia": 1. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a gene or protein "GR alpha" and a disease "hypokalemia": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a gene or protein "GR alpha" and a disease "hypokalemia" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "GR alpha" and a disease "hypoglycemia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a gene or protein "GR alpha": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. 2. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. 3. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. 4. A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. Sentences mentioning a disease "hypoglycemia": 1. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. 2. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Sentences mentioning both entities a gene or protein "GR alpha" and a disease "hypoglycemia": 1. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Task: Identify the relationship between a gene or protein "GR alpha" and a disease "hypoglycemia" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>
<s>[INST] <<SYS>> Your task involves analyzing the title and abstract of a medical article to determine the relationship between two specified entities: a gene or protein "GR" and a disease "seizure". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. - Abstract of the article: CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. Most of the reported cases are adults, demonstrating symptoms associated with mineralocorticoid and/or adrenal androgen excess caused by compensatively increased secretion of the adrenocorticotropic hormone. PATIENT: We identified a new 2-yr-old female case of generalized glucocorticoid resistance syndrome. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. She also had hypertension and premature pubarche, whereas dexamethasone effectively suppressed these clinical manifestations. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. Molecular analysis revealed that the mutant receptor had significantly impaired transactivation activity with a 2-fold reduction in affinity to ligand. It showed attenuated transactivation of the activation function (AF)-2 and reduced binding to a p160 nuclear receptor coactivator. Computer-based structural analysis revealed that replacement of arginine by glutamine at position 714 transmitted a conformational change to the LBD and the AF-2 transactivation surface, resulting in a decreased binding affinity to ligand and to the LXXLL coactivator motif. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. Tips for Analysis: Sentences mentioning a gene or protein "GR": 1. CONTEXT: Generalized glucocorticoid resistance syndrome is a rare familial or sporadic condition characterized by partial insensitivity to glucocorticoids, caused by mutations in the glucocorticoid receptor (GR) gene. 2. RESULTS: The patient's GR gene had a heterozygotic mutation (G-->A) at nucleotide position 2141 (exon 8), which resulted in substitution of arginine by glutamine at amino acid position 714 in the ligand-binding domain (LBD) of the GR alpha. 3. CONCLUSIONS: Dexamethasone treatment is effective in controlling the premature pubarche, hypoglycemia, hypertension, and hypokalemia in this child case, wherein arginine 714 plays a key role in the proper formation of the ligand-binding pocket and the AF-2 surface of the GR alpha LBD. 4. A novel point mutation in helix 10 of the human glucocorticoid receptor causes generalized glucocorticoid resistance by disrupting the structure of the ligand-binding domain. Sentences mentioning a disease "seizure": 1. The patient (TJ) presented with a generalized seizure associated with hypoglycemia and hypokalemia. Sentences mentioning both entities a gene or protein "GR" and a disease "seizure": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "GR" and a disease "seizure" using the analysis tips. Select from the options: ['Positive_Correlation', 'Negative_Correlation', 'Association']. Your choice should be based on the context and tips provided. [/INST] Association</s>

Subsets and Splits

No community queries yet

The top public SQL queries from the community will appear here once available.