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<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 "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 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 "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 gene or protein "GR alpha" 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 gene or protein "GR alpha" 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 gene or protein "glucocorticoid receptor" 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 gene or protein "glucocorticoid receptor": 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 "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 gene or protein "glucocorticoid receptor" and 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. 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. Task: Identify the relationship between a gene or protein "glucocorticoid receptor" 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] 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 "C4A" and a disease "SLE". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: MHC region and risk of systemic lupus erythematosus in African American women. - Abstract of the article: The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. We also genotyped 1,509 ancestral informative markers throughout the genome to estimate European ancestry to control for population stratification due to population admixture. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. In univariate analysis, the OR for the C4A deletion was 1.38, p = 0.075, but after simultaneous adjustment for the other four SNPs the odds ratio was 1.01, p = 0.98. A genotype score combining the four newly identified SNPs showed an additive risk according to the number of high-risk alleles (OR = 1.67 per high-risk allele, p < 0.0001). Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. Tips for Analysis: Sentences mentioning a gene or protein "C4A": 1. In univariate analysis, the OR for the C4A deletion was 1.38, p = 0.075, but after simultaneous adjustment for the other four SNPs the odds ratio was 1.01, p = 0.98. 2. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. Sentences mentioning a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. 2. MHC region and risk of systemic lupus erythematosus in African American women. 3. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. 4. In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. 5. Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. 6. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. 7. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. 8. Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). 9. The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Sentences mentioning both entities a gene or protein "C4A" and a disease "SLE": 1. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. Task: Identify the relationship between a gene or protein "C4A" and a disease "SLE" 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 "HLA-DRB1" and a disease "SLE". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: MHC region and risk of systemic lupus erythematosus in African American women. - Abstract of the article: The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. We also genotyped 1,509 ancestral informative markers throughout the genome to estimate European ancestry to control for population stratification due to population admixture. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. In univariate analysis, the OR for the C4A deletion was 1.38, p = 0.075, but after simultaneous adjustment for the other four SNPs the odds ratio was 1.01, p = 0.98. A genotype score combining the four newly identified SNPs showed an additive risk according to the number of high-risk alleles (OR = 1.67 per high-risk allele, p < 0.0001). Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. Tips for Analysis: Sentences mentioning a gene or protein "HLA-DRB1": 1. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Sentences mentioning a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. 2. MHC region and risk of systemic lupus erythematosus in African American women. 3. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. 4. In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. 5. Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. 6. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. 7. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. 8. Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). 9. The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Sentences mentioning both entities a gene or protein "HLA-DRB1" and a disease "SLE": 1. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Task: Identify the relationship between a gene or protein "HLA-DRB1" and a disease "SLE" 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 "rs2844580" and a disease "SLE". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: MHC region and risk of systemic lupus erythematosus in African American women. - Abstract of the article: The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. We also genotyped 1,509 ancestral informative markers throughout the genome to estimate European ancestry to control for population stratification due to population admixture. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. In univariate analysis, the OR for the C4A deletion was 1.38, p = 0.075, but after simultaneous adjustment for the other four SNPs the odds ratio was 1.01, p = 0.98. A genotype score combining the four newly identified SNPs showed an additive risk according to the number of high-risk alleles (OR = 1.67 per high-risk allele, p < 0.0001). Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. Tips for Analysis: Sentences mentioning a variant "rs2844580": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. Sentences mentioning a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. 2. MHC region and risk of systemic lupus erythematosus in African American women. 3. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. 4. In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. 5. Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. 6. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. 7. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. 8. Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). 9. The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Sentences mentioning both entities a variant "rs2844580" and a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. Task: Identify the relationship between a variant "rs2844580" and a disease "SLE" 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 "rs2071349" and a disease "SLE". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: MHC region and risk of systemic lupus erythematosus in African American women. - Abstract of the article: The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. We also genotyped 1,509 ancestral informative markers throughout the genome to estimate European ancestry to control for population stratification due to population admixture. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. In univariate analysis, the OR for the C4A deletion was 1.38, p = 0.075, but after simultaneous adjustment for the other four SNPs the odds ratio was 1.01, p = 0.98. A genotype score combining the four newly identified SNPs showed an additive risk according to the number of high-risk alleles (OR = 1.67 per high-risk allele, p < 0.0001). Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. Tips for Analysis: Sentences mentioning a variant "rs2071349": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. Sentences mentioning a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. 2. MHC region and risk of systemic lupus erythematosus in African American women. 3. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. 4. In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. 5. Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. 6. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. 7. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. 8. Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). 9. The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Sentences mentioning both entities a variant "rs2071349" and a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. Task: Identify the relationship between a variant "rs2071349" and a disease "SLE" 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 "rs204890" and a disease "SLE". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: MHC region and risk of systemic lupus erythematosus in African American women. - Abstract of the article: The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. We also genotyped 1,509 ancestral informative markers throughout the genome to estimate European ancestry to control for population stratification due to population admixture. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. In univariate analysis, the OR for the C4A deletion was 1.38, p = 0.075, but after simultaneous adjustment for the other four SNPs the odds ratio was 1.01, p = 0.98. A genotype score combining the four newly identified SNPs showed an additive risk according to the number of high-risk alleles (OR = 1.67 per high-risk allele, p < 0.0001). Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. Tips for Analysis: Sentences mentioning a variant "rs204890": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. Sentences mentioning a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. 2. MHC region and risk of systemic lupus erythematosus in African American women. 3. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. 4. In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. 5. Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. 6. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. 7. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. 8. Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). 9. The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Sentences mentioning both entities a variant "rs204890" and a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. Task: Identify the relationship between a variant "rs204890" and a disease "SLE" 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 "SLE" and a variant "rs9271366". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: MHC region and risk of systemic lupus erythematosus in African American women. - Abstract of the article: The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. We also genotyped 1,509 ancestral informative markers throughout the genome to estimate European ancestry to control for population stratification due to population admixture. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. In univariate analysis, the OR for the C4A deletion was 1.38, p = 0.075, but after simultaneous adjustment for the other four SNPs the odds ratio was 1.01, p = 0.98. A genotype score combining the four newly identified SNPs showed an additive risk according to the number of high-risk alleles (OR = 1.67 per high-risk allele, p < 0.0001). Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. Tips for Analysis: Sentences mentioning a disease "SLE": 1. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. 2. MHC region and risk of systemic lupus erythematosus in African American women. 3. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. 4. In addition, two SNPs found in a GWAS of European ancestry women were confirmed in our study, indicating that African Americans share some genetic risk factors for SLE with European and Chinese subjects. 5. Although SLE affects African Americans disproportionately compared to European Americans, there has been no comprehensive analysis of the MHC region in relationship to SLE in African Americans. 6. In summary, we found four independent signals in the MHC region associated with risk of SLE in African American women. 7. We conducted a screening of the MHC region for 1,536 single nucleotide polymorphisms (SNPs) and the deletion of the C4A gene in a SLE case-control study (380 cases, 765 age-matched controls) nested within the prospective Black Women's Health Study. 8. Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). 9. The major histocompatibility complex (MHC) on chromosome 6p21 is a key contributor to the genetic basis of systemic lupus erythematosus (SLE). Sentences mentioning a variant "rs9271366": 1. Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). 2. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. 3. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Sentences mentioning both entities a disease "SLE" and a variant "rs9271366": 1. Our strongest signal, the rs9271366 SNP, was also associated with higher risk of SLE in a previous Chinese genome-wide association study (GWAS). 2. Conditional haplotype analysis revealed three other SNPs, rs204890 (OR = 1.86, p = 1.2 10(-4)), rs2071349 (OR = 1.53, p = 1.0 10(-3)), and rs2844580 (OR = 1.43, p = 1.3 10(-3)), to be associated with SLE independent of the rs9271366 SNP. 3. The most strongly associated SNP with SLE was the rs9271366 (odds ratio, OR = 1.70, p = 5.6 10(-5)) near the HLA-DRB1 gene. Task: Identify the relationship between a disease "SLE" and a variant "rs9271366" 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 "triglycerides" and a disease "obese". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease. - Abstract of the article: BACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis. AIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients. MATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism. RESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 4.82) compared to controls (14.26 11.4; p < 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 4.35) compared to patients without liver fibrosis (10.61 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6). CONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients. Tips for Analysis: Sentences mentioning a chemical "triglycerides": 1. RESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. Sentences mentioning a disease "obese": 1. Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease. 2. CONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. 3. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients. 4. RESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. 5. AIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients. 6. PAI-1 serum levels observed in obese patients were significantly lower (10.63 4.82) compared to controls (14.26 11.4; p < 0.05). 7. No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 4.35) compared to patients without liver fibrosis (10.61 5.2; p = 0.985). 8. MATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Sentences mentioning both entities a chemical "triglycerides" and a disease "obese": 1. RESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. Task: Identify the relationship between a chemical "triglycerides" and a disease "obese" 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 "Plasminogen activator inhibitor type 1" and a disease "obese". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease. - Abstract of the article: BACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis. AIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients. MATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism. RESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 4.82) compared to controls (14.26 11.4; p < 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 4.35) compared to patients without liver fibrosis (10.61 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6). CONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients. Tips for Analysis: Sentences mentioning a gene or protein "Plasminogen activator inhibitor type 1": 1. Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease. 2. PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6). 3. BACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. 4. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. 5. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients. 6. No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). 7. AIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients. 8. PAI-1 serum levels observed in obese patients were significantly lower (10.63 4.82) compared to controls (14.26 11.4; p < 0.05). 9. CONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. 10. No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 4.35) compared to patients without liver fibrosis (10.61 5.2; p = 0.985). 11. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis. Sentences mentioning a disease "obese": 1. Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease. 2. CONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. 3. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients. 4. RESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. 5. AIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients. 6. PAI-1 serum levels observed in obese patients were significantly lower (10.63 4.82) compared to controls (14.26 11.4; p < 0.05). 7. No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 4.35) compared to patients without liver fibrosis (10.61 5.2; p = 0.985). 8. MATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Sentences mentioning both entities a gene or protein "Plasminogen activator inhibitor type 1" and a disease "obese": 1. Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease. 2. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients. 3. AIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients. 4. PAI-1 serum levels observed in obese patients were significantly lower (10.63 4.82) compared to controls (14.26 11.4; p < 0.05). 5. CONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. 6. No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 4.35) compared to patients without liver fibrosis (10.61 5.2; p = 0.985). Task: Identify the relationship between a gene or protein "Plasminogen activator inhibitor type 1" and a disease "obese" 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.474delA" and a disease "pulmonary arterial hypertension". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Aberrant caveolin-1-mediated Smad signaling and proliferation identified by analysis of adenine 474 deletion mutation (c.474delA) in patient fibroblasts: a new perspective on the mechanism of pulmonary hypertension. - Abstract of the article: A heterozygous caveolin-1 c.474delA mutation has been identified in a family with heritable pulmonary arterial hypertension (PAH). This frameshift mutation leads to a caveolin-1 protein that contains all known functional domains but has a change in only the final 20 amino acids of the C-terminus. Here we studied how this mutation alters caveolin-1 function, using patient-derived fibroblasts. Transmission electron microscopy showed that fibroblasts carrying the c.474delA mutation form typical caveolae. Expression of mutated caveolin-1 in caveolin-1-null mouse fibroblasts failed to induce formation of caveolae due to retention of the mutated protein in the endoplasmic reticulum. However, coexpression of wild-type caveolin-1 with mutated caveolin-1 restored the ability to form caveolae. Importantly, fibroblasts carrying the mutation showed twofold increase in proliferation rate associated with hyperphosphorylation of Smad1/5/8. This mutation impaired the antiproliferative function of caveolin-1. Inhibition of type I TGFb receptors ALK1/2/3/6 responsible for phosphorylation of Smad1/5/8 reduced the hyperproliferation seen in c.474delA fibroblasts. These results demonstrate the critical role of the final 20 amino acids of caveolin-1 in modulating fibroblast proliferation by dampening Smad signaling and suggest that augmented Smad signaling and fibroblast hyperproliferation are contributing factors in the pathogenesis of PAH in patients with caveolin-1 c.474delA mutation. Tips for Analysis: Sentences mentioning a variant "c.474delA": Sentences mentioning a disease "pulmonary arterial hypertension": Sentences mentioning both entities a variant "c.474delA" and a disease "pulmonary arterial hypertension": There is no sentence that contains both these two entities. Task: Identify the relationship between a variant "c.474delA" and a disease "pulmonary arterial 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 disease "pulmonary hypertension" and a variant "c.474delA". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Aberrant caveolin-1-mediated Smad signaling and proliferation identified by analysis of adenine 474 deletion mutation (c.474delA) in patient fibroblasts: a new perspective on the mechanism of pulmonary hypertension. - Abstract of the article: A heterozygous caveolin-1 c.474delA mutation has been identified in a family with heritable pulmonary arterial hypertension (PAH). This frameshift mutation leads to a caveolin-1 protein that contains all known functional domains but has a change in only the final 20 amino acids of the C-terminus. Here we studied how this mutation alters caveolin-1 function, using patient-derived fibroblasts. Transmission electron microscopy showed that fibroblasts carrying the c.474delA mutation form typical caveolae. Expression of mutated caveolin-1 in caveolin-1-null mouse fibroblasts failed to induce formation of caveolae due to retention of the mutated protein in the endoplasmic reticulum. However, coexpression of wild-type caveolin-1 with mutated caveolin-1 restored the ability to form caveolae. Importantly, fibroblasts carrying the mutation showed twofold increase in proliferation rate associated with hyperphosphorylation of Smad1/5/8. This mutation impaired the antiproliferative function of caveolin-1. Inhibition of type I TGFb receptors ALK1/2/3/6 responsible for phosphorylation of Smad1/5/8 reduced the hyperproliferation seen in c.474delA fibroblasts. These results demonstrate the critical role of the final 20 amino acids of caveolin-1 in modulating fibroblast proliferation by dampening Smad signaling and suggest that augmented Smad signaling and fibroblast hyperproliferation are contributing factors in the pathogenesis of PAH in patients with caveolin-1 c.474delA mutation. Tips for Analysis: Sentences mentioning a disease "pulmonary hypertension": Sentences mentioning a variant "c.474delA": Sentences mentioning both entities a disease "pulmonary hypertension" and a variant "c.474delA": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "pulmonary hypertension" and a variant "c.474delA" 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 "pulmonary hypertension" and a gene or protein "caveolin-1". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Aberrant caveolin-1-mediated Smad signaling and proliferation identified by analysis of adenine 474 deletion mutation (c.474delA) in patient fibroblasts: a new perspective on the mechanism of pulmonary hypertension. - Abstract of the article: A heterozygous caveolin-1 c.474delA mutation has been identified in a family with heritable pulmonary arterial hypertension (PAH). This frameshift mutation leads to a caveolin-1 protein that contains all known functional domains but has a change in only the final 20 amino acids of the C-terminus. Here we studied how this mutation alters caveolin-1 function, using patient-derived fibroblasts. Transmission electron microscopy showed that fibroblasts carrying the c.474delA mutation form typical caveolae. Expression of mutated caveolin-1 in caveolin-1-null mouse fibroblasts failed to induce formation of caveolae due to retention of the mutated protein in the endoplasmic reticulum. However, coexpression of wild-type caveolin-1 with mutated caveolin-1 restored the ability to form caveolae. Importantly, fibroblasts carrying the mutation showed twofold increase in proliferation rate associated with hyperphosphorylation of Smad1/5/8. This mutation impaired the antiproliferative function of caveolin-1. Inhibition of type I TGFb receptors ALK1/2/3/6 responsible for phosphorylation of Smad1/5/8 reduced the hyperproliferation seen in c.474delA fibroblasts. These results demonstrate the critical role of the final 20 amino acids of caveolin-1 in modulating fibroblast proliferation by dampening Smad signaling and suggest that augmented Smad signaling and fibroblast hyperproliferation are contributing factors in the pathogenesis of PAH in patients with caveolin-1 c.474delA mutation. Tips for Analysis: Sentences mentioning a disease "pulmonary hypertension": Sentences mentioning a gene or protein "caveolin-1": Sentences mentioning both entities a disease "pulmonary hypertension" and a gene or protein "caveolin-1": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "pulmonary hypertension" and a gene or protein "caveolin-1" 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 "caveolin-1" and a disease "PAH". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Aberrant caveolin-1-mediated Smad signaling and proliferation identified by analysis of adenine 474 deletion mutation (c.474delA) in patient fibroblasts: a new perspective on the mechanism of pulmonary hypertension. - Abstract of the article: A heterozygous caveolin-1 c.474delA mutation has been identified in a family with heritable pulmonary arterial hypertension (PAH). This frameshift mutation leads to a caveolin-1 protein that contains all known functional domains but has a change in only the final 20 amino acids of the C-terminus. Here we studied how this mutation alters caveolin-1 function, using patient-derived fibroblasts. Transmission electron microscopy showed that fibroblasts carrying the c.474delA mutation form typical caveolae. Expression of mutated caveolin-1 in caveolin-1-null mouse fibroblasts failed to induce formation of caveolae due to retention of the mutated protein in the endoplasmic reticulum. However, coexpression of wild-type caveolin-1 with mutated caveolin-1 restored the ability to form caveolae. Importantly, fibroblasts carrying the mutation showed twofold increase in proliferation rate associated with hyperphosphorylation of Smad1/5/8. This mutation impaired the antiproliferative function of caveolin-1. Inhibition of type I TGFb receptors ALK1/2/3/6 responsible for phosphorylation of Smad1/5/8 reduced the hyperproliferation seen in c.474delA fibroblasts. These results demonstrate the critical role of the final 20 amino acids of caveolin-1 in modulating fibroblast proliferation by dampening Smad signaling and suggest that augmented Smad signaling and fibroblast hyperproliferation are contributing factors in the pathogenesis of PAH in patients with caveolin-1 c.474delA mutation. Tips for Analysis: Sentences mentioning a gene or protein "caveolin-1": Sentences mentioning a disease "PAH": Sentences mentioning both entities a gene or protein "caveolin-1" and a disease "PAH": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "caveolin-1" and a disease "PAH" 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 "impaired intellectual development" and a variant "I280S". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a disease "impaired intellectual development": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Sentences mentioning a variant "I280S": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. 2. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. 3. The I280S mutation was recently reported in a heterozygous patient. Sentences mentioning both entities a disease "impaired intellectual development" and a variant "I280S": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Task: Identify the relationship between a disease "impaired intellectual development" and a variant "I280S" 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 "tachycardia" and a variant "I280S". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a disease "tachycardia": Sentences mentioning a variant "I280S": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. 2. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. 3. The I280S mutation was recently reported in a heterozygous patient. Sentences mentioning both entities a disease "tachycardia" and a variant "I280S": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "tachycardia" and a variant "I280S" 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 "hyperkinetic" and a variant "I280S". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a disease "hyperkinetic": Sentences mentioning a variant "I280S": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. 2. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. 3. The I280S mutation was recently reported in a heterozygous patient. Sentences mentioning both entities a disease "hyperkinetic" and a variant "I280S": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "hyperkinetic" and a variant "I280S" 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 "1123T-->G" and a disease "impaired intellectual development". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a variant "1123T-->G": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Sentences mentioning a disease "impaired intellectual development": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. 2. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. 3. The I280S mutation was recently reported in a heterozygous patient. Sentences mentioning both entities a variant "1123T-->G" and a disease "impaired intellectual development": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Task: Identify the relationship between a variant "1123T-->G" and a disease "impaired intellectual development" 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 "1123T-->G" and a disease "tachycardia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a variant "1123T-->G": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Sentences mentioning a disease "tachycardia": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. 2. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. 3. The I280S mutation was recently reported in a heterozygous patient. Sentences mentioning both entities a variant "1123T-->G" and a disease "tachycardia": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Task: Identify the relationship between a variant "1123T-->G" and a disease "tachycardia" 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 "1123T-->G" and a disease "hyperkinetic". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a variant "1123T-->G": 1. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. Sentences mentioning a disease "hyperkinetic": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Sentences mentioning both entities a variant "1123T-->G" and a disease "hyperkinetic": There is no sentence that contains both these two entities. Task: Identify the relationship between a variant "1123T-->G" and a disease "hyperkinetic" 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 "TR-beta" and a disease "impaired intellectual development". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a gene or protein "TR-beta": 1. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. Sentences mentioning a disease "impaired intellectual development": Sentences mentioning both entities a gene or protein "TR-beta" and a disease "impaired intellectual development": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "TR-beta" and a disease "impaired intellectual development" 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 "TR-beta" and a disease "tachycardia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a gene or protein "TR-beta": 1. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. Sentences mentioning a disease "tachycardia": Sentences mentioning both entities a gene or protein "TR-beta" and a disease "tachycardia": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "TR-beta" and a disease "tachycardia" 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 "TR-beta" and a disease "hyperkinetic". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a gene or protein "TR-beta": 1. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. Sentences mentioning a disease "hyperkinetic": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Sentences mentioning both entities a gene or protein "TR-beta" and a disease "hyperkinetic": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "TR-beta" and a disease "hyperkinetic" 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 "RTH" and a variant "1123T-->G". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a disease "RTH": 1. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. Sentences mentioning a variant "1123T-->G": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Sentences mentioning both entities a disease "RTH" and a variant "1123T-->G": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "RTH" and a variant "1123T-->G" 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 "RTH" and a variant "I280S". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a disease "RTH": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. 2. Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. 3. We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. 4. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). Sentences mentioning a variant "I280S": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Sentences mentioning both entities a disease "RTH" and a variant "I280S": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Task: Identify the relationship between a disease "RTH" and a variant "I280S" 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 "Resistance to thyroid hormone syndrome" and a gene or protein "T3 receptor". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. - Abstract of the article: Resistance to thyroid hormone syndrome (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. Patients with RTH are usually euthyroid but can occasionally present with signs and symptoms of thyrotoxicosis or rarely with hypothyroidism. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. The single nucleotide substitution I280S (1123T-->G) was present either on both alleles or in a hemizygous form with complete deletion of the second allele. The I280S mutation was recently reported in a heterozygous patient. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. Tips for Analysis: Sentences mentioning a disease "Resistance to thyroid hormone syndrome": 1. The severe phenotype with seriously impaired intellectual development, hyperkinetic behaviour, tachycardia, hearing and visual impairment is probably due to the dominant negative effect of the I280S mutant protein and the absence of any functional TR-beta. 2. Severe form of thyroid hormone resistance in a patient with homozygous/hemizygous mutation of T3 receptor gene. 3. We present a patient with RTH found to be homo-/hemizygous for a mutation in the TR-beta gene. 4. Affected individuals are usually heterozygous for mutations in the thyroid hormone receptor beta gene (TR-beta). Sentences mentioning a gene or protein "T3 receptor": Sentences mentioning both entities a disease "Resistance to thyroid hormone syndrome" and a gene or protein "T3 receptor": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "Resistance to thyroid hormone syndrome" and a gene or protein "T3 receptor" 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 "ACE" and a chemical "agarose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. - Abstract of the article: PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. EXPERIMENTAL DESIGN: Genomic DNA was purified from peripheral blood mononuclear cells or tissue specimens. Amplified ACE gene fragments were separated on agarose gels. D or I alleles were identified by the presence of 190- or 490-bp fragments, respectively. Local expression of ACE was investigated by immunohistochemistry. RESULTS: Twenty-four of 113 (21%) gastric cancer patients had the II, 57 (51%) the ID, and 32 (28%) the DD genotype. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. Patients with the II genotype had a highly significantly smaller number of lymph node metastases (P < 0.001) and a significantly lower UICC tumor stage (P = 0.01) than patients with the DD genotype. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. Tips for Analysis: Sentences mentioning a gene or protein "ACE": 1. Amplified ACE gene fragments were separated on agarose gels. 2. PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. 3. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. 4. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. 5. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. 6. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. 7. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. 8. Local expression of ACE was investigated by immunohistochemistry. 9. The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. 10. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. Sentences mentioning a chemical "agarose": 1. Amplified ACE gene fragments were separated on agarose gels. Sentences mentioning both entities a gene or protein "ACE" and a chemical "agarose": 1. Amplified ACE gene fragments were separated on agarose gels. Task: Identify the relationship between a gene or protein "ACE" and a chemical "agarose" 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 "angiotensin I-converting enzyme" and a disease "gastric cancer". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. - Abstract of the article: PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. EXPERIMENTAL DESIGN: Genomic DNA was purified from peripheral blood mononuclear cells or tissue specimens. Amplified ACE gene fragments were separated on agarose gels. D or I alleles were identified by the presence of 190- or 490-bp fragments, respectively. Local expression of ACE was investigated by immunohistochemistry. RESULTS: Twenty-four of 113 (21%) gastric cancer patients had the II, 57 (51%) the ID, and 32 (28%) the DD genotype. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. Patients with the II genotype had a highly significantly smaller number of lymph node metastases (P < 0.001) and a significantly lower UICC tumor stage (P = 0.01) than patients with the DD genotype. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. Tips for Analysis: Sentences mentioning a gene or protein "angiotensin I-converting enzyme": 1. Amplified ACE gene fragments were separated on agarose gels. 2. PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. 3. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. 4. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. 5. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. 6. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. 7. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. 8. Local expression of ACE was investigated by immunohistochemistry. 9. The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. 10. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. Sentences mentioning a disease "gastric cancer": 1. PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. 2. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. 3. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. 4. The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. 5. RESULTS: Twenty-four of 113 (21%) gastric cancer patients had the II, 57 (51%) the ID, and 32 (28%) the DD genotype. 6. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. Sentences mentioning both entities a gene or protein "angiotensin I-converting enzyme" and a disease "gastric cancer": 1. PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. 2. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. 3. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. 4. The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. 5. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. Task: Identify the relationship between a gene or protein "angiotensin I-converting enzyme" and a disease "gastric 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 "ACE" and a disease "tumor". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. - Abstract of the article: PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. EXPERIMENTAL DESIGN: Genomic DNA was purified from peripheral blood mononuclear cells or tissue specimens. Amplified ACE gene fragments were separated on agarose gels. D or I alleles were identified by the presence of 190- or 490-bp fragments, respectively. Local expression of ACE was investigated by immunohistochemistry. RESULTS: Twenty-four of 113 (21%) gastric cancer patients had the II, 57 (51%) the ID, and 32 (28%) the DD genotype. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. Patients with the II genotype had a highly significantly smaller number of lymph node metastases (P < 0.001) and a significantly lower UICC tumor stage (P = 0.01) than patients with the DD genotype. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. Tips for Analysis: Sentences mentioning a gene or protein "ACE": 1. Amplified ACE gene fragments were separated on agarose gels. 2. PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. 3. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. 4. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. 5. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. 6. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. 7. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. 8. Local expression of ACE was investigated by immunohistochemistry. 9. The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. 10. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. Sentences mentioning a disease "tumor": 1. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. 2. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. 3. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. 4. Patients with the II genotype had a highly significantly smaller number of lymph node metastases (P < 0.001) and a significantly lower UICC tumor stage (P = 0.01) than patients with the DD genotype. Sentences mentioning both entities a gene or protein "ACE" and a disease "tumor": 1. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. 2. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. 3. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. Task: Identify the relationship between a gene or protein "ACE" and a disease "tumor" 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 "lymph node metastases" and a gene or protein "ACE". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. - Abstract of the article: PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. EXPERIMENTAL DESIGN: Genomic DNA was purified from peripheral blood mononuclear cells or tissue specimens. Amplified ACE gene fragments were separated on agarose gels. D or I alleles were identified by the presence of 190- or 490-bp fragments, respectively. Local expression of ACE was investigated by immunohistochemistry. RESULTS: Twenty-four of 113 (21%) gastric cancer patients had the II, 57 (51%) the ID, and 32 (28%) the DD genotype. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. Patients with the II genotype had a highly significantly smaller number of lymph node metastases (P < 0.001) and a significantly lower UICC tumor stage (P = 0.01) than patients with the DD genotype. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. Tips for Analysis: Sentences mentioning a disease "lymph node metastases": 1. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. 2. The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. 3. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. 4. Patients with the II genotype had a highly significantly smaller number of lymph node metastases (P < 0.001) and a significantly lower UICC tumor stage (P = 0.01) than patients with the DD genotype. Sentences mentioning a gene or protein "ACE": 1. Amplified ACE gene fragments were separated on agarose gels. 2. PURPOSE: In the present study, we aimed to substantiate the putative significance of angiotensin I-converting enzyme (ACE) on gastric cancer biology by investigating the influence of its gene polymorphism on gastric cancer progression. 3. ACE was expressed by endothelial cells in all (100%) specimens and by tumor cells in 56 (56%) specimens. 4. CONCLUSIONS: Our study shows that ACE is expressed locally in gastric cancer and that the gene polymorphism influences metastatic behavior. 5. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. 6. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. 7. The distribution of the ACE genotypes did not differ significantly from the control group of 189 patients without gastric cancer. 8. Local expression of ACE was investigated by immunohistochemistry. 9. The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. 10. The expression of ACE in gastric cancer was investigated by immunohistochemistry in 100 of 113 patients. Sentences mentioning both entities a disease "lymph node metastases" and a gene or protein "ACE": 1. No correlation was found between tumor type, tumor location, local tumor growth, distant metastases, and the ACE genotype. 2. The number of lymph node metastases in gastric cancer correlates with the angiotensin I-converting enzyme gene insertion/deletion polymorphism. 3. However, the ACE genotypes correlated with the number of lymph node metastases and the Unio Internationale Contra Cancrum (UICC) tumor stage. Task: Identify the relationship between a disease "lymph node metastases" and a gene or protein "ACE" 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 "MSH2" and a disease "Lynch syndrome". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Distinct patterns of germ-line deletions in MLH1 and MSH2: the implication of Alu repetitive element in the genetic etiology of Lynch syndrome (HNPCC). - Abstract of the article: A relatively high frequency of germ-line genomic rearrangements in MLH1 and MSH2 has been reported among Lynch Syndrome (HNPCC) patients from different ethnic populations. To investigate the underlying molecular mechanisms, we characterized the DNA breakpoints of 11 germ-line deletions, six for MLH1 and five for MSH2. Distinct deletion patterns were found for the two genes. The five cases of MSH2 deletions result exclusively from intragenic unequal recombination mediated by repetitive Alu sequences. In contrast, five out of the six MLH1 deletions are due to recombinations involving sequences of no significant homology (P=0.015). A detailed analysis of the DNA breakpoints in the two genes, previously characterized by other groups, validated the observation that Alu-mediated unequal recombination is the main type of deletion in MSH2 (n=34), but not in MLH1 (n=21) (P<0.0001). Plotting the distribution of known DNA breakpoints among the introns of the two genes showed that, the highest breakpoint density is co-localized with the highest Alu density. Our study suggests that Alu is a promoting factor for the genomic recombinations in both MLH1 and MSH2, and the local Alu density may be involved in shaping the deletion pattern. Tips for Analysis: Sentences mentioning a gene or protein "MSH2": 1. A detailed analysis of the DNA breakpoints in the two genes, previously characterized by other groups, validated the observation that Alu-mediated unequal recombination is the main type of deletion in MSH2 (n=34), but not in MLH1 (n=21) (P<0.0001). 2. Our study suggests that Alu is a promoting factor for the genomic recombinations in both MLH1 and MSH2, and the local Alu density may be involved in shaping the deletion pattern. 3. The five cases of MSH2 deletions result exclusively from intragenic unequal recombination mediated by repetitive Alu sequences. 4. A relatively high frequency of germ-line genomic rearrangements in MLH1 and MSH2 has been reported among Lynch Syndrome (HNPCC) patients from different ethnic populations. 5. Distinct patterns of germ-line deletions in MLH1 and MSH2: the implication of Alu repetitive element in the genetic etiology of Lynch syndrome (HNPCC). 6. To investigate the underlying molecular mechanisms, we characterized the DNA breakpoints of 11 germ-line deletions, six for MLH1 and five for MSH2. Sentences mentioning a disease "Lynch syndrome": 1. A relatively high frequency of germ-line genomic rearrangements in MLH1 and MSH2 has been reported among Lynch Syndrome (HNPCC) patients from different ethnic populations. 2. Distinct patterns of germ-line deletions in MLH1 and MSH2: the implication of Alu repetitive element in the genetic etiology of Lynch syndrome (HNPCC). Sentences mentioning both entities a gene or protein "MSH2" and a disease "Lynch syndrome": 1. A relatively high frequency of germ-line genomic rearrangements in MLH1 and MSH2 has been reported among Lynch Syndrome (HNPCC) patients from different ethnic populations. 2. Distinct patterns of germ-line deletions in MLH1 and MSH2: the implication of Alu repetitive element in the genetic etiology of Lynch syndrome (HNPCC). Task: Identify the relationship between a gene or protein "MSH2" and a disease "Lynch 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 "MLH1" and a disease "HNPCC". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Distinct patterns of germ-line deletions in MLH1 and MSH2: the implication of Alu repetitive element in the genetic etiology of Lynch syndrome (HNPCC). - Abstract of the article: A relatively high frequency of germ-line genomic rearrangements in MLH1 and MSH2 has been reported among Lynch Syndrome (HNPCC) patients from different ethnic populations. To investigate the underlying molecular mechanisms, we characterized the DNA breakpoints of 11 germ-line deletions, six for MLH1 and five for MSH2. Distinct deletion patterns were found for the two genes. The five cases of MSH2 deletions result exclusively from intragenic unequal recombination mediated by repetitive Alu sequences. In contrast, five out of the six MLH1 deletions are due to recombinations involving sequences of no significant homology (P=0.015). A detailed analysis of the DNA breakpoints in the two genes, previously characterized by other groups, validated the observation that Alu-mediated unequal recombination is the main type of deletion in MSH2 (n=34), but not in MLH1 (n=21) (P<0.0001). Plotting the distribution of known DNA breakpoints among the introns of the two genes showed that, the highest breakpoint density is co-localized with the highest Alu density. Our study suggests that Alu is a promoting factor for the genomic recombinations in both MLH1 and MSH2, and the local Alu density may be involved in shaping the deletion pattern. Tips for Analysis: Sentences mentioning a gene or protein "MLH1": 1. A detailed analysis of the DNA breakpoints in the two genes, previously characterized by other groups, validated the observation that Alu-mediated unequal recombination is the main type of deletion in MSH2 (n=34), but not in MLH1 (n=21) (P<0.0001). 2. Our study suggests that Alu is a promoting factor for the genomic recombinations in both MLH1 and MSH2, and the local Alu density may be involved in shaping the deletion pattern. 3. A relatively high frequency of germ-line genomic rearrangements in MLH1 and MSH2 has been reported among Lynch Syndrome (HNPCC) patients from different ethnic populations. 4. In contrast, five out of the six MLH1 deletions are due to recombinations involving sequences of no significant homology (P=0.015). 5. Distinct patterns of germ-line deletions in MLH1 and MSH2: the implication of Alu repetitive element in the genetic etiology of Lynch syndrome (HNPCC). 6. To investigate the underlying molecular mechanisms, we characterized the DNA breakpoints of 11 germ-line deletions, six for MLH1 and five for MSH2. Sentences mentioning a disease "HNPCC": 1. A relatively high frequency of germ-line genomic rearrangements in MLH1 and MSH2 has been reported among Lynch Syndrome (HNPCC) patients from different ethnic populations. 2. Distinct patterns of germ-line deletions in MLH1 and MSH2: the implication of Alu repetitive element in the genetic etiology of Lynch syndrome (HNPCC). Sentences mentioning both entities a gene or protein "MLH1" and a disease "HNPCC": 1. A relatively high frequency of germ-line genomic rearrangements in MLH1 and MSH2 has been reported among Lynch Syndrome (HNPCC) patients from different ethnic populations. 2. Distinct patterns of germ-line deletions in MLH1 and MSH2: the implication of Alu repetitive element in the genetic etiology of Lynch syndrome (HNPCC). Task: Identify the relationship between a gene or protein "MLH1" and a disease "HNPCC" 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 "schizophrenia" and a gene or protein "NDE1". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. - Abstract of the article: We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. This specific DISC1 allele was later identified to associate with visual working memory, selectively in males. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. In this study, we conditioned our sample of Finnish families for the presence of the Finnish tentative risk allele for DISC1 and re-analyzed our genome-wide scan data of 443 markers on the basis of this stratification. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. Our finding would support the concept that initial gene findings in multifactorial diseases will assist in the identification of other components of complex genetic etiology. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia. Tips for Analysis: Sentences mentioning a disease "schizophrenia": 1. We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. 2. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. 3. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. 4. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. 5. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia. Sentences mentioning a gene or protein "NDE1": 1. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. 2. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. 3. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. Sentences mentioning both entities a disease "schizophrenia" and a gene or protein "NDE1": 1. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. 2. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. Task: Identify the relationship between a disease "schizophrenia" and a gene or protein "NDE1" 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 "Disrupted in Schizophrenia 1" and a gene or protein "NDE1". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. - Abstract of the article: We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. This specific DISC1 allele was later identified to associate with visual working memory, selectively in males. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. In this study, we conditioned our sample of Finnish families for the presence of the Finnish tentative risk allele for DISC1 and re-analyzed our genome-wide scan data of 443 markers on the basis of this stratification. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. Our finding would support the concept that initial gene findings in multifactorial diseases will assist in the identification of other components of complex genetic etiology. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia. Tips for Analysis: Sentences mentioning a gene or protein "Disrupted in Schizophrenia 1": 1. In this study, we conditioned our sample of Finnish families for the presence of the Finnish tentative risk allele for DISC1 and re-analyzed our genome-wide scan data of 443 markers on the basis of this stratification. 2. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. 3. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. 4. This specific DISC1 allele was later identified to associate with visual working memory, selectively in males. 5. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. 6. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia. 7. We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. Sentences mentioning a gene or protein "NDE1": 1. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. 2. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. 3. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. Sentences mentioning both entities a gene or protein "Disrupted in Schizophrenia 1" and a gene or protein "NDE1": 1. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. 2. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. Task: Identify the relationship between a gene or protein "Disrupted in Schizophrenia 1" and a gene or protein "NDE1" 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 "DISC1" and a disease "schizophrenia". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. - Abstract of the article: We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. This specific DISC1 allele was later identified to associate with visual working memory, selectively in males. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. In this study, we conditioned our sample of Finnish families for the presence of the Finnish tentative risk allele for DISC1 and re-analyzed our genome-wide scan data of 443 markers on the basis of this stratification. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. Our finding would support the concept that initial gene findings in multifactorial diseases will assist in the identification of other components of complex genetic etiology. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia. Tips for Analysis: Sentences mentioning a gene or protein "DISC1": 1. In this study, we conditioned our sample of Finnish families for the presence of the Finnish tentative risk allele for DISC1 and re-analyzed our genome-wide scan data of 443 markers on the basis of this stratification. 2. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. 3. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. 4. This specific DISC1 allele was later identified to associate with visual working memory, selectively in males. 5. Two additional loci displayed an evidence of linkage (LOD > 3) and included a locus on 16p13, proximal to the gene encoding NDE1, which has been shown to biologically interact with DISC1. 6. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia. 7. We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. Sentences mentioning a disease "schizophrenia": 1. We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. 2. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. 3. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. 4. Although none of the observed linkages remained significant after multiple test correction through simulation, further analysis of NDE1 revealed an association between a tag-haplotype and schizophrenia (P = 0.00046) specific to females, which proved to be significant (P = 0.011) after multiple test correction. 5. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia. Sentences mentioning both entities a gene or protein "DISC1" and a disease "schizophrenia": 1. Notably, this and other converging lines of evidence underline the importance of DISC1-related functional pathways in the etiology of schizophrenia. 2. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. 3. DISC1 association to schizophrenia has since been replicated in multiple independent study samples from different populations. 4. We have previously reported a robust association between an allelic haplotype of 'Disrupted in Schizophrenia 1' (DISC1) and schizophrenia in a nationwide collection of Finnish schizophrenia families. Task: Identify the relationship between a gene or protein "DISC1" and a disease "schizophrenia" 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 "benign breast tumors" and a gene or protein "prolactin receptor". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a disease "benign breast tumors": 1. Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. 2. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. Sentences mentioning a gene or protein "prolactin receptor": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 3. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 4. This is a unique description of a functional mutation of the PrlR associated with a human disease. 5. Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. 6. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. 7. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. Sentences mentioning both entities a disease "benign breast tumors" and a gene or protein "prolactin receptor": 1. Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. Task: Identify the relationship between a disease "benign breast tumors" and a gene or protein "prolactin receptor" 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 "MFA" and a variant "Ile(146)-->Leu". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a disease "MFA": 1. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. 2. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. 3. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Sentences mentioning a variant "Ile(146)-->Leu": 1. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. 2. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 3. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. Sentences mentioning both entities a disease "MFA" and a variant "Ile(146)-->Leu": 1. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. Task: Identify the relationship between a disease "MFA" and a variant "Ile(146)-->Leu" 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 "Multiple fibroadenomas" and a gene or protein "PrlR". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a disease "Multiple fibroadenomas": 1. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. 2. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. 3. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Sentences mentioning a gene or protein "PrlR": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 3. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 4. This is a unique description of a functional mutation of the PrlR associated with a human disease. 5. Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. 6. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. 7. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. Sentences mentioning both entities a disease "Multiple fibroadenomas" and a gene or protein "PrlR": 1. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. Task: Identify the relationship between a disease "Multiple fibroadenomas" and a gene or protein "PrlR" 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 "PrlR" and a gene or protein "signal transducer and activator of transcription 5". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a gene or protein "PrlR": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 3. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 4. This is a unique description of a functional mutation of the PrlR associated with a human disease. 5. Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. 6. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. 7. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. Sentences mentioning a gene or protein "signal transducer and activator of transcription 5": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. Sentences mentioning both entities a gene or protein "PrlR" and a gene or protein "signal transducer and activator of transcription 5": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. Task: Identify the relationship between a gene or protein "PrlR" and a gene or protein "signal transducer and activator of transcription 5" 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 "PrlR" and a disease "breast diseases". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a gene or protein "PrlR": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 3. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 4. This is a unique description of a functional mutation of the PrlR associated with a human disease. 5. Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. 6. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. 7. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. Sentences mentioning a disease "breast diseases": 1. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Sentences mentioning both entities a gene or protein "PrlR" and a disease "breast diseases": 1. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Task: Identify the relationship between a gene or protein "PrlR" and a disease "breast diseases" 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 "prolactin" and a disease "benign breast tumors". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a gene or protein "prolactin": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 3. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 4. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. Sentences mentioning a disease "benign breast tumors": 1. Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. 2. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. Sentences mentioning both entities a gene or protein "prolactin" and a disease "benign breast tumors": 1. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. Task: Identify the relationship between a gene or protein "prolactin" and a disease "benign breast 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] 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 "Prl" and a disease "MFA". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a gene or protein "Prl": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 3. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 4. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. Sentences mentioning a disease "MFA": 1. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. 2. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. 3. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Sentences mentioning both entities a gene or protein "Prl" and a disease "MFA": 1. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. Task: Identify the relationship between a gene or protein "Prl" and a disease "MFA" 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 "Prl" and a gene or protein "PrlR". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a gene or protein "Prl": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 3. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 4. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. Sentences mentioning a gene or protein "PrlR": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 3. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 4. This is a unique description of a functional mutation of the PrlR associated with a human disease. 5. Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. 6. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. 7. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. Sentences mentioning both entities a gene or protein "Prl" and a gene or protein "PrlR": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 3. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Task: Identify the relationship between a gene or protein "Prl" and a gene or protein "PrlR" 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] Bind</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 "Prl" and a disease "breast diseases". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Identification of a gain-of-function mutation of the prolactin receptor in women with benign breast tumors. - Abstract of the article: There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. In a prospective study involving 74 MFA patients and 170 control subjects, we identified four patients harboring a heterozygous single nucleotide polymorphism in exon 6 of the PrlR gene, encoding Ile(146)-->Leu substitution in its extracellular domain. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. Constitutive activity of PrlR(I146L) in the breast sample from a patient was supported by increased STAT5 signaling. This is a unique description of a functional mutation of the PrlR associated with a human disease. Hallmarks of constitutive activity were all reversed by a specific PrlR antagonist, which opens potential therapeutic approaches for MFA, or any other disease that could be associated with this mutation in future. Tips for Analysis: Sentences mentioning a gene or protein "Prl": 1. This sole substitution was sufficient to confer constitutive activity to the receptor variant (PrlR(I146L)), as assessed in three reconstituted cell models (Ba/F3, HEK293 and MCF-7 cells) by Prl-independent (i) PrlR tyrosine phosphorylation, (ii) activation of signal transducer and activator of transcription 5 (STAT5) signaling, (iii) transcriptional activity toward a Prl-responsive reporter gene, and (iv) cell proliferation and protection from cell death. 2. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. 3. There is currently no known genetic disease linked to prolactin (Prl) or its receptor (PrlR) in humans. 4. Multiple fibroadenomas (MFA) are benign breast tumors which appear most frequently in young women, including at puberty, when Prl has well-recognized proliferative actions on the breast. Sentences mentioning a disease "breast diseases": 1. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Sentences mentioning both entities a gene or protein "Prl" and a disease "breast diseases": 1. Given the essential role of this hormonal system in breast physiology, we reasoned that genetic anomalies of Prl/PrlR genes may be related to the occurrence of breast diseases with high proliferative potential. Task: Identify the relationship between a gene or protein "Prl" and a disease "breast diseases" 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 "metronidazole" and a disease "infection". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Reversible inferior colliculus lesion in metronidazole-induced encephalopathy: magnetic resonance findings on diffusion-weighted and fluid attenuated inversion recovery imaging. - Abstract of the article: OBJECTIVE: This is to present reversible inferior colliculus lesions in metronidazole-induced encephalopathy, to focus on the diffusion-weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) imaging. MATERIALS AND METHODS: From November 2005 to September 2007, 8 patients (5 men and 3 women) were diagnosed as having metronidazole-induced encephalopathy (age range; 43-78 years). They had been taking metronidazole (total dosage, 45-120 g; duration, 30 days to 2 months) to treat the infection in various organs. Initial brain magnetic resonance imaging (MRI) were obtained after the hospitalization, including DWI (8/8), apparent diffusion coefficient (ADC) map (4/8), FLAIR (7/8), and T2-weighted image (8/8). Follow-up MRIs were performed on 5 patients from third to 14th days after discontinuation of metronidazole administration. Findings of initial and follow-up MRIs were retrospectively evaluated by 2 neuroradiologists by consensus, to analyze the presence of abnormal signal intensities, their locations, and signal changes on follow-up images. RESULTS: Initial MRIs showed abnormal high signal intensities on DWI and FLAIR (or T2-weighted image) at the dentate nucleus (8/8), inferior colliculus (6/8), corpus callosum (2/8), pons (2/8), medulla (1/8), and bilateral cerebral white matter (1/8). High-signal intensity lesions on DWI tended to show low signal intensity on ADC map (3/4), but in one patient, high signal intensity was shown at bilateral dentate nuclei on not only DWI but also ADC map. All the lesions in dentate, inferior colliculus, pons, and medullas had been resolved completely on follow-up MRIs in 5 patients, but in 1 patient of them, corpus callosal lesion persisted. CONCLUSIONS: Reversible inferior colliculus lesions could be considered as the characteristic for metronidazole-induced encephalopathy, next to the dentate nucleus involvement. Tips for Analysis: Sentences mentioning a chemical "metronidazole": 1. They had been taking metronidazole (total dosage, 45-120 g; duration, 30 days to 2 months) to treat the infection in various organs. 2. Reversible inferior colliculus lesion in metronidazole-induced encephalopathy: magnetic resonance findings on diffusion-weighted and fluid attenuated inversion recovery imaging. 3. Follow-up MRIs were performed on 5 patients from third to 14th days after discontinuation of metronidazole administration. 4. MATERIALS AND METHODS: From November 2005 to September 2007, 8 patients (5 men and 3 women) were diagnosed as having metronidazole-induced encephalopathy (age range; 43-78 years). 5. OBJECTIVE: This is to present reversible inferior colliculus lesions in metronidazole-induced encephalopathy, to focus on the diffusion-weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) imaging. 6. CONCLUSIONS: Reversible inferior colliculus lesions could be considered as the characteristic for metronidazole-induced encephalopathy, next to the dentate nucleus involvement. Sentences mentioning a disease "infection": 1. They had been taking metronidazole (total dosage, 45-120 g; duration, 30 days to 2 months) to treat the infection in various organs. Sentences mentioning both entities a chemical "metronidazole" and a disease "infection": 1. They had been taking metronidazole (total dosage, 45-120 g; duration, 30 days to 2 months) to treat the infection in various organs. Task: Identify the relationship between a chemical "metronidazole" and a disease "infection" 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 "metronidazole" and a disease "inferior colliculus lesion". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Reversible inferior colliculus lesion in metronidazole-induced encephalopathy: magnetic resonance findings on diffusion-weighted and fluid attenuated inversion recovery imaging. - Abstract of the article: OBJECTIVE: This is to present reversible inferior colliculus lesions in metronidazole-induced encephalopathy, to focus on the diffusion-weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) imaging. MATERIALS AND METHODS: From November 2005 to September 2007, 8 patients (5 men and 3 women) were diagnosed as having metronidazole-induced encephalopathy (age range; 43-78 years). They had been taking metronidazole (total dosage, 45-120 g; duration, 30 days to 2 months) to treat the infection in various organs. Initial brain magnetic resonance imaging (MRI) were obtained after the hospitalization, including DWI (8/8), apparent diffusion coefficient (ADC) map (4/8), FLAIR (7/8), and T2-weighted image (8/8). Follow-up MRIs were performed on 5 patients from third to 14th days after discontinuation of metronidazole administration. Findings of initial and follow-up MRIs were retrospectively evaluated by 2 neuroradiologists by consensus, to analyze the presence of abnormal signal intensities, their locations, and signal changes on follow-up images. RESULTS: Initial MRIs showed abnormal high signal intensities on DWI and FLAIR (or T2-weighted image) at the dentate nucleus (8/8), inferior colliculus (6/8), corpus callosum (2/8), pons (2/8), medulla (1/8), and bilateral cerebral white matter (1/8). High-signal intensity lesions on DWI tended to show low signal intensity on ADC map (3/4), but in one patient, high signal intensity was shown at bilateral dentate nuclei on not only DWI but also ADC map. All the lesions in dentate, inferior colliculus, pons, and medullas had been resolved completely on follow-up MRIs in 5 patients, but in 1 patient of them, corpus callosal lesion persisted. CONCLUSIONS: Reversible inferior colliculus lesions could be considered as the characteristic for metronidazole-induced encephalopathy, next to the dentate nucleus involvement. Tips for Analysis: Sentences mentioning a chemical "metronidazole": 1. They had been taking metronidazole (total dosage, 45-120 g; duration, 30 days to 2 months) to treat the infection in various organs. 2. Reversible inferior colliculus lesion in metronidazole-induced encephalopathy: magnetic resonance findings on diffusion-weighted and fluid attenuated inversion recovery imaging. 3. Follow-up MRIs were performed on 5 patients from third to 14th days after discontinuation of metronidazole administration. 4. MATERIALS AND METHODS: From November 2005 to September 2007, 8 patients (5 men and 3 women) were diagnosed as having metronidazole-induced encephalopathy (age range; 43-78 years). 5. OBJECTIVE: This is to present reversible inferior colliculus lesions in metronidazole-induced encephalopathy, to focus on the diffusion-weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) imaging. 6. CONCLUSIONS: Reversible inferior colliculus lesions could be considered as the characteristic for metronidazole-induced encephalopathy, next to the dentate nucleus involvement. Sentences mentioning a disease "inferior colliculus lesion": 1. Reversible inferior colliculus lesion in metronidazole-induced encephalopathy: magnetic resonance findings on diffusion-weighted and fluid attenuated inversion recovery imaging. 2. MATERIALS AND METHODS: From November 2005 to September 2007, 8 patients (5 men and 3 women) were diagnosed as having metronidazole-induced encephalopathy (age range; 43-78 years). 3. All the lesions in dentate, inferior colliculus, pons, and medullas had been resolved completely on follow-up MRIs in 5 patients, but in 1 patient of them, corpus callosal lesion persisted. 4. OBJECTIVE: This is to present reversible inferior colliculus lesions in metronidazole-induced encephalopathy, to focus on the diffusion-weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) imaging. 5. CONCLUSIONS: Reversible inferior colliculus lesions could be considered as the characteristic for metronidazole-induced encephalopathy, next to the dentate nucleus involvement. Sentences mentioning both entities a chemical "metronidazole" and a disease "inferior colliculus lesion": 1. MATERIALS AND METHODS: From November 2005 to September 2007, 8 patients (5 men and 3 women) were diagnosed as having metronidazole-induced encephalopathy (age range; 43-78 years). 2. OBJECTIVE: This is to present reversible inferior colliculus lesions in metronidazole-induced encephalopathy, to focus on the diffusion-weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) imaging. 3. CONCLUSIONS: Reversible inferior colliculus lesions could be considered as the characteristic for metronidazole-induced encephalopathy, next to the dentate nucleus involvement. 4. Reversible inferior colliculus lesion in metronidazole-induced encephalopathy: magnetic resonance findings on diffusion-weighted and fluid attenuated inversion recovery imaging. Task: Identify the relationship between a chemical "metronidazole" and a disease "inferior colliculus lesion" 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 "PC" and a chemical "HBsAg". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a gene or protein "PC": 1. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 2. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 3. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning a chemical "HBsAg": 1. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 2. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning both entities a gene or protein "PC" and a chemical "HBsAg": 1. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Task: Identify the relationship between a gene or protein "PC" and a chemical "HBsAg" 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 "PC" and a chemical "LAM". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a gene or protein "PC": 1. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 2. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 3. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning a chemical "LAM": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. 5. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. 6. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 7. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. Sentences mentioning both entities a gene or protein "PC" and a chemical "LAM": 1. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 2. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 3. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Task: Identify the relationship between a gene or protein "PC" and a chemical "LAM" 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 "precore" and a chemical "HBeAg". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a gene or protein "precore": 1. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 2. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 3. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning a chemical "HBeAg": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. Sentences mentioning both entities a gene or protein "precore" and a chemical "HBeAg": 1. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 2. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. Task: Identify the relationship between a gene or protein "precore" and a chemical "HBeAg" 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 variant "P120T" and a chemical "HBsAg". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a variant "P120T": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 5. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. Sentences mentioning a chemical "HBsAg": 1. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 2. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning both entities a variant "P120T" and a chemical "HBsAg": 1. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. Task: Identify the relationship between a variant "P120T" and a chemical "HBsAg" 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 "P120T" and a chemical "hepatitis B virus e antigen". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a variant "P120T": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 5. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. Sentences mentioning a chemical "hepatitis B virus e antigen": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. Sentences mentioning both entities a variant "P120T" and a chemical "hepatitis B virus e antigen": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 3. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. Task: Identify the relationship between a variant "P120T" and a chemical "hepatitis B virus e antigen" 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 "lamivudine" and a variant "P120T". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a chemical "lamivudine": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. 5. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. 6. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 7. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. Sentences mentioning a variant "P120T": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 5. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. Sentences mentioning both entities a chemical "lamivudine" and a variant "P120T": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 5. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. Task: Identify the relationship between a chemical "lamivudine" and a variant "P120T" 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 "lamivudine" and a chemical "hepatitis B virus e antigen". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a chemical "lamivudine": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. 5. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. 6. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 7. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. Sentences mentioning a chemical "hepatitis B virus e antigen": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. Sentences mentioning both entities a chemical "lamivudine" and a chemical "hepatitis B virus e antigen": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 3. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. Task: Identify the relationship between a chemical "lamivudine" and a chemical "hepatitis B virus e antigen" 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 "G145R" and a chemical "HBsAg". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a variant "G145R": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 3. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 4. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning a chemical "HBsAg": 1. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 2. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning both entities a variant "G145R" and a chemical "HBsAg": 1. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Task: Identify the relationship between a variant "G145R" and a chemical "HBsAg" 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 variant "G145R" and a chemical "lamivudine". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a variant "G145R": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 3. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 4. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning a chemical "lamivudine": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. 5. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. 6. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 7. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. Sentences mentioning both entities a variant "G145R" and a chemical "lamivudine": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 3. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 4. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Task: Identify the relationship between a variant "G145R" and a chemical "lamivudine" 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 "HBeAg" and a variant "G145R". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. - Abstract of the article: Immune escape variants of the hepatitis B virus (HBV) represent an emerging clinical challenge, because they can be associated with vaccine escape, HBV reactivation, and failure of diagnostic tests. Recent data suggest a preferential selection of immune escape mutants in distinct peripheral blood leukocyte compartments of infected individuals. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Although the sP120T substitution also impaired HBsAg secretion, it did not enhance the replication of LAM-resistant clones. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. In all clones with combined immune escape and LAM resistance mutations, the nucleotide analogues adefovir and tenofovir remained effective in suppressing viral replication in vitro. These findings reveal the differential impact of immune escape variants on the replication and drug susceptibility of complex HBV mutants, supporting the need of close surveillance and treatment adjustment in response to the selection of distinct mutational patterns. Tips for Analysis: Sentences mentioning a chemical "HBeAg": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. However, the concomitant occurrence of HBeAg negativity (PC/BCP), sP120T, and LAM resistance resulted in the restoration of replication to levels of wild-type HBV. 3. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 4. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. Sentences mentioning a variant "G145R": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 3. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. 4. The sG145R mutation strongly reduced HBsAg levels and was able to fully restore the impaired replication of LAM-resistant HBV mutants to the levels of wild-type HBV, and PC or BCP mutations further enhanced viral replication. Sentences mentioning both entities a chemical "HBeAg" and a variant "G145R": 1. Differential impact of immune escape mutations G145R and P120T on the replication of lamivudine-resistant hepatitis B virus e antigen-positive and -negative strains. 2. We therefore systematically analyzed the functional impact of the most prevalent immune escape variants, the sG145R and sP120T mutants, on the viral replication efficacy and antiviral drug susceptibility of common treatment-associated mutants with resistance to lamivudine (LAM) and/or HBeAg negativity. 3. Replication-competent HBV strains with sG145R or sP120T and LAM resistance (rtM204I or rtL180M/rtM204V) were generated on an HBeAg-positive and an HBeAg-negative background with precore (PC) and basal core promoter (BCP) mutants. Task: Identify the relationship between a chemical "HBeAg" and a variant "G145R" 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 "hypospadias" and a variant "8 nucleotide deletion". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a disease "hypospadias": 1. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Sentences mentioning a variant "8 nucleotide deletion": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. Sentences mentioning both entities a disease "hypospadias" and a variant "8 nucleotide deletion": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "hypospadias" and a variant "8 nucleotide deletion" 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 "isolated micropenis" and a variant "p.G196S". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a disease "isolated micropenis": 1. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. Sentences mentioning a variant "p.G196S": 1. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. Sentences mentioning both entities a disease "isolated micropenis" and a variant "p.G196S": 1. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. Task: Identify the relationship between a disease "isolated micropenis" and a variant "p.G196S" 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 "isolated micropenis" and a gene or protein "SRD5A2". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a disease "isolated micropenis": 1. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. Sentences mentioning a gene or protein "SRD5A2": 1. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. 2. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. 3. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. 4. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 5. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. Sentences mentioning both entities a disease "isolated micropenis" and a gene or protein "SRD5A2": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "isolated micropenis" and a gene or protein "SRD5A2" 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 "hypospadias". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a gene or protein "SRD5A2": 1. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. 2. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. 3. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. 4. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 5. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. Sentences mentioning a disease "hypospadias": 1. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Sentences mentioning both entities a gene or protein "SRD5A2" and a disease "hypospadias": 1. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Task: Identify the relationship between a gene or protein "SRD5A2" and a disease "hypospadias" 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 "46,XY DSD" and a variant "g.80_87delT CGCGAAG". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a disease "46,XY DSD": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 2. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. 3. Phenotypic presentation of 46,XY DSD depends on the underlying defects. Sentences mentioning a variant "g.80_87delT CGCGAAG": 1. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Sentences mentioning both entities a disease "46,XY DSD" and a variant "g.80_87delT CGCGAAG": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "46,XY DSD" and a variant "g.80_87delT CGCGAAG" 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 "46,XY DSD" and a variant "p.A27fsX132". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a disease "46,XY DSD": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 2. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. 3. Phenotypic presentation of 46,XY DSD depends on the underlying defects. Sentences mentioning a variant "p.A27fsX132": 1. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Sentences mentioning both entities a disease "46,XY DSD" and a variant "p.A27fsX132": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "46,XY DSD" and a variant "p.A27fsX132" 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 "46,XY DSD" and a variant "p.R246Q". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a disease "46,XY DSD": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 2. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. 3. Phenotypic presentation of 46,XY DSD depends on the underlying defects. Sentences mentioning a variant "p.R246Q": 1. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. 2. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Sentences mentioning both entities a disease "46,XY DSD" and a variant "p.R246Q": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "46,XY DSD" and a variant "p.R246Q" 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 "46,XY DSD" and a gene or protein "SRD5A2". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a disease "46,XY DSD": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 2. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. 3. Phenotypic presentation of 46,XY DSD depends on the underlying defects. Sentences mentioning a gene or protein "SRD5A2": 1. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. 2. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. 3. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. 4. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 5. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. Sentences mentioning both entities a disease "46,XY DSD" and a gene or protein "SRD5A2": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 2. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. Task: Identify the relationship between a disease "46,XY DSD" and a gene or protein "SRD5A2" 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 "46,XY DSD" and a variant "8 nucleotide deletion". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. - Abstract of the article: Phenotypic presentation of 46,XY DSD depends on the underlying defects. Defect in androgen action on the target tissues or production of active metabolite share common morphological features. Molecular study may help differentiating these abnormalities with precision. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. The amplicons that showed an aberrant migration in SSCP were subjected to sequencing. Interestingly, six patients from 4 unrelated families (a pair of sibs, uncle/nephew and other two isolated) were identified with mutations in SRD5A2 gene. In five patients p.R246Q missense mutation was detected, of which four were homozygous and one was compound heterozygous: g.80_87delT CGCGAAG (p.A27fsX132) and p.R246Q. Another patient with isolated micropenis harbored a heterozygous p.G196S missense mutation. No AR gene mutation was detected. In conclusion, our study suggests that p.R246Q mutation is common amongst patients with SRD5A2 gene defect from the Northern states of India. Also, it records a novel deletion in exon 1 of SRD5A2 gene in a patient with severe hypospadias. Tips for Analysis: Sentences mentioning a disease "46,XY DSD": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. 2. Mutational analysis of androgen receptor (AR) and SRD5A2 genes was performed in 29 patients with 46,XY DSD, by PCR-SSCP. 3. Phenotypic presentation of 46,XY DSD depends on the underlying defects. Sentences mentioning a variant "8 nucleotide deletion": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. Sentences mentioning both entities a disease "46,XY DSD" and a variant "8 nucleotide deletion": 1. Molecular diagnosis of 46,XY DSD and identification of a novel 8 nucleotide deletion in exon 1 of the SRD5A2 gene. Task: Identify the relationship between a disease "46,XY DSD" and a variant "8 nucleotide deletion" 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 "5-FU" and a disease "tumors". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Safety of capecitabine: a review. - Abstract of the article: IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. AREAS COVERED IN THIS REVIEW: This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety. WHAT THE READER WILL GAIN: The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand-foot syndrome. Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions. Tips for Analysis: Sentences mentioning a chemical "5-FU": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. 2. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. Sentences mentioning a disease "tumors": Sentences mentioning both entities a chemical "5-FU" and a disease "tumors": There is no sentence that contains both these two entities. Task: Identify the relationship between a chemical "5-FU" 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] 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 "capecitabine" and a disease "renal and kidney disease". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Safety of capecitabine: a review. - Abstract of the article: IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. AREAS COVERED IN THIS REVIEW: This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety. WHAT THE READER WILL GAIN: The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand-foot syndrome. Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions. Tips for Analysis: Sentences mentioning a chemical "capecitabine": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. 2. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. Sentences mentioning a disease "renal and kidney disease": Sentences mentioning both entities a chemical "capecitabine" and a disease "renal and kidney disease": There is no sentence that contains both these two entities. Task: Identify the relationship between a chemical "capecitabine" and a disease "renal and kidney disease" 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 "Capecitabine" and a disease "hand-foot syndrome". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Safety of capecitabine: a review. - Abstract of the article: IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. AREAS COVERED IN THIS REVIEW: This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety. WHAT THE READER WILL GAIN: The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand-foot syndrome. Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions. Tips for Analysis: Sentences mentioning a chemical "Capecitabine": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. 2. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. Sentences mentioning a disease "hand-foot syndrome": Sentences mentioning both entities a chemical "Capecitabine" and a disease "hand-foot syndrome": There is no sentence that contains both these two entities. Task: Identify the relationship between a chemical "Capecitabine" and a disease "hand-foot 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] 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 "Capecitabine" and a disease "stomatitis". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Safety of capecitabine: a review. - Abstract of the article: IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. AREAS COVERED IN THIS REVIEW: This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety. WHAT THE READER WILL GAIN: The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand-foot syndrome. Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions. Tips for Analysis: Sentences mentioning a chemical "Capecitabine": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. 2. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. Sentences mentioning a disease "stomatitis": Sentences mentioning both entities a chemical "Capecitabine" and a disease "stomatitis": There is no sentence that contains both these two entities. Task: Identify the relationship between a chemical "Capecitabine" and a disease "stomatitis" 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 "capecitabine" and a disease "vomiting". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Safety of capecitabine: a review. - Abstract of the article: IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. AREAS COVERED IN THIS REVIEW: This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety. WHAT THE READER WILL GAIN: The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand-foot syndrome. Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions. Tips for Analysis: Sentences mentioning a chemical "capecitabine": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. 2. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. Sentences mentioning a disease "vomiting": Sentences mentioning both entities a chemical "capecitabine" and a disease "vomiting": There is no sentence that contains both these two entities. Task: Identify the relationship between a chemical "capecitabine" and a disease "vomiting" 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 "capecitabine" and a disease "nausea". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Safety of capecitabine: a review. - Abstract of the article: IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. AREAS COVERED IN THIS REVIEW: This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety. WHAT THE READER WILL GAIN: The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand-foot syndrome. Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions. Tips for Analysis: Sentences mentioning a chemical "capecitabine": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. 2. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. Sentences mentioning a disease "nausea": Sentences mentioning both entities a chemical "capecitabine" and a disease "nausea": There is no sentence that contains both these two entities. Task: Identify the relationship between a chemical "capecitabine" and a disease "nausea" 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 "capecitabine" and a disease "diarrhea". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Safety of capecitabine: a review. - Abstract of the article: IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. AREAS COVERED IN THIS REVIEW: This article reviews the pharmacology and efficacy of capecitabine with a special emphasis on its safety. WHAT THE READER WILL GAIN: The reader will gain better insight into the safety of capecitabine in special populations such as patients with advanced age, renal and kidney disease. We also explore different dosing and schedules of capecitabine administration. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. It has shown promising results alone or in combination with other chemotherapeutic agents in colorectal, breast, pancreaticobiliary, gastric, renal cell and head and neck cancers. The most commonly reported toxic effects of capecitabine are diarrhea, nausea, vomiting, stomatitis and hand-foot syndrome. Capecitabine has a well-established safety profile and can be given safely to patients with advanced age, hepatic and renal dysfunctions. Tips for Analysis: Sentences mentioning a chemical "capecitabine": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. 2. TAKE HOME MESSAGE: Capecitabine is an oral prodrug of 5-FU and was developed to fulfill the need for a more convenient therapy and provide an improved safety/efficacy profile. Sentences mentioning a disease "diarrhea": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. Sentences mentioning both entities a chemical "capecitabine" and a disease "diarrhea": 1. IMPORTANCE OF THE FIELD: Fluoropyrimidines, in particular 5-fluorouracil (5-FU), have been the mainstay of treatment for several solid tumors, including colorectal, breast and head and neck cancers, for > 40 years. Task: Identify the relationship between a chemical "capecitabine" and a disease "diarrhea" 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 "necrotic" and a chemical "temsirolimus". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. - Abstract of the article: Mantle cell lymphoma (MCL) is a rare and aggressive type of B-cell non-Hodgkin's lymphoma. Patients become progressively refractory to conventional chemotherapy, and their prognosis is poor. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. Tips for Analysis: Sentences mentioning a disease "necrotic": 1. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. Sentences mentioning a chemical "temsirolimus": 1. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. 2. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 3. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. 4. Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. 5. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. 6. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. 7. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Sentences mentioning both entities a disease "necrotic" and a chemical "temsirolimus": 1. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. Task: Identify the relationship between a disease "necrotic" and a chemical "temsirolimus" 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 "temsirolimus" and a gene or protein "mTOR". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. - Abstract of the article: Mantle cell lymphoma (MCL) is a rare and aggressive type of B-cell non-Hodgkin's lymphoma. Patients become progressively refractory to conventional chemotherapy, and their prognosis is poor. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. Tips for Analysis: Sentences mentioning a chemical "temsirolimus": 1. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. 2. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 3. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. 4. Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. 5. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. 6. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. 7. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Sentences mentioning a gene or protein "mTOR": 1. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. Sentences mentioning both entities a chemical "temsirolimus" and a gene or protein "mTOR": 1. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. Task: Identify the relationship between a chemical "temsirolimus" and a gene or protein "mTOR" 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 "temsirolimus" and a gene or protein "VEGF". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. - Abstract of the article: Mantle cell lymphoma (MCL) is a rare and aggressive type of B-cell non-Hodgkin's lymphoma. Patients become progressively refractory to conventional chemotherapy, and their prognosis is poor. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. Tips for Analysis: Sentences mentioning a chemical "temsirolimus": 1. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. 2. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 3. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. 4. Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. 5. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. 6. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. 7. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Sentences mentioning a gene or protein "VEGF": 1. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Sentences mentioning both entities a chemical "temsirolimus" and a gene or protein "VEGF": 1. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Task: Identify the relationship between a chemical "temsirolimus" and a gene or protein "VEGF" 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 "temsirolimus" and a disease "tumor". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. - Abstract of the article: Mantle cell lymphoma (MCL) is a rare and aggressive type of B-cell non-Hodgkin's lymphoma. Patients become progressively refractory to conventional chemotherapy, and their prognosis is poor. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. Tips for Analysis: Sentences mentioning a chemical "temsirolimus": 1. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. 2. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 3. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. 4. Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. 5. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. 6. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. 7. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Sentences mentioning a disease "tumor": 1. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 2. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. 3. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. 4. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Sentences mentioning both entities a chemical "temsirolimus" and a disease "tumor": 1. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 2. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. 3. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. 4. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Task: Identify the relationship between a chemical "temsirolimus" and a disease "tumor" 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 "mantle cell lymphoma" and a chemical "temsirolimus". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. - Abstract of the article: Mantle cell lymphoma (MCL) is a rare and aggressive type of B-cell non-Hodgkin's lymphoma. Patients become progressively refractory to conventional chemotherapy, and their prognosis is poor. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. Tips for Analysis: Sentences mentioning a disease "mantle cell lymphoma": 1. Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. 2. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 3. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. 4. Mantle cell lymphoma (MCL) is a rare and aggressive type of B-cell non-Hodgkin's lymphoma. Sentences mentioning a chemical "temsirolimus": 1. Comparison of the two biopsies showed that temsirolimus inhibited tumor cell proliferation through cell cycle arrest, but did not induce any change in the number of apoptotic tumor cells. 2. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 3. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. 4. Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. 5. Apart from this cytostatic effect, temsirolimus had an antiangiogenic effect with decrease of tumor microvessel density and of VEGF expression. 6. Moreover, numerous patchy, well-limited fibrotic areas, compatible with post-necrotic tissue repair, were found after 6-month temsirolimus therapy. 7. In this case, lymph node biopsies were performed before and six months after temsirolimus therapy. Sentences mentioning both entities a disease "mantle cell lymphoma" and a chemical "temsirolimus": 1. Cytostatic and anti-angiogenic effects of temsirolimus in refractory mantle cell lymphoma. 2. Thus, temsirolimus reduced tumor burden through associated cytostatic and anti-angiogenic effects.This dual effect of temsirolimus on tumor tissue could contribute to its recently reported efficiency in refractory MCL resistant to conventional chemotherapy. 3. However, a 38% remission rate has been recently reported in refractory MCL treated with temsirolimus, a mTOR inhibitor.Here we had the opportunity to study a case of refractory MCL who had tumor regression two months after temsirolimus treatment, and a progression-free survival of 10 months. Task: Identify the relationship between a disease "mantle cell lymphoma" and a chemical "temsirolimus" 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 "NADPH oxidases" and a chemical "ROS". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a gene or protein "NADPH oxidases": 1. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. 2. NADPH oxidases are the main source of ROS in the vasculature. Sentences mentioning a chemical "ROS": 1. NADPH oxidases are the main source of ROS in the vasculature. 2. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). Sentences mentioning both entities a gene or protein "NADPH oxidases" and a chemical "ROS": 1. NADPH oxidases are the main source of ROS in the vasculature. Task: Identify the relationship between a gene or protein "NADPH oxidases" and a chemical "ROS" 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 "ROS" and a disease "atherosclerosis". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a chemical "ROS": 1. NADPH oxidases are the main source of ROS in the vasculature. 2. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). Sentences mentioning a disease "atherosclerosis": 1. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). Sentences mentioning both entities a chemical "ROS" and a disease "atherosclerosis": 1. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). Task: Identify the relationship between a chemical "ROS" and a disease "atherosclerosis" 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 "Reactive oxygen species" and a disease "coronary artery disease". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a chemical "Reactive oxygen species": 1. NADPH oxidases are the main source of ROS in the vasculature. 2. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). Sentences mentioning a disease "coronary artery disease": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. 3. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). 4. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). 5. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 6. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. 7. The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). 8. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. Sentences mentioning both entities a chemical "Reactive oxygen species" and a disease "coronary artery disease": 1. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). Task: Identify the relationship between a chemical "Reactive oxygen species" and a disease "coronary artery disease" 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 "Overweight" and a gene or protein "CYBA". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a disease "Overweight": 1. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 2. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). Sentences mentioning a gene or protein "CYBA": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. 3. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. 4. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. Sentences mentioning both entities a disease "Overweight" and a gene or protein "CYBA": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "Overweight" and a gene or protein "CYBA" 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 "obesity" and a gene or protein "CYBA". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a disease "obesity": 1. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. 2. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 3. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). Sentences mentioning a gene or protein "CYBA": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. 3. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. 4. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. Sentences mentioning both entities a disease "obesity" and a gene or protein "CYBA": There is no sentence that contains both these two entities. Task: Identify the relationship between a disease "obesity" and a gene or protein "CYBA" 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 "-930G" and a disease "overweight". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a variant "-930G": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. 3. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. 4. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 5. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). 6. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 7. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). 8. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. 9. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. 10. The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). Sentences mentioning a disease "overweight": 1. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 2. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). Sentences mentioning both entities a variant "-930G" and a disease "overweight": 1. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 2. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). Task: Identify the relationship between a variant "-930G" and a disease "overweight" 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 "-930G" and a disease "obesity". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a variant "-930G": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. 3. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. 4. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 5. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). 6. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 7. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). 8. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. 9. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. 10. The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). Sentences mentioning a disease "obesity": 1. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. 2. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 3. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). Sentences mentioning both entities a variant "-930G" and a disease "obesity": 1. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. 2. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 3. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). Task: Identify the relationship between a variant "-930G" and a disease "obesity" 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 "-930A>G" and a disease "CAD". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a variant "-930A>G": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. 3. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. 4. A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. 5. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). 6. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 7. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). 8. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. 9. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. 10. The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). Sentences mentioning a disease "CAD": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. 3. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). 4. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). 5. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 6. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. 7. The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). 8. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. Sentences mentioning both entities a variant "-930A>G" and a disease "CAD": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. 3. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). 4. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 5. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. 6. The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). Task: Identify the relationship between a variant "-930A>G" and a disease "CAD" 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 "p22phox" and a gene or protein "NADPH oxidases". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a gene or protein "p22phox": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. 3. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. 4. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. Sentences mentioning a gene or protein "NADPH oxidases": 1. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. 2. NADPH oxidases are the main source of ROS in the vasculature. Sentences mentioning both entities a gene or protein "p22phox" and a gene or protein "NADPH oxidases": 1. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. Task: Identify the relationship between a gene or protein "p22phox" and a gene or protein "NADPH oxidases" 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 "CYBA" and a disease "coronary artery disease". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. A case-control study and gene-risk factors interactions. - Abstract of the article: Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The -930A>G polymorphism was genotyped using the TaqMan - Pre-designed SNP Genotyping Assay (Applied Biosystems). The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). A synergistic effect of the -930G allele with overweight/obesity (BMI --25) and cigarette smoking was found. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. The -930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure. Tips for Analysis: Sentences mentioning a gene or protein "CYBA": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b245 alpha) gene. 3. The -930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. 4. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. Sentences mentioning a disease "coronary artery disease": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. 3. Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). 4. Overweight/obesity was a risk factor for CAD only in the -930G allele carriers (P<10(-10)) but not in the AA homozygotes (P=1.00). 5. The aim of the present study was to analyze a possible association between the -930A>G polymorphism and CAD and to search for gene-traditional risk factors interactions. 6. The estimated CAD risk for BMI --25 and the -930G allele interaction was about 160% greater than that predicted by assuming additivity of the effects, and about 40% greater for interaction of cigarette smoking and the -930G allele. 7. The -930G allele carrier state was a risk factor for CAD (OR 2.03, 95% CI 1.21-3.44, P=0.007). 8. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. Sentences mentioning both entities a gene or protein "CYBA" and a disease "coronary artery disease": 1. The -930A>G polymorphism of the CYBA gene is associated with premature coronary artery disease. 2. In conclusion the -930A>G CYBA polymorphism is associated with CAD in the Polish population. Task: Identify the relationship between a gene or protein "CYBA" and a disease "coronary artery disease" 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 "sodium" and a chemical "glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a chemical "sodium": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning a chemical "glucose": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. 4. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 5. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 6. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. 7. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. Sentences mentioning both entities a chemical "sodium" and a chemical "glucose": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Task: Identify the relationship between a chemical "sodium" and a chemical "glucose" 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 chemical "glucose" and a chemical "phloridzin". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a chemical "glucose": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. 4. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 5. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 6. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. 7. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. Sentences mentioning a chemical "phloridzin": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning both entities a chemical "glucose" and a chemical "phloridzin": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Task: Identify the relationship between a chemical "glucose" and a chemical "phloridzin" 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 gene or protein "GLUT5" and a chemical "cytochalasin B". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT5": 1. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. Sentences mentioning a chemical "cytochalasin B": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning both entities a gene or protein "GLUT5" and a chemical "cytochalasin B": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "GLUT5" and a chemical "cytochalasin B" 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 "GLUT8" and a chemical "cytochalasin B". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT8": 1. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. Sentences mentioning a chemical "cytochalasin B": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning both entities a gene or protein "GLUT8" and a chemical "cytochalasin B": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "GLUT8" and a chemical "cytochalasin B" 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 "GLUT12" and a chemical "cytochalasin B". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT12": 1. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. Sentences mentioning a chemical "cytochalasin B": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning both entities a gene or protein "GLUT12" and a chemical "cytochalasin B": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "GLUT12" and a chemical "cytochalasin B" 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 "GLUT6" and a chemical "glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT6": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Sentences mentioning a chemical "glucose": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. 4. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 5. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 6. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. 7. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. Sentences mentioning both entities a gene or protein "GLUT6" and a chemical "glucose": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Task: Identify the relationship between a gene or protein "GLUT6" 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] 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 "GLUT6" and a chemical "cytochalasin B". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT6": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Sentences mentioning a chemical "cytochalasin B": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning both entities a gene or protein "GLUT6" and a chemical "cytochalasin B": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "GLUT6" and a chemical "cytochalasin B" 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 "GLUT4" and a gene or protein "insulin". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT4": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 4. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 5. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. Sentences mentioning a gene or protein "insulin": 1. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Sentences mentioning both entities a gene or protein "GLUT4" and a gene or protein "insulin": 1. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Task: Identify the relationship between a gene or protein "GLUT4" and a gene or protein "insulin" 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 "GLUT4" and a chemical "Glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT4": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 4. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 5. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. Sentences mentioning a chemical "Glucose": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. 4. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 5. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 6. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. 7. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. Sentences mentioning both entities a gene or protein "GLUT4" and a chemical "Glucose": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 4. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 5. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. Task: Identify the relationship between a gene or protein "GLUT4" 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 "GLUT4" and a chemical "cytochalasin B". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT4": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 4. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 5. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. Sentences mentioning a chemical "cytochalasin B": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning both entities a gene or protein "GLUT4" and a chemical "cytochalasin B": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "GLUT4" and a chemical "cytochalasin B" 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 "GLUT3" and a chemical "glucose". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT3": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Sentences mentioning a chemical "glucose": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. 3. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. 4. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. 5. GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. 6. GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. 7. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. Sentences mentioning both entities a gene or protein "GLUT3" and a chemical "glucose": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Task: Identify the relationship between a gene or protein "GLUT3" 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] 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 "GLUT3" and a chemical "cytochalasin B". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT3": 1. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. 2. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Sentences mentioning a chemical "cytochalasin B": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning both entities a gene or protein "GLUT3" and a chemical "cytochalasin B": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "GLUT3" and a chemical "cytochalasin B" 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 "GLUT2" and a chemical "cytochalasin B". Follow the context and analysis tips provided to assist in your response. <</SYS>> Context: - Title of the article: GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle. - Abstract of the article: GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake. Tips for Analysis: Sentences mentioning a gene or protein "GLUT2": 1. Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. Sentences mentioning a chemical "cytochalasin B": 1. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. Sentences mentioning both entities a gene or protein "GLUT2" and a chemical "cytochalasin B": There is no sentence that contains both these two entities. Task: Identify the relationship between a gene or protein "GLUT2" and a chemical "cytochalasin B" 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>

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