PubMed:20621845 JSON TXT

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LitCoin-entities

LitCoin-sentences

{"project":"LitCoin-sentences","denotations":[{"id":"T1","span":{"begin":0,"end":143},"obj":"Sentence"},{"id":"T2","span":{"begin":144,"end":152},"obj":"Sentence"},{"id":"T3","span":{"begin":153,"end":461},"obj":"Sentence"},{"id":"T4","span":{"begin":462,"end":470},"obj":"Sentence"},{"id":"T5","span":{"begin":471,"end":566},"obj":"Sentence"},{"id":"T6","span":{"begin":567,"end":751},"obj":"Sentence"},{"id":"T7","span":{"begin":752,"end":874},"obj":"Sentence"},{"id":"T8","span":{"begin":875,"end":883},"obj":"Sentence"},{"id":"T9","span":{"begin":884,"end":1192},"obj":"Sentence"},{"id":"T10","span":{"begin":1193,"end":1391},"obj":"Sentence"},{"id":"T11","span":{"begin":1392,"end":1558},"obj":"Sentence"},{"id":"T12","span":{"begin":1559,"end":1644},"obj":"Sentence"},{"id":"T13","span":{"begin":1645,"end":1656},"obj":"Sentence"},{"id":"T14","span":{"begin":1657,"end":1867},"obj":"Sentence"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin-entities-OrganismTaxon-PD

{"project":"LitCoin-entities-OrganismTaxon-PD","denotations":[{"id":"T1","span":{"begin":133,"end":136},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":192,"end":195},"obj":"OrganismTaxon"},{"id":"T5","span":{"begin":509,"end":513},"obj":"OrganismTaxon"},{"id":"T8","span":{"begin":1728,"end":1732},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"NCBItxid:10116"},{"id":"A2","pred":"db_id","subj":"T1","obj":"NCBItxid:10114"},{"id":"A3","pred":"db_id","subj":"T3","obj":"NCBItxid:10116"},{"id":"A4","pred":"db_id","subj":"T3","obj":"NCBItxid:10114"},{"id":"A5","pred":"db_id","subj":"T5","obj":"NCBItxid:10118"},{"id":"A6","pred":"db_id","subj":"T5","obj":"NCBItxid:10116"},{"id":"A7","pred":"db_id","subj":"T5","obj":"NCBItxid:10114"},{"id":"A8","pred":"db_id","subj":"T8","obj":"NCBItxid:10118"},{"id":"A9","pred":"db_id","subj":"T8","obj":"NCBItxid:10116"},{"id":"A10","pred":"db_id","subj":"T8","obj":"NCBItxid:10114"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin_Mondo

{"project":"LitCoin_Mondo","denotations":[{"id":"T1","span":{"begin":103,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":112,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":205,"end":229},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":214,"end":229},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":283,"end":289},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005396"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005160"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005396"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0005160"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0021178"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin-NCBITaxon-2

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":133,"end":136},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":192,"end":195},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":509,"end":513},"obj":"OrganismTaxon"},{"id":"T4","span":{"begin":1728,"end":1732},"obj":"OrganismTaxon"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin-GeneOrGeneProduct-v0

LitCoin-GeneOrGeneProduct-v2

LitCoin-Disease-MeSH

{"project":"LitCoin-Disease-MeSH","denotations":[{"id":"T1","span":{"begin":103,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":205,"end":229},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":231,"end":234},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":283,"end":289},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":447,"end":450},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1682,"end":1685},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1847,"end":1866},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A3","pred":"originalLabel","subj":"T3","obj":"D017545"},{"id":"A7","pred":"originalLabel","subj":"T7","obj":"D066253"},{"id":"A6","pred":"originalLabel","subj":"T6","obj":"D017545"},{"id":"A1","pred":"originalLabel","subj":"T1","obj":"D017545"},{"id":"A5","pred":"originalLabel","subj":"T5","obj":"D017545"},{"id":"A4","pred":"originalLabel","subj":"T4","obj":"D014947"},{"id":"A2","pred":"originalLabel","subj":"T2","obj":"D017545"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin_Mondo_095

{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":103,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":205,"end":229},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":231,"end":234},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":283,"end":289},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":447,"end":450},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1682,"end":1685},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005396"},{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005396"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0005396"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0005396"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0021178"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005396"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin-MeSH-Disease-2

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T1","span":{"begin":103,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":205,"end":229},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":231,"end":234},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":283,"end":289},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":447,"end":450},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1682,"end":1685},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1847,"end":1866},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A3","pred":"ID:","subj":"T3","obj":"D017545"},{"id":"A6","pred":"ID:","subj":"T6","obj":"D017545"},{"id":"A5","pred":"ID:","subj":"T5","obj":"D017545"},{"id":"A4","pred":"ID:","subj":"T4","obj":"D014947"},{"id":"A2","pred":"ID:","subj":"T2","obj":"D017545"},{"id":"A1","pred":"ID:","subj":"T1","obj":"D017545"},{"id":"A7","pred":"ID:","subj":"T7","obj":"D066253"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin-MONDO_bioort2019

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T1","span":{"begin":103,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":205,"end":229},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":231,"end":234},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":447,"end":450},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":1682,"end":1685},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"#label","subj":"T1","obj":"D017545"},{"id":"A2","pred":"#label","subj":"T2","obj":"D017545"},{"id":"A3","pred":"#label","subj":"T3","obj":"D017545"},{"id":"A4","pred":"#label","subj":"T4","obj":"D017545"},{"id":"A5","pred":"#label","subj":"T5","obj":"D017545"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin-Chemical-MeSH-CHEBI

LitCoin-GeneOrGeneProduct-v3

{"project":"LitCoin-GeneOrGeneProduct-v3","denotations":[{"id":"T1","span":{"begin":13,"end":19},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":21,"end":27},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":29,"end":34},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":39,"end":44},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":329,"end":340},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":345,"end":362},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":364,"end":368},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":371,"end":396},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":398,"end":402},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":756,"end":760},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":765,"end":769},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":781,"end":785},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":1113,"end":1121},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1193,"end":1198},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1200,"end":1205},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":1207,"end":1214},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":1219,"end":1226},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":1462,"end":1467},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":1469,"end":1474},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":1476,"end":1483},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":1488,"end":1495},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":1559,"end":1563},"obj":"GeneOrGeneProduct"},{"id":"T27","span":{"begin":1792,"end":1797},"obj":"GeneOrGeneProduct"},{"id":"T28","span":{"begin":1799,"end":1804},"obj":"GeneOrGeneProduct"},{"id":"T29","span":{"begin":1806,"end":1812},"obj":"GeneOrGeneProduct"},{"id":"T30","span":{"begin":1817,"end":1823},"obj":"GeneOrGeneProduct"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

LitCoin-training-merged

Allie

{"project":"Allie","denotations":[{"id":"SS1_20621845_2_0","span":{"begin":205,"end":229},"obj":"expanded"},{"id":"SS2_20621845_2_0","span":{"begin":231,"end":234},"obj":"abbr"},{"id":"SS1_20621845_2_1","span":{"begin":329,"end":362},"obj":"expanded"},{"id":"SS2_20621845_2_1","span":{"begin":364,"end":368},"obj":"abbr"},{"id":"SS1_20621845_2_2","span":{"begin":371,"end":396},"obj":"expanded"},{"id":"SS2_20621845_2_2","span":{"begin":398,"end":402},"obj":"abbr"}],"relations":[{"id":"AE1_20621845_2_0","pred":"abbreviatedTo","subj":"SS1_20621845_2_0","obj":"SS2_20621845_2_0"},{"id":"AE1_20621845_2_1","pred":"abbreviatedTo","subj":"SS1_20621845_2_1","obj":"SS2_20621845_2_1"},{"id":"AE1_20621845_2_2","pred":"abbreviatedTo","subj":"SS1_20621845_2_2","obj":"SS2_20621845_2_2"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":205,"end":229},"obj":"HP_0012727"},{"id":"T2","span":{"begin":214,"end":229},"obj":"HP_0004942"},{"id":"T3","span":{"begin":221,"end":229},"obj":"HP_0002617"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

biored-valid-deepseek-nr-ng

biored-valid

biored-valid-deepseek-nr-g

{"project":"biored-valid-deepseek-nr-g","denotations":[{"id":"T1","span":{"begin":13,"end":19},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":21,"end":27},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":29,"end":34},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":39,"end":44},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":103,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":133,"end":136},"obj":"OrganismTaxon"},{"id":"T7","span":{"begin":205,"end":229},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":231,"end":234},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":257,"end":264},"obj":"ChemicalEntity"},{"id":"T10","span":{"begin":364,"end":368},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":398,"end":402},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":437,"end":442},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":447,"end":450},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":494,"end":513},"obj":"OrganismTaxon"},{"id":"T15","span":{"begin":534,"end":541},"obj":"ChemicalEntity"},{"id":"T16","span":{"begin":560,"end":564},"obj":"ChemicalEntity"},{"id":"T17","span":{"begin":611,"end":615},"obj":"ChemicalEntity"},{"id":"T18","span":{"begin":628,"end":632},"obj":"ChemicalEntity"},{"id":"T19","span":{"begin":657,"end":661},"obj":"ChemicalEntity"},{"id":"T20","span":{"begin":756,"end":760},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":925,"end":929},"obj":"ChemicalEntity"},{"id":"T22","span":{"begin":946,"end":953},"obj":"ChemicalEntity"},{"id":"T23","span":{"begin":1193,"end":1198},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":1200,"end":1205},"obj":"GeneOrGeneProduct"},{"id":"T25","span":{"begin":1207,"end":1214},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":1219,"end":1226},"obj":"GeneOrGeneProduct"},{"id":"T27","span":{"begin":1806,"end":1812},"obj":"GeneOrGeneProduct"},{"id":"T28","span":{"begin":1817,"end":1823},"obj":"GeneOrGeneProduct"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

biored-valid-deepseek-r-ng

{"project":"biored-valid-deepseek-r-ng","denotations":[{"id":"T1","span":{"begin":13,"end":19},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":21,"end":27},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":29,"end":34},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":39,"end":44},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":61,"end":79},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":89,"end":94},"obj":"ChemicalEntity"},{"id":"T7","span":{"begin":103,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":133,"end":136},"obj":"OrganismTaxon"},{"id":"T9","span":{"begin":231,"end":234},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":239,"end":255},"obj":"ChemicalEntity"},{"id":"T11","span":{"begin":437,"end":442},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":494,"end":513},"obj":"OrganismTaxon"},{"id":"T13","span":{"begin":560,"end":564},"obj":"ChemicalEntity"},{"id":"T14","span":{"begin":1207,"end":1214},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1219,"end":1226},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":1847,"end":1866},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

biored-valid-deepseek-r-g

{"project":"biored-valid-deepseek-r-g","denotations":[{"id":"T1","span":{"begin":13,"end":19},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":21,"end":27},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":29,"end":34},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":39,"end":44},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":61,"end":79},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":89,"end":94},"obj":"ChemicalEntity"},{"id":"T7","span":{"begin":103,"end":127},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":133,"end":136},"obj":"OrganismTaxon"},{"id":"T9","span":{"begin":231,"end":234},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":239,"end":255},"obj":"ChemicalEntity"},{"id":"T11","span":{"begin":257,"end":264},"obj":"ChemicalEntity"},{"id":"T12","span":{"begin":327,"end":362},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":364,"end":368},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":371,"end":396},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":398,"end":402},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":437,"end":442},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":494,"end":513},"obj":"OrganismTaxon"},{"id":"T18","span":{"begin":989,"end":1009},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T19","span":{"begin":1067,"end":1097},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T20","span":{"begin":1103,"end":1132},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T21","span":{"begin":1193,"end":1198},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":1200,"end":1205},"obj":"GeneOrGeneProduct"},{"id":"T23","span":{"begin":1207,"end":1214},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":1219,"end":1226},"obj":"GeneOrGeneProduct"},{"id":"T25","span":{"begin":1792,"end":1797},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":1799,"end":1804},"obj":"GeneOrGeneProduct"},{"id":"T27","span":{"begin":1806,"end":1812},"obj":"GeneOrGeneProduct"},{"id":"T28","span":{"begin":1817,"end":1823},"obj":"GeneOrGeneProduct"}],"text":"Elevation of ADAM10, ADAM17, MMP-2 and MMP-9 expression with media degeneration features CaCl2-induced thoracic aortic aneurysm in a rat model.\nPURPOSE: This study was designed to establish a rat model of thoracic aortic aneurysm (TAA) by calcium chloride (CaCl(2))-induced arterial injury and to explore the potential role of a disintegrin and metalloproteinase (ADAM), matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) in TAA formation.\nMETHODS: Thoracic aorta of male Sprague-Dawley rats was exposed to 0.5M CaCl(2) or normal saline (NaCl). After 12weeks, animals were euthanized, and CaCl(2)-treated, CaCl(2)-untreated (n=12) and NaCl-treated aortic segments (n=12) were collected for histological and molecular assessments. MMP-TIMP and ADAM mRNAs were semi-quantitatively analyzed and protein expressions were determined by immunohistochemistry.\nRESULTS: Despite similar external diameters among CaCl(2)-treated, non-CaCl(2)-treated and NaCl-treated segments, aneurymal alteration (n=6, 50%), media degeneration with regional disruption, fragmentation of elastic fiber, and increased collagen deposition (n=12, 100%) were demonstrated in CaCl(2)-treated segments. MMP-2, MMP-9, ADAM-10 and ADAM-17 mRNA levels were increased in CaCl(2)-treated segments (all p\u003c0.01), with trends of elevation in CaCl(2)-untreated segments, as compared with NaCl-treated segments. Immunohistochemistry displayed significantly increased expressions of MMP-2, MMP-9, ADAM-10 and ADAM-17 (all p\u003c0.01) in intima and media for CaCl(2)-treated segments. TIMP mRNA and tissue levels did not differ obviously among the three aortic segments.\nCONCLUSION: This study establishes a TAA model by periarterial CaCl(2) exposure in rats, and demonstrates a significant elevation of expression of MMP-2, MMP-9, ADAM10 and ADAM17 in the pathogenesis of vascular remodeling."}

biored-valid-gemini-nr-ng

biored-valid-gemini-r-g

biored-valid-gemini-r-ng

biored-valid-gpt-nr-ng

biored-valid-gpt-nr-g

biored-valid-gpt-r-g

biored-valid-gpt-r-ng

biored-valid-gemini-nr-g

biored-valid-gpt-r-m

biored-valid-gemini-r-m

biored-valid-deepseek-r-m