PMC:7373848 / 19069-19910 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T320","span":{"begin":43,"end":53},"obj":"Body_part"},{"id":"T321","span":{"begin":55,"end":64},"obj":"Body_part"},{"id":"T322","span":{"begin":96,"end":112},"obj":"Body_part"},{"id":"T323","span":{"begin":108,"end":112},"obj":"Body_part"},{"id":"T324","span":{"begin":226,"end":237},"obj":"Body_part"},{"id":"T325","span":{"begin":242,"end":253},"obj":"Body_part"},{"id":"T326","span":{"begin":307,"end":318},"obj":"Body_part"},{"id":"T327","span":{"begin":415,"end":422},"obj":"Body_part"},{"id":"T328","span":{"begin":442,"end":453},"obj":"Body_part"},{"id":"T329","span":{"begin":522,"end":526},"obj":"Body_part"},{"id":"T330","span":{"begin":522,"end":524},"obj":"Body_part"},{"id":"T331","span":{"begin":531,"end":533},"obj":"Body_part"},{"id":"T332","span":{"begin":564,"end":581},"obj":"Body_part"},{"id":"T333","span":{"begin":576,"end":581},"obj":"Body_part"},{"id":"T334","span":{"begin":681,"end":690},"obj":"Body_part"},{"id":"T335","span":{"begin":738,"end":754},"obj":"Body_part"},{"id":"T336","span":{"begin":750,"end":754},"obj":"Body_part"},{"id":"T337","span":{"begin":805,"end":815},"obj":"Body_part"}],"attributes":[{"id":"A320","pred":"fma_id","subj":"T320","obj":"http://purl.org/sig/ont/fma/fma241981"},{"id":"A321","pred":"fma_id","subj":"T321","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A322","pred":"fma_id","subj":"T322","obj":"http://purl.org/sig/ont/fma/fma66772"},{"id":"A323","pred":"fma_id","subj":"T323","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A324","pred":"fma_id","subj":"T324","obj":"http://purl.org/sig/ont/fma/fma62860"},{"id":"A325","pred":"fma_id","subj":"T325","obj":"http://purl.org/sig/ont/fma/fma63261"},{"id":"A326","pred":"fma_id","subj":"T326","obj":"http://purl.org/sig/ont/fma/fma62860"},{"id":"A327","pred":"fma_id","subj":"T327","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A328","pred":"fma_id","subj":"T328","obj":"http://purl.org/sig/ont/fma/fma62860"},{"id":"A329","pred":"fma_id","subj":"T329","obj":"http://purl.org/sig/ont/fma/fma86583"},{"id":"A330","pred":"fma_id","subj":"T330","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A331","pred":"fma_id","subj":"T331","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A332","pred":"fma_id","subj":"T332","obj":"http://purl.org/sig/ont/fma/fma66772"},{"id":"A333","pred":"fma_id","subj":"T333","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A334","pred":"fma_id","subj":"T334","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A335","pred":"fma_id","subj":"T335","obj":"http://purl.org/sig/ont/fma/fma66772"},{"id":"A336","pred":"fma_id","subj":"T336","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A337","pred":"fma_id","subj":"T337","obj":"http://purl.org/sig/ont/fma/fma62860"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"LitCovid-PubTator","denotations":[{"id":"312","span":{"begin":370,"end":373},"obj":"Gene"},{"id":"313","span":{"begin":515,"end":520},"obj":"Gene"},{"id":"314","span":{"begin":522,"end":526},"obj":"Gene"},{"id":"315","span":{"begin":531,"end":535},"obj":"Gene"},{"id":"316","span":{"begin":692,"end":700},"obj":"Gene"},{"id":"317","span":{"begin":0,"end":23},"obj":"Disease"},{"id":"318","span":{"begin":283,"end":298},"obj":"Disease"},{"id":"319","span":{"begin":470,"end":482},"obj":"Disease"}],"attributes":[{"id":"A312","pred":"tao:has_database_id","subj":"312","obj":"Gene:207"},{"id":"A313","pred":"tao:has_database_id","subj":"313","obj":"Gene:7124"},{"id":"A314","pred":"tao:has_database_id","subj":"314","obj":"Gene:3552"},{"id":"A315","pred":"tao:has_database_id","subj":"315","obj":"Gene:3576"},{"id":"A316","pred":"tao:has_database_id","subj":"316","obj":"Gene:2147"},{"id":"A317","pred":"tao:has_database_id","subj":"317","obj":"MESH:D008659"},{"id":"A318","pred":"tao:has_database_id","subj":"318","obj":"MESH:D057772"},{"id":"A319","pred":"tao:has_database_id","subj":"319","obj":"MESH:D007249"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T68","span":{"begin":113,"end":119},"obj":"Disease"},{"id":"T69","span":{"begin":292,"end":298},"obj":"Disease"},{"id":"T70","span":{"begin":470,"end":482},"obj":"Disease"},{"id":"T71","span":{"begin":495,"end":501},"obj":"Disease"}],"attributes":[{"id":"A68","pred":"mondo_id","subj":"T68","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A69","pred":"mondo_id","subj":"T69","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A70","pred":"mondo_id","subj":"T70","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A71","pred":"mondo_id","subj":"T71","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T320","span":{"begin":96,"end":112},"obj":"http://purl.obolibrary.org/obo/CL_0000115"},{"id":"T321","span":{"begin":176,"end":179},"obj":"http://purl.obolibrary.org/obo/CLO_0002941"},{"id":"T322","span":{"begin":203,"end":213},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T323","span":{"begin":335,"end":344},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T324","span":{"begin":405,"end":414},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T325","span":{"begin":531,"end":535},"obj":"http://purl.obolibrary.org/obo/CLO_0053704"},{"id":"T326","span":{"begin":555,"end":557},"obj":"http://purl.obolibrary.org/obo/CLO_0053794"},{"id":"T327","span":{"begin":564,"end":581},"obj":"http://purl.obolibrary.org/obo/CL_0000115"},{"id":"T328","span":{"begin":738,"end":754},"obj":"http://purl.obolibrary.org/obo/CL_0000115"},{"id":"T329","span":{"begin":786,"end":795},"obj":"http://purl.obolibrary.org/obo/UBERON_0007651"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T107","span":{"begin":379,"end":381},"obj":"Chemical"},{"id":"T110","span":{"begin":415,"end":422},"obj":"Chemical"},{"id":"T111","span":{"begin":522,"end":524},"obj":"Chemical"},{"id":"T113","span":{"begin":531,"end":533},"obj":"Chemical"}],"attributes":[{"id":"A107","pred":"chebi_id","subj":"T107","obj":"http://purl.obolibrary.org/obo/CHEBI_141424"},{"id":"A108","pred":"chebi_id","subj":"T107","obj":"http://purl.obolibrary.org/obo/CHEBI_25573"},{"id":"A109","pred":"chebi_id","subj":"T107","obj":"http://purl.obolibrary.org/obo/CHEBI_1224"},{"id":"A110","pred":"chebi_id","subj":"T110","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A111","pred":"chebi_id","subj":"T111","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A112","pred":"chebi_id","subj":"T111","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A113","pred":"chebi_id","subj":"T113","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A114","pred":"chebi_id","subj":"T113","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T20","span":{"begin":0,"end":23},"obj":"Phenotype"},{"id":"T21","span":{"begin":25,"end":41},"obj":"Phenotype"}],"attributes":[{"id":"A20","pred":"hp_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/HP_0001939"},{"id":"A21","pred":"hp_id","subj":"T21","obj":"http://purl.obolibrary.org/obo/HP_0025464"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T78","span":{"begin":188,"end":198},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T79","span":{"begin":335,"end":353},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T80","span":{"begin":335,"end":344},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T81","span":{"begin":365,"end":369},"obj":"http://purl.obolibrary.org/obo/GO_0016303"},{"id":"T82","span":{"begin":389,"end":393},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T83","span":{"begin":400,"end":404},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T84","span":{"begin":470,"end":482},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"LitCovid-sentences","denotations":[{"id":"T133","span":{"begin":0,"end":125},"obj":"Sentence"},{"id":"T134","span":{"begin":126,"end":270},"obj":"Sentence"},{"id":"T135","span":{"begin":271,"end":431},"obj":"Sentence"},{"id":"T136","span":{"begin":432,"end":563},"obj":"Sentence"},{"id":"T137","span":{"begin":564,"end":724},"obj":"Sentence"},{"id":"T138","span":{"begin":725,"end":841},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T647","span":{"begin":0,"end":9},"obj":"GO:0008152"},{"id":"T648","span":{"begin":25,"end":34},"obj":"MOP:0000568"},{"id":"T649","span":{"begin":84,"end":89},"obj":"CHEBI:51231;CHEBI:51231"},{"id":"T650","span":{"begin":96,"end":107},"obj":"UBERON:0001986;CL:0000115"},{"id":"T651","span":{"begin":108,"end":112},"obj":"CL:0000115"},{"id":"T652","span":{"begin":180,"end":187},"obj":"SO:0000704"},{"id":"T653","span":{"begin":188,"end":198},"obj":"GO:0065007"},{"id":"T654","span":{"begin":203,"end":216},"obj":"GO:0042116"},{"id":"T655","span":{"begin":226,"end":237},"obj":"CL:0000775"},{"id":"T656","span":{"begin":242,"end":253},"obj":"CL:0000235"},{"id":"T657","span":{"begin":307,"end":318},"obj":"CL:0000775"},{"id":"T658","span":{"begin":370,"end":373},"obj":"PR:000002190"},{"id":"T659","span":{"begin":379,"end":381},"obj":"GO:0005883"},{"id":"T660","span":{"begin":389,"end":393},"obj":"PR:000000104"},{"id":"T661","span":{"begin":396,"end":399},"obj":"PR:000008220"},{"id":"T662","span":{"begin":400,"end":404},"obj":"PR:000000103"},{"id":"T663","span":{"begin":442,"end":453},"obj":"CL:0000775"},{"id":"T664","span":{"begin":515,"end":520},"obj":"PR:000000134"},{"id":"T665","span":{"begin":531,"end":535},"obj":"PR:000001395"},{"id":"T666","span":{"begin":564,"end":575},"obj":"UBERON:0001986;CL:0000115"},{"id":"T667","span":{"begin":576,"end":581},"obj":"CL:0000115"},{"id":"T668","span":{"begin":590,"end":603},"obj":"GO:0031982"},{"id":"T669","span":{"begin":647,"end":669},"obj":"CHEBI:67079;CHEBI:67079"},{"id":"T670","span":{"begin":692,"end":700},"obj":"CHEBI:9574;CHEBI:9574"},{"id":"T671","span":{"begin":738,"end":749},"obj":"UBERON:0001986;CL:0000115"},{"id":"T672","span":{"begin":750,"end":754},"obj":"CL:0000115"},{"id":"T673","span":{"begin":756,"end":769},"obj":"GO:0031982"},{"id":"T674","span":{"begin":805,"end":815},"obj":"CL:0000775"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}

{"project":"2_test","denotations":[{"id":"32700024-30030160-64991477","span":{"begin":121,"end":123},"obj":"30030160"},{"id":"32700024-23777751-64991478","span":{"begin":555,"end":557},"obj":"23777751"},{"id":"32700024-26228903-64991479","span":{"begin":559,"end":561},"obj":"26228903"}],"text":"Metabolic abnormalities, oxidative stress, chemokines, cytokines and by products of DAMPs cause endothelial cell injury [40]. While the toxic effect(s) can be direct, impaired epi-genetic regulation and activation of resident neutrophils and macrophages also contribute. Products of vascular injury recruit neutrophils through several signaling pathways, including PI3K/AKt/eNOS/NF-Kβ and ERK1/2/P38 MAPK-activated protein kinases. Recruited neutrophils subsets promote inflammation and further injury by releasing TNF-α, IL-1 and IL-8, and forming NETs [41, 42]. Endothelial cells produce macrovesicles in response to inflammatory conditions and inflammatory mediators, including cytokines, thrombin and complement 5a [43]. In turn, the endothelial cell  macrovesicles impair adherans junctions, promote neutrophil binding and release NETs."}