PMC:7381711 / 17433-18514 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T153","span":{"begin":48,"end":55},"obj":"Body_part"},{"id":"T154","span":{"begin":94,"end":98},"obj":"Body_part"},{"id":"T155","span":{"begin":292,"end":296},"obj":"Body_part"},{"id":"T156","span":{"begin":390,"end":394},"obj":"Body_part"},{"id":"T157","span":{"begin":509,"end":526},"obj":"Body_part"},{"id":"T158","span":{"begin":631,"end":637},"obj":"Body_part"},{"id":"T159","span":{"begin":737,"end":745},"obj":"Body_part"},{"id":"T160","span":{"begin":907,"end":915},"obj":"Body_part"},{"id":"T161","span":{"begin":1022,"end":1029},"obj":"Body_part"}],"attributes":[{"id":"A153","pred":"fma_id","subj":"T153","obj":"http://purl.org/sig/ont/fma/fma82839"},{"id":"A154","pred":"fma_id","subj":"T154","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A155","pred":"fma_id","subj":"T155","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A156","pred":"fma_id","subj":"T156","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A157","pred":"fma_id","subj":"T157","obj":"http://purl.org/sig/ont/fma/fma9639"},{"id":"A158","pred":"fma_id","subj":"T158","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A159","pred":"fma_id","subj":"T159","obj":"http://purl.org/sig/ont/fma/fma264783"},{"id":"A160","pred":"fma_id","subj":"T160","obj":"http://purl.org/sig/ont/fma/fma264783"},{"id":"A161","pred":"fma_id","subj":"T161","obj":"http://purl.org/sig/ont/fma/fma82839"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T13","span":{"begin":94,"end":98},"obj":"Body_part"},{"id":"T14","span":{"begin":292,"end":296},"obj":"Body_part"},{"id":"T15","span":{"begin":390,"end":394},"obj":"Body_part"},{"id":"T16","span":{"begin":520,"end":526},"obj":"Body_part"},{"id":"T17","span":{"begin":631,"end":637},"obj":"Body_part"}],"attributes":[{"id":"A13","pred":"uberon_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A14","pred":"uberon_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A15","pred":"uberon_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A16","pred":"uberon_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A17","pred":"uberon_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}

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{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T148","span":{"begin":169,"end":177},"obj":"Disease"},{"id":"T149","span":{"begin":230,"end":240},"obj":"Disease"},{"id":"T150","span":{"begin":297,"end":303},"obj":"Disease"},{"id":"T151","span":{"begin":464,"end":479},"obj":"Disease"},{"id":"T152","span":{"begin":470,"end":479},"obj":"Disease"},{"id":"T153","span":{"begin":575,"end":594},"obj":"Disease"},{"id":"T154","span":{"begin":585,"end":594},"obj":"Disease"},{"id":"T155","span":{"begin":675,"end":684},"obj":"Disease"},{"id":"T156","span":{"begin":693,"end":699},"obj":"Disease"},{"id":"T157","span":{"begin":864,"end":873},"obj":"Disease"},{"id":"T158","span":{"begin":1071,"end":1080},"obj":"Disease"}],"attributes":[{"id":"A148","pred":"mondo_id","subj":"T148","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A149","pred":"mondo_id","subj":"T149","obj":"http://purl.obolibrary.org/obo/MONDO_0000831"},{"id":"A150","pred":"mondo_id","subj":"T150","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A151","pred":"mondo_id","subj":"T151","obj":"http://purl.obolibrary.org/obo/MONDO_0006012"},{"id":"A152","pred":"mondo_id","subj":"T152","obj":"http://purl.obolibrary.org/obo/MONDO_0005249"},{"id":"A153","pred":"mondo_id","subj":"T153","obj":"http://purl.obolibrary.org/obo/MONDO_0005812"},{"id":"A154","pred":"mondo_id","subj":"T154","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A155","pred":"mondo_id","subj":"T155","obj":"http://purl.obolibrary.org/obo/MONDO_0005812"},{"id":"A156","pred":"mondo_id","subj":"T156","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A157","pred":"mondo_id","subj":"T157","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A158","pred":"mondo_id","subj":"T158","obj":"http://purl.obolibrary.org/obo/MONDO_0005249"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T116","span":{"begin":94,"end":98},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T117","span":{"begin":94,"end":98},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T118","span":{"begin":241,"end":244},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T119","span":{"begin":275,"end":281},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_33208"},{"id":"T120","span":{"begin":292,"end":296},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T121","span":{"begin":292,"end":296},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T122","span":{"begin":351,"end":358},"obj":"http://purl.obolibrary.org/obo/UBERON_0001005"},{"id":"T123","span":{"begin":359,"end":362},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T124","span":{"begin":390,"end":394},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T125","span":{"begin":390,"end":394},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T126","span":{"begin":410,"end":412},"obj":"http://purl.obolibrary.org/obo/CLO_0001302"},{"id":"T127","span":{"begin":447,"end":453},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_33208"},{"id":"T128","span":{"begin":509,"end":526},"obj":"http://purl.obolibrary.org/obo/UBERON_0000483"},{"id":"T129","span":{"begin":552,"end":558},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_33208"},{"id":"T130","span":{"begin":768,"end":769},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T202","span":{"begin":48,"end":55},"obj":"Chemical"},{"id":"T203","span":{"begin":988,"end":1002},"obj":"Chemical"},{"id":"T204","span":{"begin":1022,"end":1029},"obj":"Chemical"}],"attributes":[{"id":"A202","pred":"chebi_id","subj":"T202","obj":"http://purl.obolibrary.org/obo/CHEBI_28304"},{"id":"A203","pred":"chebi_id","subj":"T203","obj":"http://purl.obolibrary.org/obo/CHEBI_50249"},{"id":"A204","pred":"chebi_id","subj":"T204","obj":"http://purl.obolibrary.org/obo/CHEBI_28304"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T34","span":{"begin":123,"end":134},"obj":"http://purl.obolibrary.org/obo/GO_0050817"},{"id":"T35","span":{"begin":310,"end":321},"obj":"http://purl.obolibrary.org/obo/GO_0050817"},{"id":"T36","span":{"begin":746,"end":757},"obj":"http://purl.obolibrary.org/obo/GO_0050817"},{"id":"T37","span":{"begin":934,"end":945},"obj":"http://purl.obolibrary.org/obo/GO_0050817"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}

{"project":"LitCovid-sentences","denotations":[{"id":"T106","span":{"begin":0,"end":178},"obj":"Sentence"},{"id":"T107","span":{"begin":179,"end":414},"obj":"Sentence"},{"id":"T108","span":{"begin":415,"end":599},"obj":"Sentence"},{"id":"T109","span":{"begin":600,"end":700},"obj":"Sentence"},{"id":"T110","span":{"begin":701,"end":874},"obj":"Sentence"},{"id":"T111","span":{"begin":875,"end":1081},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T41","span":{"begin":470,"end":479},"obj":"Phenotype"},{"id":"T42","span":{"begin":1071,"end":1080},"obj":"Phenotype"}],"attributes":[{"id":"A41","pred":"hp_id","subj":"T41","obj":"http://purl.obolibrary.org/obo/HP_0002090"},{"id":"A42","pred":"hp_id","subj":"T42","obj":"http://purl.obolibrary.org/obo/HP_0002090"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}

{"project":"2_test","denotations":[{"id":"32519894-11734456-2138205","span":{"begin":305,"end":307},"obj":"11734456"},{"id":"32519894-23033361-2138206","span":{"begin":407,"end":408},"obj":"23033361"},{"id":"32519894-25884207-2138207","span":{"begin":410,"end":412},"obj":"25884207"},{"id":"32519894-26947929-2138208","span":{"begin":596,"end":597},"obj":"26947929"},{"id":"32519894-27288618-2138209","span":{"begin":1031,"end":1032},"obj":"27288618"}],"text":"It is also possible that the intended effect of heparin (i.e., anticoagulation) can interrupt lung-protective processes of coagulation that may improve host survival in COVID-19. Although critical illness-associated intravascular thrombosis has been recognized as harmful in animal models of lung injury (44), coagulation occurring within alveoli and airways has generally been found to be lung protective (9, 34). This is particularly notable in animal models of viral pneumonia, in which transgenic loss of epithelial tissue factor markedly worsened animal mortality after influenza infection (3). Transgenic loss of endothelial tissue factor, conversely, had no effect on influenza-induced injury. It is therefore possible that intra-alveolar coagulation may serve a teleological function of isolating pulmonary pathogens, protecting the host from disseminated infection. Such divergent effects of intra-alveolar and intravascular coagulation may in part explain the muted benefits of anticoagulants [including inhaled heparin (6)] in randomized controlled studies of pneumonia."}