PMC:7102662 / 12324-12975 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T31","span":{"begin":91,"end":100},"obj":"Body_part"},{"id":"T32","span":{"begin":515,"end":531},"obj":"Body_part"},{"id":"T33","span":{"begin":575,"end":580},"obj":"Body_part"}],"attributes":[{"id":"A31","pred":"fma_id","subj":"T31","obj":"http://purl.org/sig/ont/fma/fma62338"},{"id":"A32","pred":"fma_id","subj":"T32","obj":"http://purl.org/sig/ont/fma/fma67095"},{"id":"A33","pred":"fma_id","subj":"T33","obj":"http://purl.org/sig/ont/fma/fma7088"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T14","span":{"begin":575,"end":580},"obj":"Body_part"}],"attributes":[{"id":"A14","pred":"uberon_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T117","span":{"begin":64,"end":70},"obj":"Disease"},{"id":"T118","span":{"begin":118,"end":126},"obj":"Disease"},{"id":"T119","span":{"begin":241,"end":247},"obj":"Disease"},{"id":"T120","span":{"begin":255,"end":272},"obj":"Disease"},{"id":"T121","span":{"begin":261,"end":272},"obj":"Disease"},{"id":"T122","span":{"begin":299,"end":311},"obj":"Disease"},{"id":"T123","span":{"begin":446,"end":450},"obj":"Disease"},{"id":"T124","span":{"begin":470,"end":474},"obj":"Disease"},{"id":"T125","span":{"begin":631,"end":637},"obj":"Disease"}],"attributes":[{"id":"A117","pred":"mondo_id","subj":"T117","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A118","pred":"mondo_id","subj":"T118","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A119","pred":"mondo_id","subj":"T119","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A120","pred":"mondo_id","subj":"T120","obj":"http://purl.obolibrary.org/obo/MONDO_0023161"},{"id":"A121","pred":"mondo_id","subj":"T121","obj":"http://purl.obolibrary.org/obo/MONDO_0004496"},{"id":"A122","pred":"mondo_id","subj":"T122","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A123","pred":"mondo_id","subj":"T123","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A124","pred":"mondo_id","subj":"T124","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A125","pred":"mondo_id","subj":"T125","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T70","span":{"begin":176,"end":179},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T71","span":{"begin":389,"end":390},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T72","span":{"begin":485,"end":487},"obj":"http://purl.obolibrary.org/obo/CLO_0053733"},{"id":"T73","span":{"begin":548,"end":550},"obj":"http://purl.obolibrary.org/obo/CLO_0001000"},{"id":"T74","span":{"begin":569,"end":574},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T75","span":{"begin":575,"end":580},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"T76","span":{"begin":575,"end":580},"obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"T77","span":{"begin":575,"end":580},"obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"T78","span":{"begin":575,"end":580},"obj":"http://www.ebi.ac.uk/efo/EFO_0000815"},{"id":"T79","span":{"begin":645,"end":650},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T16","span":{"begin":515,"end":531},"obj":"Chemical"},{"id":"T17","span":{"begin":527,"end":531},"obj":"Chemical"}],"attributes":[{"id":"A16","pred":"chebi_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/CHEBI_33697"},{"id":"A17","pred":"chebi_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/CHEBI_37527"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T32","span":{"begin":261,"end":272},"obj":"Phenotype"}],"attributes":[{"id":"A32","pred":"hp_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/HP_0012819"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T17","span":{"begin":299,"end":311},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-sentences","denotations":[{"id":"T102","span":{"begin":0,"end":127},"obj":"Sentence"},{"id":"T103","span":{"begin":128,"end":352},"obj":"Sentence"},{"id":"T104","span":{"begin":353,"end":489},"obj":"Sentence"},{"id":"T105","span":{"begin":490,"end":651},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T222","span":{"begin":56,"end":63},"obj":"UBERON:0000948"},{"id":"T223","span":{"begin":83,"end":90},"obj":"UBERON:0000948"},{"id":"T224","span":{"begin":118,"end":126},"obj":"SP_7"},{"id":"T225","span":{"begin":220,"end":228},"obj":"UBERON:0001621"},{"id":"T226","span":{"begin":230,"end":240},"obj":"UBERON:0002349"},{"id":"T227","span":{"begin":255,"end":260},"obj":"NCBITaxon:10239"},{"id":"T228","span":{"begin":434,"end":438},"obj":"GO:0016265"},{"id":"T229","span":{"begin":446,"end":450},"obj":"SP_10"},{"id":"T230","span":{"begin":470,"end":474},"obj":"SP_10"},{"id":"T231","span":{"begin":509,"end":514},"obj":"NCBITaxon:10239"},{"id":"T232","span":{"begin":569,"end":574},"obj":"SP_6;NCBITaxon:9606"},{"id":"T233","span":{"begin":575,"end":580},"obj":"UBERON:0000948"},{"id":"T234","span":{"begin":620,"end":630},"obj":"UBERON:0002349"},{"id":"T235","span":{"begin":645,"end":650},"obj":"NCBITaxon:10239"},{"id":"T36","span":{"begin":56,"end":63},"obj":"UBERON:0000948"},{"id":"T27626","span":{"begin":620,"end":630},"obj":"UBERON:0002349"},{"id":"T22127","span":{"begin":41,"end":49},"obj":"UBERON:0005985"},{"id":"T81653","span":{"begin":50,"end":55},"obj":"UBERON:0000178"},{"id":"T33438","span":{"begin":110,"end":120},"obj":"UBERON:0002349"},{"id":"T74631","span":{"begin":133,"end":146},"obj":"GO:0007596"},{"id":"T1706","span":{"begin":273,"end":278},"obj":"CHEBI:36044;CHEBI:36044"},{"id":"T69753","span":{"begin":280,"end":295},"obj":"CHEBI:50858;CHEBI:50858"},{"id":"T40512","span":{"begin":333,"end":341},"obj":"SP_7"},{"id":"T95131","span":{"begin":549,"end":556},"obj":"UBERON:0000948"},{"id":"T55330","span":{"begin":618,"end":626},"obj":"SP_7"},{"id":"T47609","span":{"begin":10,"end":17},"obj":"UBERON:0000948"},{"id":"T90774","span":{"begin":329,"end":339},"obj":"UBERON:0000948"},{"id":"T51367","span":{"begin":400,"end":407},"obj":"UBERON:0000948"},{"id":"T20059","span":{"begin":626,"end":634},"obj":"SP_7"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"2_test","denotations":[{"id":"32247212-19453650-25241181","span":{"begin":485,"end":487},"obj":"19453650"}],"text":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}

{"project":"LitCovid-PubTator","denotations":[{"id":"378","span":{"begin":104,"end":112},"obj":"Species"},{"id":"379","span":{"begin":417,"end":425},"obj":"Species"},{"id":"380","span":{"begin":569,"end":574},"obj":"Species"},{"id":"381","span":{"begin":56,"end":79},"obj":"Disease"},{"id":"382","span":{"begin":118,"end":126},"obj":"Disease"},{"id":"383","span":{"begin":230,"end":247},"obj":"Disease"},{"id":"384","span":{"begin":261,"end":272},"obj":"Disease"},{"id":"385","span":{"begin":299,"end":311},"obj":"Disease"},{"id":"386","span":{"begin":434,"end":438},"obj":"Disease"},{"id":"387","span":{"begin":620,"end":637},"obj":"Disease"}],"attributes":[{"id":"A378","pred":"tao:has_database_id","subj":"378","obj":"Tax:9606"},{"id":"A379","pred":"tao:has_database_id","subj":"379","obj":"Tax:9606"},{"id":"A380","pred":"tao:has_database_id","subj":"380","obj":"Tax:9606"},{"id":"A381","pred":"tao:has_database_id","subj":"381","obj":"MESH:D006331"},{"id":"A382","pred":"tao:has_database_id","subj":"382","obj":"MESH:C000657245"},{"id":"A383","pred":"tao:has_database_id","subj":"383","obj":"MESH:D009202"},{"id":"A384","pred":"tao:has_database_id","subj":"384","obj":"MESH:D009205"},{"id":"A385","pred":"tao:has_database_id","subj":"385","obj":"MESH:D007249"},{"id":"A386","pred":"tao:has_database_id","subj":"386","obj":"MESH:D003643"},{"id":"A387","pred":"tao:has_database_id","subj":"387","obj":"MESH:D009202"}],"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":"Any of the mechanisms described above can lead to acute cardiac injury and rise in cardiac troponins in patients with COVID-19. The relative role of these different mechanisms has not been described but direct (i.e. non-coronary) myocardial injury due to viral myocarditis or the effect of systemic inflammation appear to be the most common mechanisms. These observations are supported by a previous autopsy study in patients who had died due to SARS during the Toronto SARS outbreak [11]. In this study, the viral ribonucleic acid was detected in 35% of the autopsied human heart samples, providing evidence for direct myocardial injury by the virus."}