PMC:7464116 / 30745-32151 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T201","span":{"begin":44,"end":55},"obj":"Body_part"},{"id":"T202","span":{"begin":76,"end":85},"obj":"Body_part"},{"id":"T203","span":{"begin":159,"end":181},"obj":"Body_part"},{"id":"T204","span":{"begin":204,"end":215},"obj":"Body_part"},{"id":"T205","span":{"begin":293,"end":304},"obj":"Body_part"},{"id":"T206","span":{"begin":499,"end":511},"obj":"Body_part"},{"id":"T207","span":{"begin":589,"end":606},"obj":"Body_part"},{"id":"T208","span":{"begin":601,"end":606},"obj":"Body_part"},{"id":"T209","span":{"begin":614,"end":620},"obj":"Body_part"},{"id":"T210","span":{"begin":696,"end":707},"obj":"Body_part"},{"id":"T211","span":{"begin":1240,"end":1245},"obj":"Body_part"},{"id":"T212","span":{"begin":1265,"end":1269},"obj":"Body_part"},{"id":"T213","span":{"begin":1346,"end":1358},"obj":"Body_part"},{"id":"T214","span":{"begin":1383,"end":1400},"obj":"Body_part"},{"id":"T215","span":{"begin":1395,"end":1400},"obj":"Body_part"}],"attributes":[{"id":"A201","pred":"fma_id","subj":"T201","obj":"http://purl.org/sig/ont/fma/fma62845"},{"id":"A202","pred":"fma_id","subj":"T202","obj":"http://purl.org/sig/ont/fma/fma62851"},{"id":"A203","pred":"fma_id","subj":"T203","obj":"http://purl.org/sig/ont/fma/fma274259"},{"id":"A204","pred":"fma_id","subj":"T204","obj":"http://purl.org/sig/ont/fma/fma62845"},{"id":"A205","pred":"fma_id","subj":"T205","obj":"http://purl.org/sig/ont/fma/fma62845"},{"id":"A206","pred":"fma_id","subj":"T206","obj":"http://purl.org/sig/ont/fma/fma62845"},{"id":"A207","pred":"fma_id","subj":"T207","obj":"http://purl.org/sig/ont/fma/fma66772"},{"id":"A208","pred":"fma_id","subj":"T208","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A209","pred":"fma_id","subj":"T209","obj":"http://purl.org/sig/ont/fma/fma7203"},{"id":"A210","pred":"fma_id","subj":"T210","obj":"http://purl.org/sig/ont/fma/fma63916"},{"id":"A211","pred":"fma_id","subj":"T211","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A212","pred":"fma_id","subj":"T212","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A213","pred":"fma_id","subj":"T213","obj":"http://purl.org/sig/ont/fma/fma62925"},{"id":"A214","pred":"fma_id","subj":"T214","obj":"http://purl.org/sig/ont/fma/fma66772"},{"id":"A215","pred":"fma_id","subj":"T215","obj":"http://purl.org/sig/ont/fma/fma68646"}],"text":"Su et al. [66] demonstrated the presence of erythrocyte aggregates, without platelets or fibrinoid fragments, which obstructs the lumen of the peritubular and glomerular capillaries in COVID-19 patients. Erythrocyte aggregation, presumably induced by inflammation (reflected by a high rate of erythrocyte sedimentation) and hypotension, can potentiate oxidative stress, inflammation and complement activation, aggravating microvascular damage [64]. Furthermore, occlusion of microvascular lumens by erythrocytes has been associated with a variety of endothelial lesions [66]. Normally, in endothelial cells of the kidney, only ACE is expressed without detectable ACE-2 [79]. Therefore, the renal endothelium cannot be infected directly by SARS-CoV-2. However, this cannot be totally excluded, since ACE-2expressioncan be changed in pathological states or by drugs [66]. Varga et al. recently concluded that SARS-CoV-2 infection induces endothelitis in various organs, directly and indirectly, and that could explain the systemic impairment of microcirculation [80]. Further studies are necessary to better understand the genesis of renal endothelial lesions. Of note, a recent study has proposed a new route for SARS-CoV-2 invasion of host cells via an alternative cell receptor known as CD147 (and also called basigin), which is a transmembrane glycoprotein and is expressed on all endothelial cells [81]."}

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{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T335","span":{"begin":185,"end":193},"obj":"Disease"},{"id":"T336","span":{"begin":251,"end":263},"obj":"Disease"},{"id":"T337","span":{"begin":324,"end":335},"obj":"Disease"},{"id":"T338","span":{"begin":370,"end":382},"obj":"Disease"},{"id":"T339","span":{"begin":739,"end":747},"obj":"Disease"},{"id":"T340","span":{"begin":739,"end":743},"obj":"Disease"},{"id":"T341","span":{"begin":907,"end":915},"obj":"Disease"},{"id":"T342","span":{"begin":907,"end":911},"obj":"Disease"},{"id":"T343","span":{"begin":918,"end":927},"obj":"Disease"},{"id":"T344","span":{"begin":1212,"end":1220},"obj":"Disease"},{"id":"T345","span":{"begin":1212,"end":1216},"obj":"Disease"}],"attributes":[{"id":"A335","pred":"mondo_id","subj":"T335","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A336","pred":"mondo_id","subj":"T336","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A337","pred":"mondo_id","subj":"T337","obj":"http://purl.obolibrary.org/obo/MONDO_0005468"},{"id":"A338","pred":"mondo_id","subj":"T338","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A339","pred":"mondo_id","subj":"T339","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A340","pred":"mondo_id","subj":"T340","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A341","pred":"mondo_id","subj":"T341","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A342","pred":"mondo_id","subj":"T342","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A343","pred":"mondo_id","subj":"T343","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A344","pred":"mondo_id","subj":"T344","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A345","pred":"mondo_id","subj":"T345","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"}],"text":"Su et al. [66] demonstrated the presence of erythrocyte aggregates, without platelets or fibrinoid fragments, which obstructs the lumen of the peritubular and glomerular capillaries in COVID-19 patients. Erythrocyte aggregation, presumably induced by inflammation (reflected by a high rate of erythrocyte sedimentation) and hypotension, can potentiate oxidative stress, inflammation and complement activation, aggravating microvascular damage [64]. Furthermore, occlusion of microvascular lumens by erythrocytes has been associated with a variety of endothelial lesions [66]. Normally, in endothelial cells of the kidney, only ACE is expressed without detectable ACE-2 [79]. Therefore, the renal endothelium cannot be infected directly by SARS-CoV-2. However, this cannot be totally excluded, since ACE-2expressioncan be changed in pathological states or by drugs [66]. Varga et al. recently concluded that SARS-CoV-2 infection induces endothelitis in various organs, directly and indirectly, and that could explain the systemic impairment of microcirculation [80]. Further studies are necessary to better understand the genesis of renal endothelial lesions. Of note, a recent study has proposed a new route for SARS-CoV-2 invasion of host cells via an alternative cell receptor known as CD147 (and also called basigin), which is a transmembrane glycoprotein and is expressed on all endothelial cells [81]."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T443","span":{"begin":44,"end":55},"obj":"http://purl.obolibrary.org/obo/CL_0000232"},{"id":"T444","span":{"begin":204,"end":215},"obj":"http://purl.obolibrary.org/obo/CL_0000232"},{"id":"T445","span":{"begin":278,"end":279},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T446","span":{"begin":293,"end":304},"obj":"http://purl.obolibrary.org/obo/CL_0000232"},{"id":"T447","span":{"begin":398,"end":408},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T448","span":{"begin":499,"end":511},"obj":"http://purl.obolibrary.org/obo/CL_0000232"},{"id":"T449","span":{"begin":512,"end":515},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T450","span":{"begin":537,"end":538},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T451","span":{"begin":589,"end":606},"obj":"http://purl.obolibrary.org/obo/CL_0000115"},{"id":"T452","span":{"begin":614,"end":620},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T453","span":{"begin":614,"end":620},"obj":"http://www.ebi.ac.uk/efo/EFO_0000927"},{"id":"T454","span":{"begin":614,"end":620},"obj":"http://www.ebi.ac.uk/efo/EFO_0000929"},{"id":"T455","span":{"begin":696,"end":707},"obj":"http://purl.obolibrary.org/obo/UBERON_0001986"},{"id":"T456","span":{"begin":960,"end":966},"obj":"http://purl.obolibrary.org/obo/UBERON_0003103"},{"id":"T457","span":{"begin":1168,"end":1169},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T458","span":{"begin":1183,"end":1186},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T459","span":{"begin":1196,"end":1197},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T460","span":{"begin":1240,"end":1245},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T461","span":{"begin":1265,"end":1269},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T462","span":{"begin":1330,"end":1331},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T463","span":{"begin":1383,"end":1400},"obj":"http://purl.obolibrary.org/obo/CL_0000115"}],"text":"Su et al. [66] demonstrated the presence of erythrocyte aggregates, without platelets or fibrinoid fragments, which obstructs the lumen of the peritubular and glomerular capillaries in COVID-19 patients. Erythrocyte aggregation, presumably induced by inflammation (reflected by a high rate of erythrocyte sedimentation) and hypotension, can potentiate oxidative stress, inflammation and complement activation, aggravating microvascular damage [64]. Furthermore, occlusion of microvascular lumens by erythrocytes has been associated with a variety of endothelial lesions [66]. Normally, in endothelial cells of the kidney, only ACE is expressed without detectable ACE-2 [79]. Therefore, the renal endothelium cannot be infected directly by SARS-CoV-2. However, this cannot be totally excluded, since ACE-2expressioncan be changed in pathological states or by drugs [66]. Varga et al. recently concluded that SARS-CoV-2 infection induces endothelitis in various organs, directly and indirectly, and that could explain the systemic impairment of microcirculation [80]. Further studies are necessary to better understand the genesis of renal endothelial lesions. Of note, a recent study has proposed a new route for SARS-CoV-2 invasion of host cells via an alternative cell receptor known as CD147 (and also called basigin), which is a transmembrane glycoprotein and is expressed on all endothelial cells [81]."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T86","span":{"begin":858,"end":863},"obj":"Chemical"},{"id":"T87","span":{"begin":1346,"end":1358},"obj":"Chemical"}],"attributes":[{"id":"A86","pred":"chebi_id","subj":"T86","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"},{"id":"A87","pred":"chebi_id","subj":"T87","obj":"http://purl.obolibrary.org/obo/CHEBI_17089"}],"text":"Su et al. [66] demonstrated the presence of erythrocyte aggregates, without platelets or fibrinoid fragments, which obstructs the lumen of the peritubular and glomerular capillaries in COVID-19 patients. Erythrocyte aggregation, presumably induced by inflammation (reflected by a high rate of erythrocyte sedimentation) and hypotension, can potentiate oxidative stress, inflammation and complement activation, aggravating microvascular damage [64]. Furthermore, occlusion of microvascular lumens by erythrocytes has been associated with a variety of endothelial lesions [66]. Normally, in endothelial cells of the kidney, only ACE is expressed without detectable ACE-2 [79]. Therefore, the renal endothelium cannot be infected directly by SARS-CoV-2. However, this cannot be totally excluded, since ACE-2expressioncan be changed in pathological states or by drugs [66]. Varga et al. recently concluded that SARS-CoV-2 infection induces endothelitis in various organs, directly and indirectly, and that could explain the systemic impairment of microcirculation [80]. Further studies are necessary to better understand the genesis of renal endothelial lesions. Of note, a recent study has proposed a new route for SARS-CoV-2 invasion of host cells via an alternative cell receptor known as CD147 (and also called basigin), which is a transmembrane glycoprotein and is expressed on all endothelial cells [81]."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T63","span":{"begin":44,"end":66},"obj":"http://purl.obolibrary.org/obo/GO_0034117"},{"id":"T64","span":{"begin":204,"end":227},"obj":"http://purl.obolibrary.org/obo/GO_0034117"},{"id":"T65","span":{"begin":251,"end":263},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T66","span":{"begin":370,"end":382},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T67","span":{"begin":387,"end":408},"obj":"http://purl.obolibrary.org/obo/GO_0006956"},{"id":"T68","span":{"begin":1223,"end":1239},"obj":"http://purl.obolibrary.org/obo/GO_0044409"}],"text":"Su et al. [66] demonstrated the presence of erythrocyte aggregates, without platelets or fibrinoid fragments, which obstructs the lumen of the peritubular and glomerular capillaries in COVID-19 patients. Erythrocyte aggregation, presumably induced by inflammation (reflected by a high rate of erythrocyte sedimentation) and hypotension, can potentiate oxidative stress, inflammation and complement activation, aggravating microvascular damage [64]. Furthermore, occlusion of microvascular lumens by erythrocytes has been associated with a variety of endothelial lesions [66]. Normally, in endothelial cells of the kidney, only ACE is expressed without detectable ACE-2 [79]. Therefore, the renal endothelium cannot be infected directly by SARS-CoV-2. However, this cannot be totally excluded, since ACE-2expressioncan be changed in pathological states or by drugs [66]. Varga et al. recently concluded that SARS-CoV-2 infection induces endothelitis in various organs, directly and indirectly, and that could explain the systemic impairment of microcirculation [80]. Further studies are necessary to better understand the genesis of renal endothelial lesions. Of note, a recent study has proposed a new route for SARS-CoV-2 invasion of host cells via an alternative cell receptor known as CD147 (and also called basigin), which is a transmembrane glycoprotein and is expressed on all endothelial cells [81]."}

{"project":"LitCovid-sentences","denotations":[{"id":"T188","span":{"begin":0,"end":203},"obj":"Sentence"},{"id":"T189","span":{"begin":204,"end":448},"obj":"Sentence"},{"id":"T190","span":{"begin":449,"end":575},"obj":"Sentence"},{"id":"T191","span":{"begin":576,"end":674},"obj":"Sentence"},{"id":"T192","span":{"begin":675,"end":750},"obj":"Sentence"},{"id":"T193","span":{"begin":751,"end":869},"obj":"Sentence"},{"id":"T194","span":{"begin":870,"end":1065},"obj":"Sentence"},{"id":"T195","span":{"begin":1066,"end":1158},"obj":"Sentence"},{"id":"T196","span":{"begin":1159,"end":1406},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Su et al. [66] demonstrated the presence of erythrocyte aggregates, without platelets or fibrinoid fragments, which obstructs the lumen of the peritubular and glomerular capillaries in COVID-19 patients. Erythrocyte aggregation, presumably induced by inflammation (reflected by a high rate of erythrocyte sedimentation) and hypotension, can potentiate oxidative stress, inflammation and complement activation, aggravating microvascular damage [64]. Furthermore, occlusion of microvascular lumens by erythrocytes has been associated with a variety of endothelial lesions [66]. Normally, in endothelial cells of the kidney, only ACE is expressed without detectable ACE-2 [79]. Therefore, the renal endothelium cannot be infected directly by SARS-CoV-2. However, this cannot be totally excluded, since ACE-2expressioncan be changed in pathological states or by drugs [66]. Varga et al. recently concluded that SARS-CoV-2 infection induces endothelitis in various organs, directly and indirectly, and that could explain the systemic impairment of microcirculation [80]. Further studies are necessary to better understand the genesis of renal endothelial lesions. Of note, a recent study has proposed a new route for SARS-CoV-2 invasion of host cells via an alternative cell receptor known as CD147 (and also called basigin), which is a transmembrane glycoprotein and is expressed on all endothelial cells [81]."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T108","span":{"begin":324,"end":335},"obj":"Phenotype"},{"id":"T109","span":{"begin":352,"end":368},"obj":"Phenotype"}],"attributes":[{"id":"A108","pred":"hp_id","subj":"T108","obj":"http://purl.obolibrary.org/obo/HP_0002615"},{"id":"A109","pred":"hp_id","subj":"T109","obj":"http://purl.obolibrary.org/obo/HP_0025464"}],"text":"Su et al. [66] demonstrated the presence of erythrocyte aggregates, without platelets or fibrinoid fragments, which obstructs the lumen of the peritubular and glomerular capillaries in COVID-19 patients. Erythrocyte aggregation, presumably induced by inflammation (reflected by a high rate of erythrocyte sedimentation) and hypotension, can potentiate oxidative stress, inflammation and complement activation, aggravating microvascular damage [64]. Furthermore, occlusion of microvascular lumens by erythrocytes has been associated with a variety of endothelial lesions [66]. Normally, in endothelial cells of the kidney, only ACE is expressed without detectable ACE-2 [79]. Therefore, the renal endothelium cannot be infected directly by SARS-CoV-2. However, this cannot be totally excluded, since ACE-2expressioncan be changed in pathological states or by drugs [66]. Varga et al. recently concluded that SARS-CoV-2 infection induces endothelitis in various organs, directly and indirectly, and that could explain the systemic impairment of microcirculation [80]. Further studies are necessary to better understand the genesis of renal endothelial lesions. Of note, a recent study has proposed a new route for SARS-CoV-2 invasion of host cells via an alternative cell receptor known as CD147 (and also called basigin), which is a transmembrane glycoprotein and is expressed on all endothelial cells [81]."}

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{"project":"2_test","denotations":[{"id":"32759645-32327202-58096209","span":{"begin":11,"end":13},"obj":"32327202"},{"id":"32759645-32366514-58096210","span":{"begin":444,"end":446},"obj":"32366514"},{"id":"32759645-32327202-58096211","span":{"begin":571,"end":573},"obj":"32327202"},{"id":"32759645-25664248-58096212","span":{"begin":670,"end":672},"obj":"25664248"},{"id":"32759645-32327202-58096213","span":{"begin":865,"end":867},"obj":"32327202"}],"text":"Su et al. [66] demonstrated the presence of erythrocyte aggregates, without platelets or fibrinoid fragments, which obstructs the lumen of the peritubular and glomerular capillaries in COVID-19 patients. Erythrocyte aggregation, presumably induced by inflammation (reflected by a high rate of erythrocyte sedimentation) and hypotension, can potentiate oxidative stress, inflammation and complement activation, aggravating microvascular damage [64]. Furthermore, occlusion of microvascular lumens by erythrocytes has been associated with a variety of endothelial lesions [66]. Normally, in endothelial cells of the kidney, only ACE is expressed without detectable ACE-2 [79]. Therefore, the renal endothelium cannot be infected directly by SARS-CoV-2. However, this cannot be totally excluded, since ACE-2expressioncan be changed in pathological states or by drugs [66]. Varga et al. recently concluded that SARS-CoV-2 infection induces endothelitis in various organs, directly and indirectly, and that could explain the systemic impairment of microcirculation [80]. Further studies are necessary to better understand the genesis of renal endothelial lesions. Of note, a recent study has proposed a new route for SARS-CoV-2 invasion of host cells via an alternative cell receptor known as CD147 (and also called basigin), which is a transmembrane glycoprotein and is expressed on all endothelial cells [81]."}