PMC:7319613 / 4650-5532 JSONTXT

{"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T73","span":{"begin":24,"end":32},"obj":"SP_7"},{"id":"T74","span":{"begin":51,"end":60},"obj":"MOP:0000568"},{"id":"T75","span":{"begin":75,"end":84},"obj":"MOP:0000568"},{"id":"T76","span":{"begin":142,"end":152},"obj":"GO:0065007"},{"id":"T77","span":{"begin":243,"end":252},"obj":"MOP:0000568"},{"id":"T78","span":{"begin":281,"end":289},"obj":"MOP:0000568;CHEBI:60156;CHEBI:60156"},{"id":"T79","span":{"begin":290,"end":303},"obj":"CHEBI:60156;CHEBI:60156"},{"id":"T80","span":{"begin":325,"end":333},"obj":"SP_7"},{"id":"T81","span":{"begin":342,"end":347},"obj":"UBERON:0000170"},{"id":"T82","span":{"begin":349,"end":357},"obj":"MOP:0000568;CHEBI:60156;CHEBI:60156"},{"id":"T83","span":{"begin":358,"end":371},"obj":"CHEBI:60156;CHEBI:60156"},{"id":"T84","span":{"begin":392,"end":403},"obj":"GO:0050817"},{"id":"T85","span":{"begin":426,"end":434},"obj":"CL:0000233"},{"id":"T86","span":{"begin":488,"end":496},"obj":"SP_7"},{"id":"T87","span":{"begin":534,"end":542},"obj":"SP_7"},{"id":"T88","span":{"begin":602,"end":611},"obj":"MOP:0000568"},{"id":"T89","span":{"begin":729,"end":737},"obj":"SP_7"},{"id":"T90","span":{"begin":774,"end":783},"obj":"MOP:0000568"},{"id":"T91","span":{"begin":808,"end":819},"obj":"GO:0007567"},{"id":"T79446","span":{"begin":24,"end":32},"obj":"SP_7"},{"id":"T97104","span":{"begin":51,"end":60},"obj":"MOP:0000568"},{"id":"T588","span":{"begin":75,"end":84},"obj":"MOP:0000568"},{"id":"T3518","span":{"begin":142,"end":152},"obj":"GO:0065007"},{"id":"T20606","span":{"begin":243,"end":252},"obj":"MOP:0000568"},{"id":"T20774","span":{"begin":281,"end":289},"obj":"MOP:0000568;CHEBI:60156;CHEBI:60156"},{"id":"T1362","span":{"begin":290,"end":303},"obj":"CHEBI:60156;CHEBI:60156"},{"id":"T87866","span":{"begin":325,"end":333},"obj":"SP_7"},{"id":"T66042","span":{"begin":342,"end":347},"obj":"UBERON:0000170"},{"id":"T4721","span":{"begin":349,"end":357},"obj":"MOP:0000568;CHEBI:60156;CHEBI:60156"},{"id":"T89600","span":{"begin":358,"end":371},"obj":"CHEBI:60156;CHEBI:60156"},{"id":"T43418","span":{"begin":392,"end":403},"obj":"GO:0050817"},{"id":"T82797","span":{"begin":426,"end":434},"obj":"CL:0000233"},{"id":"T81388","span":{"begin":488,"end":496},"obj":"SP_7"},{"id":"T88622","span":{"begin":534,"end":542},"obj":"SP_7"},{"id":"T2753","span":{"begin":602,"end":611},"obj":"MOP:0000568"},{"id":"T37382","span":{"begin":729,"end":737},"obj":"SP_7"},{"id":"T83273","span":{"begin":774,"end":783},"obj":"MOP:0000568"},{"id":"T53875","span":{"begin":808,"end":819},"obj":"GO:0007567"}],"text":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T9","span":{"begin":290,"end":303},"obj":"Body_part"},{"id":"T10","span":{"begin":342,"end":347},"obj":"Body_part"},{"id":"T11","span":{"begin":358,"end":371},"obj":"Body_part"},{"id":"T12","span":{"begin":426,"end":434},"obj":"Body_part"}],"attributes":[{"id":"A9","pred":"fma_id","subj":"T9","obj":"http://purl.org/sig/ont/fma/fma82779"},{"id":"A10","pred":"fma_id","subj":"T10","obj":"http://purl.org/sig/ont/fma/fma68877"},{"id":"A11","pred":"fma_id","subj":"T11","obj":"http://purl.org/sig/ont/fma/fma82779"},{"id":"A12","pred":"fma_id","subj":"T12","obj":"http://purl.org/sig/ont/fma/fma62851"}],"text":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T20","span":{"begin":0,"end":12},"obj":"Disease"},{"id":"T21","span":{"begin":24,"end":32},"obj":"Disease"},{"id":"T22","span":{"begin":114,"end":126},"obj":"Disease"},{"id":"T23","span":{"begin":325,"end":333},"obj":"Disease"},{"id":"T24","span":{"begin":488,"end":496},"obj":"Disease"},{"id":"T25","span":{"begin":534,"end":542},"obj":"Disease"},{"id":"T26","span":{"begin":729,"end":737},"obj":"Disease"}],"attributes":[{"id":"A20","pred":"mondo_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A21","pred":"mondo_id","subj":"T21","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A22","pred":"mondo_id","subj":"T22","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A23","pred":"mondo_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A24","pred":"mondo_id","subj":"T24","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A25","pred":"mondo_id","subj":"T25","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A26","pred":"mondo_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T22","span":{"begin":128,"end":129},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T23","span":{"begin":342,"end":347},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"}],"text":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T6","span":{"begin":281,"end":303},"obj":"Chemical"},{"id":"T7","span":{"begin":290,"end":303},"obj":"Chemical"},{"id":"T8","span":{"begin":358,"end":371},"obj":"Chemical"}],"attributes":[{"id":"A6","pred":"chebi_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_60156"},{"id":"A7","pred":"chebi_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_16247"},{"id":"A8","pred":"chebi_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/CHEBI_16247"}],"text":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}

{"project":"LitCovid-PubTator","denotations":[{"id":"97","span":{"begin":334,"end":341},"obj":"Species"},{"id":"98","span":{"begin":290,"end":303},"obj":"Chemical"},{"id":"99","span":{"begin":358,"end":371},"obj":"Chemical"},{"id":"100","span":{"begin":0,"end":12},"obj":"Disease"},{"id":"101","span":{"begin":24,"end":32},"obj":"Disease"},{"id":"102","span":{"begin":114,"end":126},"obj":"Disease"},{"id":"103","span":{"begin":325,"end":333},"obj":"Disease"},{"id":"104","span":{"begin":392,"end":417},"obj":"Disease"},{"id":"105","span":{"begin":488,"end":496},"obj":"Disease"},{"id":"106","span":{"begin":534,"end":542},"obj":"Disease"},{"id":"107","span":{"begin":729,"end":737},"obj":"Disease"}],"attributes":[{"id":"A97","pred":"tao:has_database_id","subj":"97","obj":"Tax:9606"},{"id":"A98","pred":"tao:has_database_id","subj":"98","obj":"MESH:D010743"},{"id":"A99","pred":"tao:has_database_id","subj":"99","obj":"MESH:D010743"},{"id":"A100","pred":"tao:has_database_id","subj":"100","obj":"MESH:D007249"},{"id":"A101","pred":"tao:has_database_id","subj":"101","obj":"MESH:C000657245"},{"id":"A102","pred":"tao:has_database_id","subj":"102","obj":"MESH:D007249"},{"id":"A103","pred":"tao:has_database_id","subj":"103","obj":"MESH:C000657245"},{"id":"A104","pred":"tao:has_database_id","subj":"104","obj":"MESH:D025861"},{"id":"A105","pred":"tao:has_database_id","subj":"105","obj":"MESH:C000657245"},{"id":"A106","pred":"tao:has_database_id","subj":"106","obj":"MESH:C000657245"},{"id":"A107","pred":"tao:has_database_id","subj":"107","obj":"MESH:C000657245"}],"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":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T15","span":{"begin":51,"end":67},"obj":"Phenotype"},{"id":"T16","span":{"begin":75,"end":91},"obj":"Phenotype"},{"id":"T17","span":{"begin":243,"end":259},"obj":"Phenotype"},{"id":"T18","span":{"begin":392,"end":417},"obj":"Phenotype"},{"id":"T19","span":{"begin":422,"end":441},"obj":"Phenotype"},{"id":"T20","span":{"begin":602,"end":618},"obj":"Phenotype"},{"id":"T21","span":{"begin":774,"end":790},"obj":"Phenotype"}],"attributes":[{"id":"A15","pred":"hp_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/HP_0025464"},{"id":"A16","pred":"hp_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/HP_0025464"},{"id":"A17","pred":"hp_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/HP_0025464"},{"id":"A18","pred":"hp_id","subj":"T18","obj":"http://purl.obolibrary.org/obo/HP_0001928"},{"id":"A19","pred":"hp_id","subj":"T19","obj":"http://purl.obolibrary.org/obo/HP_0001873"},{"id":"A20","pred":"hp_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/HP_0025464"},{"id":"A21","pred":"hp_id","subj":"T21","obj":"http://purl.obolibrary.org/obo/HP_0025464"}],"text":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T7","span":{"begin":0,"end":12},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T8","span":{"begin":114,"end":126},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T9","span":{"begin":142,"end":152},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T10","span":{"begin":392,"end":403},"obj":"http://purl.obolibrary.org/obo/GO_0050817"}],"text":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}

{"project":"LitCovid-sentences","denotations":[{"id":"T28","span":{"begin":0,"end":127},"obj":"Sentence"},{"id":"T29","span":{"begin":128,"end":242},"obj":"Sentence"},{"id":"T30","span":{"begin":243,"end":348},"obj":"Sentence"},{"id":"T31","span":{"begin":349,"end":522},"obj":"Sentence"},{"id":"T32","span":{"begin":523,"end":738},"obj":"Sentence"},{"id":"T33","span":{"begin":739,"end":882},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status."}