PMC:7102662 / 6321-8729 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T14","span":{"begin":42,"end":45},"obj":"Body_part"},{"id":"T15","span":{"begin":303,"end":320},"obj":"Body_part"},{"id":"T16","span":{"begin":359,"end":368},"obj":"Body_part"},{"id":"T17","span":{"begin":554,"end":559},"obj":"Body_part"},{"id":"T18","span":{"begin":675,"end":680},"obj":"Body_part"},{"id":"T19","span":{"begin":685,"end":690},"obj":"Body_part"},{"id":"T20","span":{"begin":751,"end":760},"obj":"Body_part"},{"id":"T21","span":{"begin":939,"end":943},"obj":"Body_part"},{"id":"T22","span":{"begin":1077,"end":1085},"obj":"Body_part"},{"id":"T23","span":{"begin":1232,"end":1241},"obj":"Body_part"},{"id":"T24","span":{"begin":1683,"end":1688},"obj":"Body_part"},{"id":"T25","span":{"begin":2020,"end":2029},"obj":"Body_part"}],"attributes":[{"id":"A14","pred":"fma_id","subj":"T14","obj":"http://purl.org/sig/ont/fma/fma67095"},{"id":"A15","pred":"fma_id","subj":"T15","obj":"http://purl.org/sig/ont/fma/fma265130"},{"id":"A16","pred":"fma_id","subj":"T16","obj":"http://purl.org/sig/ont/fma/fma7161"},{"id":"A17","pred":"fma_id","subj":"T17","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A18","pred":"fma_id","subj":"T18","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A19","pred":"fma_id","subj":"T19","obj":"http://purl.org/sig/ont/fma/fma68877"},{"id":"A20","pred":"fma_id","subj":"T20","obj":"http://purl.org/sig/ont/fma/fma7161"},{"id":"A21","pred":"fma_id","subj":"T21","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A22","pred":"fma_id","subj":"T22","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A23","pred":"fma_id","subj":"T23","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A24","pred":"fma_id","subj":"T24","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A25","pred":"fma_id","subj":"T25","obj":"http://purl.org/sig/ont/fma/fma7161"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T8","span":{"begin":303,"end":320},"obj":"Body_part"},{"id":"T9","span":{"begin":675,"end":680},"obj":"Body_part"},{"id":"T10","span":{"begin":939,"end":943},"obj":"Body_part"},{"id":"T11","span":{"begin":1132,"end":1138},"obj":"Body_part"},{"id":"T12","span":{"begin":1683,"end":1688},"obj":"Body_part"}],"attributes":[{"id":"A8","pred":"uberon_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/UBERON_0000065"},{"id":"A9","pred":"uberon_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A10","pred":"uberon_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A11","pred":"uberon_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/UBERON_0000062"},{"id":"A12","pred":"uberon_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

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Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T36","span":{"begin":24,"end":25},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T37","span":{"begin":125,"end":130},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T38","span":{"begin":359,"end":368},"obj":"http://purl.obolibrary.org/obo/UBERON_0004535"},{"id":"T39","span":{"begin":548,"end":559},"obj":"http://purl.obolibrary.org/obo/CLO_0053065"},{"id":"T40","span":{"begin":614,"end":615},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T41","span":{"begin":616,"end":624},"obj":"http://purl.obolibrary.org/obo/UBERON_0000158"},{"id":"T42","span":{"begin":675,"end":680},"obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"T43","span":{"begin":675,"end":680},"obj":"http://purl.obolibrary.org/obo/UBERON_0007100"},{"id":"T44","span":{"begin":675,"end":680},"obj":"http://purl.obolibrary.org/obo/UBERON_0015228"},{"id":"T45","span":{"begin":675,"end":680},"obj":"http://www.ebi.ac.uk/efo/EFO_0000815"},{"id":"T46","span":{"begin":685,"end":690},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T47","span":{"begin":751,"end":760},"obj":"http://purl.obolibrary.org/obo/UBERON_0004535"},{"id":"T48","span":{"begin":887,"end":896},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T49","span":{"begin":939,"end":943},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T50","span":{"begin":939,"end":943},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T51","span":{"begin":1132,"end":1138},"obj":"http://purl.obolibrary.org/obo/UBERON_0003103"},{"id":"T52","span":{"begin":1683,"end":1688},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T53","span":{"begin":1683,"end":1688},"obj":"http://www.ebi.ac.uk/efo/EFO_0000296"},{"id":"T54","span":{"begin":2020,"end":2029},"obj":"http://purl.obolibrary.org/obo/UBERON_0004535"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T5","span":{"begin":46,"end":50},"obj":"Chemical"},{"id":"T6","span":{"begin":87,"end":91},"obj":"Chemical"},{"id":"T7","span":{"begin":574,"end":585},"obj":"Chemical"},{"id":"T8","span":{"begin":1486,"end":1492},"obj":"Chemical"},{"id":"T9","span":{"begin":1899,"end":1914},"obj":"Chemical"},{"id":"T10","span":{"begin":1899,"end":1908},"obj":"Chemical"},{"id":"T11","span":{"begin":1909,"end":1914},"obj":"Chemical"},{"id":"T12","span":{"begin":1916,"end":1931},"obj":"Chemical"},{"id":"T13","span":{"begin":2308,"end":2319},"obj":"Chemical"},{"id":"T14","span":{"begin":2320,"end":2331},"obj":"Chemical"}],"attributes":[{"id":"A5","pred":"chebi_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_10545"},{"id":"A6","pred":"chebi_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_10545"},{"id":"A7","pred":"chebi_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_48433"},{"id":"A8","pred":"chebi_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/CHEBI_25805"},{"id":"A9","pred":"chebi_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/CHEBI_36044"},{"id":"A10","pred":"chebi_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A11","pred":"chebi_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"},{"id":"A12","pred":"chebi_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/CHEBI_50858"},{"id":"A13","pred":"chebi_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/CHEBI_48433"},{"id":"A14","pred":"chebi_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/CHEBI_27584"},{"id":"A15","pred":"chebi_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/CHEBI_30834"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T20","span":{"begin":1077,"end":1091},"obj":"Phenotype"},{"id":"T21","span":{"begin":1420,"end":1427},"obj":"Phenotype"},{"id":"T22","span":{"begin":1444,"end":1463},"obj":"Phenotype"},{"id":"T23","span":{"begin":1744,"end":1765},"obj":"Phenotype"},{"id":"T24","span":{"begin":2141,"end":2152},"obj":"Phenotype"},{"id":"T25","span":{"begin":2239,"end":2250},"obj":"Phenotype"},{"id":"T26","span":{"begin":2344,"end":2355},"obj":"Phenotype"}],"attributes":[{"id":"A20","pred":"hp_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/HP_0033041"},{"id":"A21","pred":"hp_id","subj":"T21","obj":"http://purl.obolibrary.org/obo/HP_0012418"},{"id":"A22","pred":"hp_id","subj":"T22","obj":"http://purl.obolibrary.org/obo/HP_0002086"},{"id":"A23","pred":"hp_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/HP_0001658"},{"id":"A24","pred":"hp_id","subj":"T24","obj":"http://purl.obolibrary.org/obo/HP_0011675"},{"id":"A25","pred":"hp_id","subj":"T25","obj":"http://purl.obolibrary.org/obo/HP_0002900"},{"id":"A26","pred":"hp_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/HP_0002900"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T10","span":{"begin":737,"end":747},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T11","span":{"begin":887,"end":905},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T12","span":{"begin":887,"end":896},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T13","span":{"begin":971,"end":983},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T14","span":{"begin":1051,"end":1072},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T15","span":{"begin":1610,"end":1622},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T16","span":{"begin":1808,"end":1820},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

{"project":"LitCovid-sentences","denotations":[{"id":"T57","span":{"begin":0,"end":63},"obj":"Sentence"},{"id":"T58","span":{"begin":64,"end":293},"obj":"Sentence"},{"id":"T59","span":{"begin":294,"end":412},"obj":"Sentence"},{"id":"T60","span":{"begin":413,"end":502},"obj":"Sentence"},{"id":"T61","span":{"begin":504,"end":691},"obj":"Sentence"},{"id":"T62","span":{"begin":692,"end":819},"obj":"Sentence"},{"id":"T63","span":{"begin":820,"end":957},"obj":"Sentence"},{"id":"T64","span":{"begin":958,"end":960},"obj":"Sentence"},{"id":"T65","span":{"begin":962,"end":1169},"obj":"Sentence"},{"id":"T66","span":{"begin":1170,"end":1290},"obj":"Sentence"},{"id":"T67","span":{"begin":1291,"end":1293},"obj":"Sentence"},{"id":"T68","span":{"begin":1295,"end":1556},"obj":"Sentence"},{"id":"T69","span":{"begin":1557,"end":1559},"obj":"Sentence"},{"id":"T70","span":{"begin":1561,"end":1766},"obj":"Sentence"},{"id":"T71","span":{"begin":1767,"end":1848},"obj":"Sentence"},{"id":"T72","span":{"begin":1849,"end":1851},"obj":"Sentence"},{"id":"T73","span":{"begin":1853,"end":2030},"obj":"Sentence"},{"id":"T74","span":{"begin":2031,"end":2033},"obj":"Sentence"},{"id":"T75","span":{"begin":2035,"end":2204},"obj":"Sentence"},{"id":"T76","span":{"begin":2205,"end":2343},"obj":"Sentence"},{"id":"T77","span":{"begin":2344,"end":2408},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

{"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T111","span":{"begin":0,"end":10},"obj":"SP_7"},{"id":"T112","span":{"begin":51,"end":62},"obj":"NCBITaxon:11118"},{"id":"T113","span":{"begin":70,"end":77},"obj":"NCBITaxon:species"},{"id":"T114","span":{"begin":92,"end":105},"obj":"NCBITaxon:11118"},{"id":"T115","span":{"begin":125,"end":130},"obj":"SP_6;NCBITaxon:9606"},{"id":"T116","span":{"begin":256,"end":260},"obj":"SP_10"},{"id":"T117","span":{"begin":262,"end":266},"obj":"SP_9"},{"id":"T118","span":{"begin":283,"end":291},"obj":"SP_7"},{"id":"T119","span":{"begin":303,"end":320},"obj":"UBERON:0000065"},{"id":"T120","span":{"begin":347,"end":357},"obj":"SP_7"},{"id":"T121","span":{"begin":485,"end":493},"obj":"SP_7"},{"id":"T122","span":{"begin":511,"end":521},"obj":"UBERON:0002349"},{"id":"T123","span":{"begin":530,"end":540},"obj":"SP_7"},{"id":"T124","span":{"begin":548,"end":553},"obj":"SP_6;NCBITaxon:9606"},{"id":"T125","span":{"begin":574,"end":605},"obj":"PG_10;PR:000003622"},{"id":"T126","span":{"begin":607,"end":611},"obj":"G_3;PG_10;PR:000003622"},{"id":"T127","span":{"begin":616,"end":624},"obj":"GO:0016020"},{"id":"T128","span":{"begin":662,"end":671},"obj":"GO:0010467"},{"id":"T129","span":{"begin":675,"end":680},"obj":"UBERON:0000948"},{"id":"T130","span":{"begin":685,"end":690},"obj":"UBERON:0000170"},{"id":"T131","span":{"begin":692,"end":696},"obj":"G_3;PG_10;PR:000003622"},{"id":"T132","span":{"begin":737,"end":747},"obj":"GO:0065007"},{"id":"T133","span":{"begin":751,"end":753},"obj":"UBERON:0001017"},{"id":"T134","span":{"begin":835,"end":845},"obj":"SP_7"},{"id":"T135","span":{"begin":849,"end":853},"obj":"G_3;PG_10;PR:000003622"},{"id":"T136","span":{"begin":882,"end":886},"obj":"G_3;PG_10;PR:000003622"},{"id":"T137","span":{"begin":924,"end":934},"obj":"UBERON:0002349"},{"id":"T138","span":{"begin":939,"end":943},"obj":"UBERON:0002048"},{"id":"T177","span":{"begin":1006,"end":1014},"obj":"SP_7"},{"id":"T178","span":{"begin":1132,"end":1138},"obj":"UBERON:0000062"},{"id":"T179","span":{"begin":1150,"end":1160},"obj":"UBERON:0000062"},{"id":"T180","span":{"begin":1275,"end":1283},"obj":"SP_7"},{"id":"T181","span":{"begin":1303,"end":1313},"obj":"UBERON:0002349"},{"id":"T182","span":{"begin":1444,"end":1455},"obj":"UBERON:0001004"},{"id":"T183","span":{"begin":1475,"end":1485},"obj":"UBERON:0002349"},{"id":"T184","span":{"begin":1538,"end":1548},"obj":"UBERON:0002349"},{"id":"T185","span":{"begin":1580,"end":1588},"obj":"UBERON:0005985"},{"id":"T186","span":{"begin":1589,"end":1599},"obj":"GO:0007596"},{"id":"T187","span":{"begin":1674,"end":1682},"obj":"UBERON:0005985"},{"id":"T188","span":{"begin":1683,"end":1688},"obj":"UBERON:0000178"},{"id":"T189","span":{"begin":1744,"end":1754},"obj":"UBERON:0002349"},{"id":"T190","span":{"begin":1767,"end":1780},"obj":"GO:0007596"},{"id":"T191","span":{"begin":1909,"end":1914},"obj":"CHEBI:36044;CHEBI:36044"},{"id":"T192","span":{"begin":1916,"end":1931},"obj":"CHEBI:50858;CHEBI:50858"},{"id":"T193","span":{"begin":1970,"end":1978},"obj":"SP_7"},{"id":"T194","span":{"begin":2187,"end":2194},"obj":"UBERON:0000948"},{"id":"T195","span":{"begin":2254,"end":2262},"obj":"SP_7"},{"id":"T196","span":{"begin":2286,"end":2296},"obj":"SP_7"},{"id":"T197","span":{"begin":2302,"end":2307},"obj":"PR:000013883"},{"id":"T90623","span":{"begin":1502,"end":1510},"obj":"SP_7"},{"id":"T3419","span":{"begin":1556,"end":1564},"obj":"UBERON:0000948"},{"id":"T78722","span":{"begin":1812,"end":1820},"obj":"SP_7"},{"id":"T53635","span":{"begin":1825,"end":1834},"obj":"GO:0007612"},{"id":"T94419","span":{"begin":1854,"end":1865},"obj":"NCBITaxon:11118"},{"id":"T38989","span":{"begin":1884,"end":1889},"obj":"SP_10"},{"id":"T67414","span":{"begin":1927,"end":1931},"obj":"SP_9"},{"id":"T60021","span":{"begin":2161,"end":2169},"obj":"SP_7"},{"id":"T3699","span":{"begin":2193,"end":2201},"obj":"SP_7"},{"id":"T86101","span":{"begin":2208,"end":2219},"obj":"NCBITaxon:11118"},{"id":"T88588","span":{"begin":2252,"end":2259},"obj":"UBERON:0000948"},{"id":"T53986","span":{"begin":2263,"end":2277},"obj":"UBERON:0004535"},{"id":"T35855","span":{"begin":2295,"end":2305},"obj":"UBERON:0002349"},{"id":"T55568","span":{"begin":2335,"end":2340},"obj":"UBERON:0000948"},{"id":"T45400","span":{"begin":2404,"end":2408},"obj":"SP_10"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

{"project":"2_test","denotations":[{"id":"32247212-31986264-25241178","span":{"begin":1287,"end":1288},"obj":"31986264"}],"text":"SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. Systemic inflammation- More severe forms of COVID-19 are characterized by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of proinflammatory cytokines in patients with severe/critical COVID-19 [5,6].\n3. Altered myocardial demand-supply ratio- Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.\n4. Plaque rupture and coronary thrombosis- Systemic inflammation as well as increased shear stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk.\n5. Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}

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is caused by a novel enveloped RNA beta-coronavirus. Seven species of these beta-coronaviruses are known to cause human infections, with four mainly causing mild flulike symptoms and the remaining three resulting in potentially fatal illnesses (SARS, MERS and the ongoing COVID-19). Although respiratory tract is the primary target for SARS-CoV-2, CV system may get involved in several different ways. Following are the common mechanisms responsible for CV complications in COVID-19 [3,4]-1. Direct myocardial injury- SARS-CoV-2 enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signaling pathways, leading to acute myocardial and lung injury [3,4].\n2. 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Adverse effects of various therapies- Various antiviral drugs, corticosteroids and other therapies aimed at treating COVID-19 can also have deleterious effects on the CV system.\n6. Electrolyte imbalances- Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, esp. in patients with underlying cardiac disorder. There is particular concern about hypokalemia in COVID-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system [7]. Hypokalemia increases vulnerability to various tachyarrhythmias."}