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LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T26","span":{"begin":290,"end":294},"obj":"Body_part"},{"id":"T27","span":{"begin":583,"end":593},"obj":"Body_part"},{"id":"T28","span":{"begin":683,"end":692},"obj":"Body_part"},{"id":"T29","span":{"begin":724,"end":737},"obj":"Body_part"},{"id":"T30","span":{"begin":740,"end":742},"obj":"Body_part"},{"id":"T31","span":{"begin":1081,"end":1089},"obj":"Body_part"}],"attributes":[{"id":"A26","pred":"fma_id","subj":"T26","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A27","pred":"fma_id","subj":"T27","obj":"http://purl.org/sig/ont/fma/fma63261"},{"id":"A28","pred":"fma_id","subj":"T28","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A29","pred":"fma_id","subj":"T29","obj":"http://purl.org/sig/ont/fma/fma264829"},{"id":"A30","pred":"fma_id","subj":"T30","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A31","pred":"fma_id","subj":"T31","obj":"http://purl.org/sig/ont/fma/fma84050"}],"text":"Introduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique qualities."}

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T3","span":{"begin":290,"end":294},"obj":"Body_part"}],"attributes":[{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"Introduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique qualities."}

LitCovid-PD-MONDO

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T15","span":{"begin":290,"end":294},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T16","span":{"begin":290,"end":294},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T17","span":{"begin":566,"end":571},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T18","span":{"begin":594,"end":604},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T19","span":{"begin":642,"end":649},"obj":"http://purl.obolibrary.org/obo/CLO_0009985"},{"id":"T20","span":{"begin":724,"end":737},"obj":"http://purl.obolibrary.org/obo/PR_000001393"},{"id":"T21","span":{"begin":767,"end":783},"obj":"http://purl.obolibrary.org/obo/PR_000000017"},{"id":"T22","span":{"begin":1192,"end":1193},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T23","span":{"begin":1228,"end":1229},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"Introduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique qualities."}

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T15","span":{"begin":246,"end":255},"obj":"Chemical"},{"id":"T16","span":{"begin":740,"end":742},"obj":"Chemical"},{"id":"T18","span":{"begin":751,"end":762},"obj":"Chemical"},{"id":"T19","span":{"begin":767,"end":777},"obj":"Chemical"},{"id":"T20","span":{"begin":778,"end":783},"obj":"Chemical"}],"attributes":[{"id":"A15","pred":"chebi_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A16","pred":"chebi_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A17","pred":"chebi_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A18","pred":"chebi_id","subj":"T18","obj":"http://purl.obolibrary.org/obo/CHEBI_64360"},{"id":"A19","pred":"chebi_id","subj":"T19","obj":"http://purl.obolibrary.org/obo/CHEBI_52999"},{"id":"A20","pred":"chebi_id","subj":"T20","obj":"http://purl.obolibrary.org/obo/CHEBI_30212"}],"text":"Introduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique qualities."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T3","span":{"begin":290,"end":302},"obj":"Phenotype"},{"id":"T4","span":{"begin":431,"end":451},"obj":"Phenotype"},{"id":"T5","span":{"begin":466,"end":478},"obj":"Phenotype"},{"id":"T6","span":{"begin":1081,"end":1095},"obj":"Phenotype"}],"attributes":[{"id":"A3","pred":"hp_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/HP_0002088"},{"id":"A4","pred":"hp_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/HP_0002098"},{"id":"A5","pred":"hp_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/HP_0003256"},{"id":"A6","pred":"hp_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/HP_0033041"}],"text":"Introduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique qualities."}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T2","span":{"begin":394,"end":406},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T3","span":{"begin":583,"end":604},"obj":"http://purl.obolibrary.org/obo/GO_0042116"},{"id":"T4","span":{"begin":937,"end":949},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"Introduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique qualities."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T10","span":{"begin":0,"end":12},"obj":"Sentence"},{"id":"T11","span":{"begin":13,"end":188},"obj":"Sentence"},{"id":"T12","span":{"begin":189,"end":620},"obj":"Sentence"},{"id":"T13","span":{"begin":621,"end":1060},"obj":"Sentence"},{"id":"T14","span":{"begin":1061,"end":1272},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Introduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique qualities."}

LitCovid-PubTator

2_test

{"project":"2_test","denotations":[{"id":"33073244-30774631-66244503","span":{"begin":807,"end":808},"obj":"30774631"}],"text":"Introduction\nIntensive efforts are underway to unravel the immunopathology of COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and to control the pandemic. Given the public health emergency, scarcity of effective antiviral therapies, and rapid evolution of lung disease associated with COVID-19, patients who are critically ill with COVID-19 and have exuberant inflammation, life-threatening acute respiratory distress syndrome, and coagulopathy, are basically treated as if they had secondary haemophagocytic lymphohistiocytosis or virus-associated macrophage activation syndrome (MAS). These treatments are focused on therapies that neutralise key cytokines driving classical MAS, such as interleukin-6 ([IL]-6; eg, tocilizumab) or interferon gamma (IFNγ; eg, emapalumab).1, 2 In fact, some fatal cases of COVID-19 are accompanied not only by severe respiratory disease, but also by increased systemic inflammation as shown by higher ferritin concentrations.2 However, in many aspects, COVID-19 does not resemble typical MAS. We propose that the cytokine storm syndrome seen in COVID-19 is dissimilar to that seen in canonical MAS and should be regarded as a distinct entity and approached in a novel way reflecting its unique qualities."}

PMC:7546716 / 1426-2698 JSONTXT

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PMC:7546716 / 1426-2698 JSON TXT