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LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

LitCovid-PD-MONDO

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-HP

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T12","span":{"begin":217,"end":239},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T13","span":{"begin":224,"end":239},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T14","span":{"begin":416,"end":438},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T15","span":{"begin":423,"end":438},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T16","span":{"begin":1066,"end":1081},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T17","span":{"begin":2070,"end":2080},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T18","span":{"begin":2287,"end":2296},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T19","span":{"begin":2287,"end":2296},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T20","span":{"begin":2575,"end":2591},"obj":"http://purl.obolibrary.org/obo/GO_0042310"},{"id":"T21","span":{"begin":3398,"end":3408},"obj":"http://purl.obolibrary.org/obo/GO_0065007"}],"text":"SARS-CoV-2 likely binds to epithelial cells in the nasal cavity during the asymptomatic state of the disease (initial 1–2 days of infection) where there might be some local propagation of the virus but with a limited innate immune response. Within the next few days the infection starts in the upper airway and during this stage the infection can be detected by nasal swabs or sputum as well as early markers of the innate immune response. About 80% of infected patients show mild symptoms that are mostly restricted to the upper and conducting airways.13 However, about 20% of infected patients will progress to develop a lower respiratory tract infection leading to hypoxia, and lung damage. These patients are liable to succumb to acute respiratory distress syndrome (ARDS), which is frequently fatal. Patients with comorbidities such as cardiovascular disease, diabetes mellitus, hypertension, chronic lung disease, cancer, chronic kidney disease, and obesity (body mass index ≥30) and ARDS are at increased risk of death.14 The available data indicate that the viral infection can produce an excessive immune reaction known as cytokine release syndrome (CRS) or “cytokine storm” associated with elevated levels of interleukin-6 (IL-6).15 Laboratory findings associated with worse clinical outcomes include lymphopenia, and elevations in liver enzymes, lactate dehydrogenase (LDH), inflammatory markers (e.g., C-reactive protein [CRP], ferritin), d-dimer, prothrombin time (PT), troponin and creatine phosphokinase (CPK), and acute kidney injury.15 Chest CT scans in patients with COVID-19 commonly show ground-glass opacification, consistent with viral pneumonia with abnormalities more likely to be bilateral with a peripheral distribution involving the lower lobes.16 While SARS-CoV-2 entry is dependent on ACE2 in lung cells,8 ACE2 expression is not exclusive to the lungs, and higher relative ACE2 expression is observed in heart, kidney, GIT, and testes (Gene ID: 59272). The organ- and cell-specific expression of ACE2 suggests that it may play a role in the regulation of cardiovascular and renal function as well as fertility. Surprisingly, the 2003 SARS-CoV infection was shown to downregulate the expression of ACE2 in lung tissue reducing transmissibility but increasing virulence.17 ACE2, a component of the renin-angiotensin system (RAS), catalyzes the cleavage of angiotensin I into angiotensin 1–9 and angiotensin II into the vasodilator angiotensin 1–7.18 The balance between angiotensin II and angiotensin (1–7) is critical since angiotensin II elicits vasoconstriction via the angiotensin AT1 receptor, whereas angiotensin (1–7) exerts a vasodilatory effect mediated by AT2 with multiple beneficial effects on the cardiovascular and respiratory system.18 While ACE2 appears to be involved in the hypertension and respiratory manifestations of severely ill patients, the benefits and merits of ACE inhibitors (ACEI) or angiotensin receptor 1 blockers (ARBs) in the SARS-CoV-2 patient is still controversial.18 The priming of the S viral protein by TMPRSS2 is crucial for viral entry where TMPRSS2 expression is very high in the lungs, kidneys, and prostate tissue (Gene ID: 7113).8 TMPRSS2 is predominantly expressed in the luminal cells of the prostate epithelium, where its expression is regulated positively by androgens and negatively regulated by estrogens. The hormonal regulation of TMPRSS2 has been suggested to be linked to the fact that men are at higher risk than women to become seriously ill with COVID-19.19 TMPRSS2 knockout in mice is not lethal. In contrast, humans are intolerant to the loss of function of ACE2.19 Concerns about the effect of ACEI and AT receptor blockers in COVID-19 patients are actively being investigated in the clinic, with the most recent reports offering encouragement that they may have a beneficial effect."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T26","span":{"begin":0,"end":240},"obj":"Sentence"},{"id":"T27","span":{"begin":241,"end":439},"obj":"Sentence"},{"id":"T28","span":{"begin":440,"end":693},"obj":"Sentence"},{"id":"T29","span":{"begin":694,"end":804},"obj":"Sentence"},{"id":"T30","span":{"begin":805,"end":1973},"obj":"Sentence"},{"id":"T31","span":{"begin":1974,"end":1981},"obj":"Sentence"},{"id":"T32","span":{"begin":1982,"end":2139},"obj":"Sentence"},{"id":"T33","span":{"begin":2140,"end":3195},"obj":"Sentence"},{"id":"T34","span":{"begin":3196,"end":3384},"obj":"Sentence"},{"id":"T35","span":{"begin":3385,"end":3583},"obj":"Sentence"},{"id":"T36","span":{"begin":3584,"end":3872},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"SARS-CoV-2 likely binds to epithelial cells in the nasal cavity during the asymptomatic state of the disease (initial 1–2 days of infection) where there might be some local propagation of the virus but with a limited innate immune response. Within the next few days the infection starts in the upper airway and during this stage the infection can be detected by nasal swabs or sputum as well as early markers of the innate immune response. About 80% of infected patients show mild symptoms that are mostly restricted to the upper and conducting airways.13 However, about 20% of infected patients will progress to develop a lower respiratory tract infection leading to hypoxia, and lung damage. These patients are liable to succumb to acute respiratory distress syndrome (ARDS), which is frequently fatal. Patients with comorbidities such as cardiovascular disease, diabetes mellitus, hypertension, chronic lung disease, cancer, chronic kidney disease, and obesity (body mass index ≥30) and ARDS are at increased risk of death.14 The available data indicate that the viral infection can produce an excessive immune reaction known as cytokine release syndrome (CRS) or “cytokine storm” associated with elevated levels of interleukin-6 (IL-6).15 Laboratory findings associated with worse clinical outcomes include lymphopenia, and elevations in liver enzymes, lactate dehydrogenase (LDH), inflammatory markers (e.g., C-reactive protein [CRP], ferritin), d-dimer, prothrombin time (PT), troponin and creatine phosphokinase (CPK), and acute kidney injury.15 Chest CT scans in patients with COVID-19 commonly show ground-glass opacification, consistent with viral pneumonia with abnormalities more likely to be bilateral with a peripheral distribution involving the lower lobes.16 While SARS-CoV-2 entry is dependent on ACE2 in lung cells,8 ACE2 expression is not exclusive to the lungs, and higher relative ACE2 expression is observed in heart, kidney, GIT, and testes (Gene ID: 59272). The organ- and cell-specific expression of ACE2 suggests that it may play a role in the regulation of cardiovascular and renal function as well as fertility. Surprisingly, the 2003 SARS-CoV infection was shown to downregulate the expression of ACE2 in lung tissue reducing transmissibility but increasing virulence.17 ACE2, a component of the renin-angiotensin system (RAS), catalyzes the cleavage of angiotensin I into angiotensin 1–9 and angiotensin II into the vasodilator angiotensin 1–7.18 The balance between angiotensin II and angiotensin (1–7) is critical since angiotensin II elicits vasoconstriction via the angiotensin AT1 receptor, whereas angiotensin (1–7) exerts a vasodilatory effect mediated by AT2 with multiple beneficial effects on the cardiovascular and respiratory system.18 While ACE2 appears to be involved in the hypertension and respiratory manifestations of severely ill patients, the benefits and merits of ACE inhibitors (ACEI) or angiotensin receptor 1 blockers (ARBs) in the SARS-CoV-2 patient is still controversial.18 The priming of the S viral protein by TMPRSS2 is crucial for viral entry where TMPRSS2 expression is very high in the lungs, kidneys, and prostate tissue (Gene ID: 7113).8 TMPRSS2 is predominantly expressed in the luminal cells of the prostate epithelium, where its expression is regulated positively by androgens and negatively regulated by estrogens. The hormonal regulation of TMPRSS2 has been suggested to be linked to the fact that men are at higher risk than women to become seriously ill with COVID-19.19 TMPRSS2 knockout in mice is not lethal. In contrast, humans are intolerant to the loss of function of ACE2.19 Concerns about the effect of ACEI and AT receptor blockers in COVID-19 patients are actively being investigated in the clinic, with the most recent reports offering encouragement that they may have a beneficial effect."}

LitCovid-PubTator

2_test

{"project":"2_test","denotations":[{"id":"32388976-32171076-144038","span":{"begin":1240,"end":1242},"obj":"32171076"},{"id":"32388976-32171076-144039","span":{"begin":1550,"end":1552},"obj":"32171076"},{"id":"32388976-32133578-144040","span":{"begin":1772,"end":1774},"obj":"32133578"},{"id":"32388976-32142651-144041","span":{"begin":1833,"end":1834},"obj":"32142651"},{"id":"32388976-16007097-144042","span":{"begin":2297,"end":2299},"obj":"16007097"},{"id":"32388976-32125455-144043","span":{"begin":2474,"end":2476},"obj":"32125455"},{"id":"32388976-32125455-144044","span":{"begin":2775,"end":2777},"obj":"32125455"},{"id":"32388976-32125455-144045","span":{"begin":3029,"end":3031},"obj":"32125455"},{"id":"32388976-32142651-144046","span":{"begin":3202,"end":3203},"obj":"32142651"}],"text":"SARS-CoV-2 likely binds to epithelial cells in the nasal cavity during the asymptomatic state of the disease (initial 1–2 days of infection) where there might be some local propagation of the virus but with a limited innate immune response. Within the next few days the infection starts in the upper airway and during this stage the infection can be detected by nasal swabs or sputum as well as early markers of the innate immune response. About 80% of infected patients show mild symptoms that are mostly restricted to the upper and conducting airways.13 However, about 20% of infected patients will progress to develop a lower respiratory tract infection leading to hypoxia, and lung damage. These patients are liable to succumb to acute respiratory distress syndrome (ARDS), which is frequently fatal. Patients with comorbidities such as cardiovascular disease, diabetes mellitus, hypertension, chronic lung disease, cancer, chronic kidney disease, and obesity (body mass index ≥30) and ARDS are at increased risk of death.14 The available data indicate that the viral infection can produce an excessive immune reaction known as cytokine release syndrome (CRS) or “cytokine storm” associated with elevated levels of interleukin-6 (IL-6).15 Laboratory findings associated with worse clinical outcomes include lymphopenia, and elevations in liver enzymes, lactate dehydrogenase (LDH), inflammatory markers (e.g., C-reactive protein [CRP], ferritin), d-dimer, prothrombin time (PT), troponin and creatine phosphokinase (CPK), and acute kidney injury.15 Chest CT scans in patients with COVID-19 commonly show ground-glass opacification, consistent with viral pneumonia with abnormalities more likely to be bilateral with a peripheral distribution involving the lower lobes.16 While SARS-CoV-2 entry is dependent on ACE2 in lung cells,8 ACE2 expression is not exclusive to the lungs, and higher relative ACE2 expression is observed in heart, kidney, GIT, and testes (Gene ID: 59272). The organ- and cell-specific expression of ACE2 suggests that it may play a role in the regulation of cardiovascular and renal function as well as fertility. Surprisingly, the 2003 SARS-CoV infection was shown to downregulate the expression of ACE2 in lung tissue reducing transmissibility but increasing virulence.17 ACE2, a component of the renin-angiotensin system (RAS), catalyzes the cleavage of angiotensin I into angiotensin 1–9 and angiotensin II into the vasodilator angiotensin 1–7.18 The balance between angiotensin II and angiotensin (1–7) is critical since angiotensin II elicits vasoconstriction via the angiotensin AT1 receptor, whereas angiotensin (1–7) exerts a vasodilatory effect mediated by AT2 with multiple beneficial effects on the cardiovascular and respiratory system.18 While ACE2 appears to be involved in the hypertension and respiratory manifestations of severely ill patients, the benefits and merits of ACE inhibitors (ACEI) or angiotensin receptor 1 blockers (ARBs) in the SARS-CoV-2 patient is still controversial.18 The priming of the S viral protein by TMPRSS2 is crucial for viral entry where TMPRSS2 expression is very high in the lungs, kidneys, and prostate tissue (Gene ID: 7113).8 TMPRSS2 is predominantly expressed in the luminal cells of the prostate epithelium, where its expression is regulated positively by androgens and negatively regulated by estrogens. The hormonal regulation of TMPRSS2 has been suggested to be linked to the fact that men are at higher risk than women to become seriously ill with COVID-19.19 TMPRSS2 knockout in mice is not lethal. In contrast, humans are intolerant to the loss of function of ACE2.19 Concerns about the effect of ACEI and AT receptor blockers in COVID-19 patients are actively being investigated in the clinic, with the most recent reports offering encouragement that they may have a beneficial effect."}

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PMC:7216760 / 6414-10286 JSON TXT