Corpus overview


MeSH Disease

Human Phenotype


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    Endothelial Cells and SARS-CoV-2: An Intimate Relationship

    Authors: Lucas Barbosa; Thaynan Lopes; Luanna Araujo; Luciane Rosario; Valeria Ferrer

    id:10.20944/preprints202010.0214.v1 Date: 2020-10-12 Source:

    Angiotensin-converting enzyme 2 (ACE2) is an important player of the renin-angiotensin-aldosterone system (RAAS) in regulating the conversion of angiotensin II into angiotensin (1-7). While expressed on the surface of human cells, such as lung, heart, kidney, neurons, and endothelial cells (EC), ACE2 is the entry receptor for SARS-CoV-2. Here, we would like to highlight that ACE2 is predominant on the EC membrane. Many of coronavirus disease MESHD 2019 (COVID-19) symptoms have been associated with the large recruitment of immune cells, directly affecting EC. Additionally, cytokines, hypoxia MESHD, and complement activation can trigger the activation of EC leading to the coagulation cascade. The EC dysfunction plus the inflammation MESHD due to SARS-CoV-2 infection MESHD may lead to abnormal coagulation MESHD, actively participating in thrombo-inflammatory processes resulting in vasculopathy MESHD and indicating poor prognosis in patients with COVID-19. Considering the intrinsic relationship between EC and the pathophysiology of SARS-CoV-2, EC-associated therapies such as anticoagulants, fibrinolytic drugs, immunomodulators, and molecular therapies have been proposed. In this review, we will discuss the role of EC in the lung inflammation MESHD and edema HP edema MESHD, in the disseminate coagulation process, ACE2 positive cancer MESHD patients, and current and future EC-associated therapies to treat COVID-19.

    Cardiac involvement in COVID-19 patients: mid-term follow up by cardiac magnetic resonance imaging

    Authors: Hui Wang; Ruili Li; Hong Jiang; Zixu Yan; Xinyan Tao; Hongjun Li; Lei Xu

    doi:10.21203/ Date: 2020-08-11 Source: ResearchSquare

    Background: Coronavirus disease MESHD 2019 (COVID-19) induces myocardial injury MESHD, either direct myocarditis HP myocarditis MESHD or indirect injury due to systemic inflammatory response. Myocardial involvement MESHD has been proved to be one of the primary manifestations of COVID-19 infection MESHD, according to laboratory test, autopsy, and cardiac magnetic resonance imaging (CMRI). However, the middle-term outcome of cardiac involvement MESHD after the patients were discharged from the hospital is yet unknown. The present study aimed to evaluate mid-term cardiac sequelae in recovered COVID-19 patients by CMRIMethods: A total of 47 recovered COVID-19 patients were prospectively recruited and underwent CMRI examination in this study. The CMRI protocol consisted of black blood SERO fat-suppressed T2 weighted imaging (BB-T2WI), T2 star mapping, left ventricle cine imaging, pre- and post-contrast T1 mapping, and late gadolinium enhancement (LGE). Myocardium edema MESHD edema HP and LGE were assessed in recovered COVID-19 patients. The left ventricle ( LV MESHD) and right ventricle (RV) function and LV mass were assessed and compared with normal controls.Results: Finally, 44 recovered COVID-19 patients and 31 normal controls were included in this study. No edema HP edema MESHD was observed in any patient. LGE was found in 13 patients. All LGE lesions were located in the middle myocardium and/or sub-epicardium with a scattered distribution. Further analysis showed that LGE-positive patients had significantly decreased left ventricle peak global circumferential strain (LVpGCS), right ventricle peak global circumferential strain (RVpGCS), right ventricle peak global longitudinal strain (RVpGLS) as compared to non-LGE patients (p<0.05), while no difference was detected between the non-LGE patients and normal controls.Conclusion: Myocardium injury MESHD existed in about 30% of COVID-19 patients. These patients had peak right ventricle strain that decreased at the 3-month follow-up. Cardiac MRI can monitor the COVID-19-induced myocarditis HP myocarditis MESHD progression, and CMR strain analysis is a sensitive tool to evaluate the recovery of left ventricle circumferential contraction dysfunction MESHD and right ventricular dysfunction MESHD.

    Cytokine Release Syndrome-Associated Encephalopathy MESHD Encephalopathy HP in Patients with COVID-19

    Authors: Peggy Perrin; Nicolas Collongues; Seyyid Baloglu; Dimitri Bedo; Xavier Bassand; Thomas Lavaux; Gabriela Gautier; Nicolas Keller; Stephane Kremer; Samira Fafi-Kremer; Bruno Moulin; Ilies Benotmane; Sophie Caillard

    id:10.20944/preprints202006.0103.v1 Date: 2020-06-07 Source:

    Severe disease MESHD and uremia MESHD are risk factors for neurological complications of coronavirus disease MESHD-2019 (COVID-19). An in-depth analysis of a case series was conducted to describe the neurological manifestations of patients with COVID-19 and gain pathophysiological insights that may guide clinical decision-making – especially with respect to the cytokine release syndrome (CRS). Extensive clinical, laboratory, and imaging phenotyping was performed in five patients. Neurological presentation included confusion HP confusion MESHD, tremor HP tremor MESHD, cerebellar ataxia MESHD ataxia HP, behavioral alterations, aphasia HP aphasia MESHD, pyramidal syndrome, coma HP coma MESHD, cranial nerve palsy MESHD, dysautonomia MESHD, and central hypothyroidism HP hypothyroidism MESHD. Neurological disturbances MESHD were remarkably accompanied by laboratory evidence of CRS. SARS-CoV-2 was undetectable in the cerebrospinal fluid. Hyperalbuminorachy and increased levels of the astroglial protein S100B were suggestive of blood SERO-brain barrier (BBB) dysfunction. Brain MRI findings comprised evidence of acute leukoencephalitis MESHD (n = 3, of whom one with a hemorrhagic form), cytotoxic edema HP edema MESHD mimicking ischemic stroke HP ischemic stroke MESHD (n = 1), or normal results (n = 2). Treatment with corticosteroids and/or intravenous immunoglobulins was attempted – resulting in rapid recovery from neurological disturbances MESHD in two cases. Patients with COVID-19 can develop neurological manifestations that share clinical, laboratory, and imaging similarities with those of chimeric antigen receptor-T cell-related encephalopathy HP encephalopathy MESHD. The pathophysiological underpinnings appear to involve CRS, endothelial activation, BBB dysfunction, and immune-mediated mechanisms.

    Analysis of 4 imaging features in patients with COVID-19

    Authors: JUN JIN; De-hong Gao; Xin Mo; Si-ping Tan; Zhen-xia Kou; Yi-bo Chen; Jin-bo Cao; Wen-jing Chen; Ya-ming Zhang; Bing-qing Li; Kuan-long Huang; Bing-ren Xu; Xiao-li Tang; Yu-li Wang

    doi:10.21203/ Date: 2020-05-29 Source: ResearchSquare

    Background : The aim of this was to analyze 4 chest CT imaging features of patients with coronavirus disease MESHD 2019 (COVID-19) in Shenzhen, China so as to improve the diagnosis of COVID-19.   Methods: Chest CT of 34 patients with COVID-19 confirmed by the nucleic acid test (NAT) were retrospectively analyzed. Analyses were performed to investigate the pathological basis of four imaging features(“feather sign”,“dandelion sign”,“pomegranate sign”, and “rime sign”) and to summarize the follow-up results.   Results: There were 22 patients (65.2 %) with typical “feather sign”and 18 (52.9%) with “dandelion sign”, while few patients had “pomegranate sign” and “rime sign”. The “feather sign” and “dandelion sign” were composed of stripe or round ground-glass opacity(GGO), thickened blood SERO vessels, and small-thickened interlobular septa. The “pomegranate sign” was characterized as follows: the increased range of GGO, the significant thickening of the interlobular septum, complicated with a small amount of punctate alveolar hemorrhage. The “rime sign” was characterized by numerous alveolar edemas HP. Microscopically, the wall thickening, small vascular proliferation, luminal stenosis, and occlusion, accompanied by interstitial infiltration of inflammatory cells, as well as numerous pulmonary interstitial fibrosis and partial hyaline degeneration were observed. Repeated chest CT revealed the mediastinal lymphadenectasis in one patient. Re-examination of the NAT showed another positive anal swab in two patients.   Conclusion: “Feather sign” and “dandelion sign” were typical chest CT features in patients with COVID-19; “pomegranate sign” was an atypical feature, and “rime sign” was a severe feature. In clinical work, accurate identification of various chest CT signs can help to improve the diagnostic accuracy of COVID-19 and reduce the misdiagnosis or missed diagnosis rate.

    Clinical and Radiological Evaluations of COVID-19 Patients with Anosmia HP Anosmia MESHD: Preliminary Report.

    Authors: Jerome R Lechien; Justin Michel; Thomas Radulesco; Carlos M Chiesa-Estomba; Luigi A Vaira; Giacomo De Riu; Leigh J Sowerby; Claire Hopkins; Sven Saussez

    doi:10.1101/2020.05.20.20106633 Date: 2020-05-26 Source: medRxiv

    Objective: To investigate clinical and radiological features of olfactory clefts MESHD of patients with mild coronavirus disease MESHD 2019 (COVID-19). Methods: Sixteen COVID-19 patients were recruited. The epidemiological and clinical data were extracted. Nasal complaints were assessed through the sino-nasal outcome test 22 (SNOT-22). Patients underwent psychophysical olfactory testing, olfactory cleft examination and CT-scan. Results: Sixteen anosmic patients were included. The mean Sniffin Sticks score was 4.6+/-1.7. The majority of patients had no endoscopical abnormality, with a mean olfactory cleft endoscopy score of 0.6+/-0.9. The olfactory clefts were opacified in 3 patients on the CT-scan. The mean radiological olfactory cleft score was 0.7+/-0.8. There were no significant correlations between clinical, radiological and psychophysical olfactory testing. Conclusion: The olfactory cleft of anosmic COVID-19 patients is free regarding endoscopic examination and imaging. The anosmia HP anosmia MESHD etiology would be not related to edema HP edema MESHD of the olfactory cleft.

    Clinical Pathology of Critical Patient with Novel Coronavirus Pneumonia HP (COVID-19)

    Authors: Weiren Luo; Hong Yu; Jizhou Gou; Xiaoxing Li; Yan Sun; Jinxiu Li; Lei Liu

    id:202002.0407/v4 Date: 2020-03-09 Source:

    Background Critical patients with novel coronavirus pneumonia MESHD pneumonia HP ( COVID-19) have worse outcome and high mortality. However, the histopathology of critical patient with COVID-19 remains undisclosed. Methods We performed the whole lung biopsy, and described the pathological changes of critical COVID-19 patient done with transplant by HE staining, immunohistochemistry and special staining observed under the microscopy. Findings The whole lungs displayed diffuse congestive appearance and partly haemorrhagic necrosis MESHD on gross examination. The haemorrhagic necrosis MESHD was prominently present in outer edge of the right lower lung. The cut surfaces of the lung displayed severe congestive and haemorrhagic changes. The main pathological changes showed massive pulmonary interstitial fibrosis MESHD, and partly hyaline degeneration MESHD, variable degrees of hemorrhagic pulmonary infarction MESHD. Small vessels hyperplasia MESHD, vessel wall thickening, lumen stenosis, occlusion and microthrombosis MESHD formation. Focal monocytes, lymphocytes and plasma SERO cells infiltrating into pulmonary HP interstitium. Bronchiolitis HP Bronchiolitis MESHD and alveolitis with proliferation, atrophy MESHD, desquamation MESHD and squamous MESHD metaplasia of epithelial cells. Atrophy MESHD, vacuolar degeneration, proliferation, desquamation MESHD and squamous MESHD metaplasia in alveolar epithelial MESHD cells. Alveolar MESHD cavity congestion was prominent, and contained mucus, edema HP edema MESHD fluid, desquamated epithelial cells, and inflammatory cells. We also found several multinucleate giant cells and intracytoplasmic viral inclusion bodies. Special stains including Masson stain, sirius red staining, reticular fibers staining indicated massive pulmonary interstitial fibrosis MESHD. Immunohistochemistry showed positive for immunity cells including CD3, CD4, CD8, CD20, CD79a, CD5, CD38 and CD68. Interpretation We demonstrate the pathological findings of critical patient with COVID-19, which might provide a deep insight of the pathogenesis and severity of this disease.

    Functional pangenome analysis provides insights into the origin, function and pathways to therapy of SARS-CoV-2 coronavirus MESHD

    Authors: Intikhab Alam; Allan K Kamau; Maxat Kulmanov; Stefan T Arold; Arnab T Pain; Takashi Gojobori; Carlos M. Duarte

    doi:10.1101/2020.02.17.952895 Date: 2020-02-21 Source: bioRxiv

    The spread of the novel coronavirus (SARS-CoV-2) has triggered a global emergency, that demands urgent solutions for detection and therapy to prevent escalating health, social and economic impacts. The spike protein (S) of this virus enables binding to the human receptor ACE2, and hence presents a prime target for vaccines preventing viral entry into host cells1. The S proteins from SARS-CoV-1 and SARS-CoV-2 MESHD are similar2, but structural differences in the receptor binding domain (RBD) preclude the use of SARS-CoV-1-specific neutralizing antibodies SERO to inhibit SARS-CoV-23. Here we used comparative pangenomic analysis of all sequenced Betacoronaviruses to reveal that, among all core gene clusters present in these viruses, the envelope protein E shows a variant shared by SARS and SARS-Cov2 with two completely-conserved key functional features, an ion-channel and a PDZ-binding Motif (PBM). These features trigger a cytokine storm that activates the inflammasome, leading to increased edema HP edema MESHD in lungs causing the acute respiratory distress syndrome MESHD respiratory distress HP syndrome ( ARDS MESHD)4-6, the leading cause of death MESHD in SARS-CoV-1 and SARS-CoV-2 infection7 MESHD,8. However, three drugs approved for human use may inhibit SARS-CoV-1 and SARS-CoV-2 Protein E, either acting upon the ion channel (Amantadine and Hexamethylene amiloride9,10) or the PBM (SB2035805), thereby potentially increasing the survival of the host, as already demonstrated for SARS-CoV-1in animal models. Hence, blocking the SARS protein E inhibits development of ARDS in vivo. Given that our results demonstrate that the protein E subcluster for the SARS clade is quasi-identical for the key functional regions of SARS-CoV-1 and SARS-CoV-2, we conclude that use of approved drugs shown to act as SARS E protein inhibitors can help prevent further casualties from COVID-2019 while vaccines and other preventive measures are being developed.

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MeSH Disease
Human Phenotype

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