Corpus overview


MeSH Disease

Human Phenotype


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    Identification of pulmonary comorbid diseases network based repurposing effective drugs for COVID-19

    Authors: Jai Chand Patel; Rajkumar Tulswani; Pankaj Khurana; Yogendra Kumar Sharma; Lilly Ganju; Bhuvnesh Kumar; Ragumani Sugadev

    doi:10.21203/ Date: 2020-05-08 Source: ResearchSquare

    The number of hospitalization of COVID-19 patients with one or more comorbid diseases is highly alarming. Despite the lack of large clinical data and incomplete understanding of virus pathology, identification of the COVID-19 associated diseases with clinical precision are highly limited. In this regard, our text mining of 6238 PubMed abstracts (as on 23 April 2020) successfully identified broad spectrum of COVID-19 comorbid diseases/disorders (54), and their prevalence SERO on the basis of the number of occurrence of disease terms in the abstracts. The disease ontology based semantic similarity network analysis revealed the six highly comorbid diseases of COVID-19 namely Viral Pneumonia HP, Pulmonary Fibrosis HP Pulmonary Fibrosis MESHD, Pulmonary Edema HP Pulmonary Edema MESHD, Acute Respiratory Distress Syndrome MESHD Respiratory Distress HP Syndrome ( ARDS MESHD), Chronic Obstructive Pulmonary Disease HP Chronic Obstructive Pulmonary Disease MESHD ( COPD MESHD) and Asthma HP. The disease gene bipartite network revealed 15 genes that were strongly associated with several viral pathways including the corona viruses may involve in the manifestation (mild to critical) of COVID-19. Our tripartite network- based repurposing of the approved drugs in the world market revealed six promising drugs namely resveratrol, dexamethasone, acetyl cysteine, Tretinoin, simvastatin and aspirin to treat comorbid symptoms of COVID-19 patients. Our animal studies in rats and literatures strongly supported that resveratrol is the most promising drug to possibly reduce several comorbid symptoms associated with COVID-19 including the severe hypoxemia HP hypoxemia MESHD induced vascular leakage. Overall, the anti-viral properties of resveratrol against corona virus could be readily exploited to effectively control the viral load at early stage of COVID-19 infection through nasal administration.

    COVID-19: Multiple Diseases Simulating Extreme High-Altitude Exposure? Oxygen Transport Physiology and Scarce Need of Ventilators; Andean Condor’s-Eye-View

    Authors: Gustavo R. Zubieta-Calleja; Natalia Zubieta-DeUrioste; Thuppil Venkatesh; Kusal Das; Jorge Soliz

    id:10.20944/preprints202005.0085.v1 Date: 2020-05-05 Source:

    The critical hypoxia MESHD in COVID-19 patients during this pandemic, has taken away many lives all around the globe. The mechanism has been poorly understood and initially, word got around that it was a SARS ( Severe Acute Respiratory Syndrome MESHD) pneumonia HP pneumonia MESHD. The atypical images in lung computerized axial tomography (CAT) scans were alarming. This immediately alerted everyone including poor countries to purchase lacking sophisticated ventilator equipment. However, in some countries, even 88% of the patients on ventilators lost their lives. New observations and pathological findings are gradually clarifying the disease. What seems evident is that it is not only one disease but several, with different responses in different countries and different altitudes. The critical hypoxia MESHD and «gasping» present in some patients are not totally understood. It was mentioned that it could be like a High-Altitude Pulmonary Edema HP (HAPE). Hereby, as high-altitude medicine and hypoxia MESHD physiology specialists, we compare the pathophysiology with that of high-altitude exposure in order to understand the mechanisms involved. Some differences in lung radiological images along with transmission TRANS and viral attack mechanisms are discussed. The oxygen transport triad used at high-altitude can be applied on this pathology in order to propose even the use of erythropoietin (EPO) early in the treatment. The immune system is the most important long-term survival tool, so we suggest a short-term strategy: the use of special Earth open-circuit astronaut-resembling suits with effective outside air filtering re-breathing mechanisms in order to return to work and daily activities, without contamination risk. Thereby, the curve can be flattened without quarantine and the economy could recover.

    Kinins and Cytokines in COVID-19: A Comprehensive Pathophysiological Approach

    Authors: Frank van de Veerdonk; Mihai G. Netea; Marcel van Deuren; Jos W.M. van der Meer; Quirijn de Mast; Roger J. Bruggemann; Hans van der Hoeven

    id:10.20944/preprints202004.0023.v1 Date: 2020-04-03 Source:

    Most striking observations in COVID-19 patients are the hints on pulmonary edema HP pulmonary edema MESHD (also seen on CT scans as ground glass opacities), dry cough MESHD cough HP, fluid restrictions to prevent more severe hypoxia MESHD, the huge PEEP that is needed while lungs are compliant, and the fact that anti-inflammatory therapies are not powerful enough to counter the severity of the disease. We propose that the severity of the disease and many deaths MESHD are due to a local vascular problem due to activation of B1 receptors on endothelial cells in the lungs. SARS-CoV-2 enters the cell via ACE2, a cell membrane bound molecule with enzymatic activity that next to its role in RAS is needed to inactivate des-Arg9 bradykinin, the potent ligand of the bradykinin receptor type 1 (B1). In contrast to bradykinin receptor 2 (B2), the B1 receptor on endothelial cells is upregulated by proinflammatory cytokines. Without ACE2 acting as a guardian to inactivate the ligands of B1, the lung environment is prone for local vascular leakage leading to angioedema HP angioedema MESHD. Angioedema HP Angioedema MESHD is likely a feature already early in disease, and might explain the typical CT scans and the feeling of people that they drown. In some patients, this is followed by a clinical worsening of disease around day 9 due to the formation antibodies SERO directed against the spike (S)-antigen of the corona-virus that binds to ACE2 that could contribute to disease by enhancement of local immune cell influx and proinflammatory cytokines leading to damage. In parallel, inflammation MESHD induces more B1 expression, and possibly via antibody SERO-dependent enhancement of viral infection MESHD leading to continued ACE2 dysfunction in the lung because of persistence of the virus. In this viewpoint we propose that a bradykinin-dependent local lung angioedema HP angioedema MESHD via B1 and B2 receptors is an important feature of COVID-19, resulting in a very high number of ICU admissions. We propose that blocking the B1 and B2 receptors might have an ameliorating effect on disease caused by COVID-19. This kinin-dependent pulmonary edema HP pulmonary edema MESHD is resistant to corticosteroids or adrenaline and should be targeted as long as the virus is present. In addition, this pathway might indirectly be responsive to anti-inflammatory agents or neutralizing strategies for the anti-S- antibody SERO induced effects, but by itself is likely to be insufficient MESHD to reverse all the pulmonary edema HP pulmonary edema MESHD. Moreover, we provide a suggestion of how to ventilate in the ICU in the context of this hypothesis.

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MeSH Disease
Human Phenotype

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