Corpus overview


Overview

MeSH Disease

Human Phenotype

Transmission

Seroprevalence

antibody (3)

    displaying 1 - 3 records in total 3
    records per page




    Kawasaki Disease MESHD Outbreak in Children TRANS During COVID-19 Pandemic.

    Authors: Ewelina Gowin; Jacek Wysocki; Magdalena Frydrychowicz; Danuta Januszkiewicz-Lewandowska

    doi:10.21203/rs.3.rs-70123/v1 Date: 2020-09-01 Source: ResearchSquare

    BackgroundIn response to the recent information about the outbreak of Kawasaki disease MESHD ( KD MESHD) in children TRANS connected to SARS-Cov-2 pandemic, we would like to present a group of six patients hospitalized from March to May 2020 with an inflammatory disease similar to KD MESHD. Findings There were four girls and two boys, aged TRANS from 15 months to 16 years. They all presented with fever HP fever MESHD lasting at least five days, irritability HP irritability MESHD, bilateral nonexudative conjunctivitis HP conjunctivitis MESHD, lymphadenopathy, mucus membrane changes, rash MESHD, edema HP edema MESHD.Neither the patients nor the other members of the patients' households had a positive history of COVID-19 infection MESHD. None of the six children TRANS had a positive PCR result for SARS-CoV-2 or a positive results for antibodies to SARS-CoV-2 SERO. All patients received empiric antibiotic therapy. Four patients were diagnosed with KD MESHD. Three children TRANS received standard treatment. One boy did not respond and received an additional 14-days course of methylprednisolone.In two girls, the diagnosis of KD MESHD was not made. All patients survived ConclusionFinding a correlation with the Covid-19 pandemic is difficult regarding the situation in our country. According to ECDC, in May 2020 Poland wass still before the peak of the epidemy. The intention of this article is to report that increased hospitalization of children TRANS with the inflammatory syndrome MESHD is also observed in countries with low levels of transmission TRANS of the SARS-Cov-2 virus. Our observation may broaden the knowledge of new inflammatory syndrome MESHD, which is not necessarily caused by SARS-Cov-2 but may be worsened by co-infection MESHD.

    Myocardial Injury MESHD in Post Mortem Biopsies of Patients with COVID-19

    Authors: Camila Hartmann; Anna Flavia dos Santos Miggiolaro; Jarbas da Silva Motta Junior; Lucas Baena Carstens; Caroline Busatta Vaz De Paula; Larissa Hermann de Souza Nunes; Gustavo Lenci Marques; Lidia Zytinsky Moura; Jose Rocha Faria Neto; Lucia de Noronha; Cristina Pellegrino Baena

    doi:10.21203/rs.3.rs-45192/v1 Date: 2020-07-17 Source: ResearchSquare

    Background: Myocardial injury MESHD is significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury MESHD in COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide.Aim: This histopathological and immunohistochemical study seeks to clarify the pathogenesis of myocardial injury MESHD in COVID-19.Methods: Postmortem minimally invasive autopsies were performed in two patients who died from COVID-19, and the myocardium samples were compared to a control patient. Immunohistochemistry (IHC) staining was performed using monoclonal antibodies SERO against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen.Results: The histopathological analysis showed severe pericellular interstitial edema HP edema MESHD surrounding each of the cardiomyocytes. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. On the other hand, no difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. Conclusion: Our findings point to a pathogenesis related with pyroptosis leading to endothelial disfunction. The subsequent inflammation MESHD with associated interstitial edema HP edema MESHD could explain the myocardial disfunction and arrythmias MESHD in COVID-19 patients. The presence of Th2 response, MMP-9 and type-3 collagen suggests progression to myocardial fibrosis HP myocardial fibrosis MESHD in the long term.

    The Pathogenisis of COVID-19 Myocardial Injury MESHD: an Immunohistochemical Study of Postmortem Biopsies 

    Authors: Camila Hartmann; Anna Flavia dos Santos Miggiolaro; Jarbas da Silva Motta Junior; Lucas Baena Carstens; Caroline Busatta Vaz De Paula; Sarah Fagundes Grobe; Larissa Hermann de Souza Nunes; Gustavo Lenci Marques; Lidia Zytynski Moura; Lucia de Noronha; Cristina Pellegrino Baena

    doi:10.21203/rs.3.rs-45192/v2 Date: 2020-07-17 Source: ResearchSquare

    Rationale: M yocardial injury MESHDis significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of m yocardial injury MESHDin COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide. Objective: This histopathological and immunohistochemical study seeks to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 m yocardial injury. MESHD Methods and Results: Postmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control patient. Histopathological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies SERO against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen. The samples were also subjected to a TUNEL assay to detect potential apoptosis. The histopathological analysis showed severe pericellular interstitial edema HP dema MESHDsurrounding each of the cardiomyocytes and higher mast cells count by high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. No difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. The TUNEL assay was positive in all the COVID-19 samples confirming the presence of endothelial apoptosis. Conclusions: The pathogenesis of COVID-19 m yocardial injury MESHDseems to be related with pyroptosis leading to endothelial cell injury and disfunction. The subsequent i nflammation MESHDwith associated interstitial edema HP dema MESHDcould explain the myocardial disfunction and a rrythmias MESHDin these patients. Our findings also show that COVID-19 m yocardial injury MESHDmay cause myocardial fibrosis HP yocardial fibrosis MESHDin the long term. These patients should be monitored for m yocardial dysfunction MESHDand a rrythmias MESHDafter the acute phase of COVID-19.

The ZB MED preprint Viewer preVIEW includes all COVID-19 related preprints from medRxiv and bioRxiv, from ChemRxiv, from ResearchSquare, from arXiv and from Preprints.org and is updated on a daily basis (7am CET/CEST).
The web page can also be accessed via API.

Sources


Annotations

All
None
MeSH Disease
Human Phenotype
Transmission
Seroprevalence


Export subcorpus as...

This service is developed in the project nfdi4health task force covid-19 which is a part of nfdi4health.

nfdi4health is one of the funded consortia of the National Research Data Infrastructure programme of the DFG.