Corpus overview


Overview

MeSH Disease

Fibrosis (31)

Disease (19)

Infections (17)

Pneumonia (11)

Death (9)


Human Phenotype

Transmission

Seroprevalence
    displaying 1 - 10 records in total 31
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    Molecular Basis of Kidney Defects in COVID-19 Patients

    Authors: Smartya Pulai; Madhurima Basu; Chinmay Saha; Nitai P. Bhattacharyya; Arpita Ray Chaudhury; Sujoy Ghosh

    id:10.20944/preprints202007.0452.v1 Date: 2020-07-20 Source: Preprints.org

    Background: Kidney damage is considered to be one of the risk factors for severity and mortality among COVID-19 patients. However, molecular nature of such observations remains unknown. Hypothesis: Altered gene expressions due to infection MESHD infection and in chronic HP and in chronic kidney disease MESHD could explain severity in COVID-19 with kidney defects. Methods: We collected gene expression data from publicly available resources Gene Expression Omnibus CKD, Enrichr for deregulated genes in SARS-CoV infected cells in vitro, DisGeNET and others and carried out enrichment analysis using Enrichr. Result: Number of common genes altered in chronic kidney disease HP kidney disease MESHD (CKD) and SARS-CoV infected cells was 2834. Enrichment analysis revealed that biological processes related viral life cycle and growth, cytokines, immunity, interferon, inflammation MESHD, apoptosis, autophagy, oxidative stress and others were significantly enriched with common deregulated genes. Similarly, significantly enriched pathways related to viral and bacterial infections MESHD, immunity and inflammation MESHD, cell cycle, ubiquitin mediated proteolysis, signaling pathways like Relaxin signaling pathway, mTOR signaling pathway, IL-17 signaling pathway, NF-kappa B signaling pathway were enriched with the common deregulated genes. These processes and pathways are known to be related to kidney damage. DisGeNET terms enriched include and related to Dengue MESHD fever MESHD fever HP, chronic Hepatitis MESHD chronic Hepatitis HP, measles MESHD, retroviridae infections MESHD, respiratory syncytial virus Infections MESHD and many others. Kidney dysfunction related terms ischemia MESHD of kidney, renal fibrosis HP fibrosis MESHD and diabetic nephropathy MESHD nephropathy HP. Conclusion: Common deregulated genes in SARS-CoV infected cells and chronic kidney disease HP kidney disease MESHD, as well as their enrichment with molecular processes and pathways relevant for viral pathogenesis and renal dysfunctions, could explain the severity of COVID-19 with kidney disease MESHD. This observation not only provides molecular relation of severity in COVID-19 with renal dysfunctions but might also help in the management and treatment targets for these cases.

    Myocardial Injury 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 is significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury 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 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 MESHD edema HP 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 MESHD edema HP could explain the myocardial disfunction and arrythmias in COVID-19 patients. The presence of Th2 response, MMP-9 and type-3 collagen suggests progression to myocardial fibrosis HP fibrosis MESHD in the long term.

    CT as a Tool to Depict Pulmonary Fibrosis MESHD Pulmonary Fibrosis HP in Patients With COVID-19: a Radiopathological Correlation 

    Authors: Anna Alguersuari; Miguel Angel Carrasco; Gemma Munné; Maria Eulalia Oliva; Cristina Simon; Maria Dolores Bosque; Melcior Martínez; Natalia Lugo; Xavier Herranz; Mariana Rovira

    doi:10.21203/rs.3.rs-44197/v1 Date: 2020-07-16 Source: ResearchSquare

    OBJECTIVESCT findings of COVID-19 infected patients has been well described, but it it’s roll in depicting signs of fibrosis MESHD in critically ill patients remains unclear. To our knowledge, there are no radiopathological correlations of the pulmonary pathology. Exudative and proliferative diffuse alveolar damage (DAD) are the most commonly reported injury. Few studies describe fibrosis MESHD, the last phase of DAD. Our study correlates post-mortem chest US and CT findings of COVID-19 infected patients with the histopathology from biopsies taken of the lung. It focuses on the role of CT to depict fibrosis MESHD. METHODSThis is a prospective observational study of six consecutive deceased patients infected with COVID-19. Post-mortem chest CTs and US were performed within 24 hours of death MESHD. CT and US were used to obtain biopsies of different radiological patterns. Pre-mortem CT examinations were also retrospectively evaluated. RESULTSOn CT, all patients presented with extensive areas of consolidation and ground-glass opacities affecting most segments of the lung. Pleural effusion MESHD Pleural effusion HP was present in all cases. Four of the patients showed signs of fibrosis MESHD. On US, subpleural consolidation, pleural thickening HP, and B-pattern were present.All patients showed different stages of DAD, mostly proliferative DAD. Four patients presented with fibrotic DAD, all of which had been admitted for over three weeks and correlated with the CT findings of fibrosis MESHD. CONCLUSIONIn our study, signs of fibrosis MESHD on CT show a histopathological correlation. CT may be useful to identify the group of COVID-infected patients that develop fibrosis MESHD as a marker of poor prognosis, in the late stage of the disease MESHD.

    Clinical characteristics of 134 convalescent patients with COVID-19 in Guizhou, China

    Authors: Siqin Zhang; Lin Liu; Bin Yang; Rou Li; Jianhua Luo; Jing Huang; Yanjun Long; Ying Huang; Jianping Zhou; Yan Zha; Xiangyan Zhang

    doi:10.21203/rs.3.rs-41986/v1 Date: 2020-07-13 Source: ResearchSquare

    Background: Previous studies have focused on the clinical characteristics of hospitalized patients with the novel 2019 coronavirus disease MESHD (COVID-19). Limited data are available for convalescent patients. This study aimed to evaluate the clinical characteristics of discharged COVID-19 patients.Methods: In this retrospective study, we extracted data for 134 convalescent patients with COVID-19 in Guizhou Provincial Staff Hospital from February 15 to March 31, 2020. Cases were analyzed on the basis of demographic, clinical, and laboratory data as well as radiological features. Results: Of 134 convalescent patients with COVID-19, 19 (14.2%) were severe cases, while 115 (85.8%) were non-severe cases. The median patient age TRANS was 33 years (IQR, 21.8 to 46.3), and the cohort included 69 men and 65 women. Compared with non-severe cases, severe patients were older and had more chronic comorbidities, especially hypertension MESHD hypertension HP, diabetes, and thyroid disease MESHD (P<0.05). Leukopenia MESHD Leukopenia HP was present in 32.1% of the convalescent patients and lymphocytopenia was present in 6.7%, both of which were more common in severe patients. 48 (35.8%) of discharged patients had elevated levels of alanine aminotransferase, which was more common in adults TRANS than in children TRANS (40.2% vs 13.6%, P=0.018). A normal chest CT was found in 61 (45.5%) patients during rehabilitation. Severe patients had more ground-glass opacity, bilateral patchy shadowing, and fibrosis MESHD. No significant differences were observed in the positive rate of IgG and/or IgM antibodies SERO between severe and non-severe patients.Conclusion: Leukopenia MESHD Leukopenia HP, lymphopenia MESHD lymphopenia HP, ground-glass opacity, and fibrosis MESHD are common in discharged severe COVID-19 patients, and liver injury is common in discharged adult TRANS patients. We suggest physicians develop follow-up treatment plans based on the different clinical characteristics of convalescent patients. 

    Discriminating Mild from Critical COVID-19 by Innate and Adaptive Immune Single-cell Profiling of Bronchoalveolar Lavages

    Authors: Els Wauters; Pierre Van Mol; Abhishek D. Garg; Sander Jansen; Yannick Van Herck; Lore Vanderbeke; Ayse Bassez; Bram Boeckx; Bert Malengier-Devlies; Anna Timmerman; Thomas Van Brussel; Tina Van Buyten; Rogier Schepers; Elisabeth Heylen; Dieter Dauwe; Christophe Dooms; Jan Gunst; Greet Hermans; Philippe Meersseman; Dries Testelmans; Jonas Yserbyt; Patrick Matthys; Sabine Tejpar; - CONTAGIOUS collaborators; Johan Neyts; Joost Wauters; Junbin Qian; Diether Lambrechts

    doi:10.1101/2020.07.09.196519 Date: 2020-07-10 Source: bioRxiv

    How innate and adaptive lung immune responses to SARS-CoV-2 synchronize during COVID-19 pneumonitis and regulate disease MESHD severity is poorly established. To address this, we applied single-cell profiling to bronchoalveolar lavages from 44 patients with mild or critical COVID-19 versus non-COVID-19 pneumonia MESHD pneumonia HP as control. Viral RNA-tracking delineated the infection MESHD phenotype to epithelial cells, but positioned mainly neutrophils at the forefront of viral clearance activity during COVID-19. In mild disease MESHD, neutrophils could execute their antiviral function in an immunologically controlled fashion, regulated by fully-differentiated T-helper-17 (TH17)-cells, as well as T-helper-1 (TH1)-cells, CD8+ resident-memory (TRM) and partially-exhausted (TEX) T-cells with good effector functions. This was paralleled by orderly phagocytic disposal of dead/stressed cells by fully-differentiated macrophages, otherwise characterized by anti-inflammatory and antigen-presenting characteristics, hence facilitating lung tissue repair. In critical disease MESHD, CD4+ TH1- and CD8+ TEX-cells were characterized by inflammation MESHD-associated stress and metabolic exhaustion, while CD4+ TH17- and CD8+ TRM-cells failed to differentiate. Consequently, T-cell effector function was largely impaired thereby possibly facilitating excessive neutrophil-based inflammation MESHD. This was accompanied by impaired monocyte-to-macrophage differentiation, with monocytes exhibiting an ATP-purinergic signalling-inflammasome footprint, thereby enabling COVID-19 associated fibrosis MESHD and worsening disease MESHD severity. Our work represents a major resource for understanding the lung-localised immunity and inflammation MESHD landscape during COVID-19.

    Genes associated with liver damage signalling pathways may impact the severity of COVID-19 symptoms in Spanish and Italian populations

    Authors: Leire Moya; Samaneh Farashi; Prashanth Suravajhala; Panchadsaram Janaththani; Jyotsna Batra

    doi:10.1101/2020.07.03.179028 Date: 2020-07-08 Source: bioRxiv

    AimThe novel SARS-CoV-2 virus, which causes the COVID-19 disease MESHD, has infected more than 10 million people and caused 500K deaths MESHD worldwide. In Europe, over 2 million confirmed cases TRANS have been reported, while nearly 200K people have died from the disease MESHD. Despite strict containment measures in Spain and Italy after the first reported COVID-19 patient, these two countries have remained in the top five European nations with the highest mortality rate for over two months. We hypothesised that a genetic mechanism could partially explain the poor survival outcome observed in these two countries. MethodsAn extensive literature search to identify human candidate genes linked to SARS-CoV infection MESHD, host immune evasion and disease MESHD aggressiveness was carried out. Pathway analysis (IPA) was performed to select the most significantly associated canonical signalling pathways with the genes of interest. The genetic variants at these genes with {+/-}1Mb flanking region was extracted (GRCh37/hg19 built). Over 80 million single nucleotide polymorphisms (SNPs) were analysed in genome-wide data of 2,504 individuals (1000 genomes, phase III, https://www.internationalgenome.org/). Principal component (PC) analysis was performed, ancestry by the whole genome was inferred and subsets of the regions of interest were extracted (PLINK v1.9b, http://pngu.mgh.harvard.edu/purcell/plink/). PC1 to PC20 values from five European ancestries, including the Spanish and Italian populations, were used for PC analysis. Gene function predictions were run with our genes of interest as a query to the GeneMANIA Cytoscape plugin (https://genemania.org/). ResultsA total of 437 candidate genes associated with SARS were identified, including 21 correlated with COVID-19 aggressiveness. The two most significant pathways associated with all 437 genes (Caveolar-mediated Endocytosis and MSP-RON Signalling) did not show any segregation at the population level. However, the most significant canonical pathway associated with genes linked to COVID-19 aggressiveness, the Hepatic Fibrosis HP Fibrosis MESHD and Hepatic Stellate Cell Activation, showed population-specific segregation. Both the Spanish and Italian populations clustered together from the rest of Europe. This was also observed for the Finnish population but in the opposite direction. These results suggest some of the severe COVID-19 cases reported in Spain and Italy could be partially explained by a pre-existing liver condition (especially liver cancer) and/or may lead to further COVID-19 related liver complications.

    Cerium oxide nanoparticles conjugated to anti-inflammatory microRNA-146a prevent bleomycin-induced acute lung injury MESHD

    Authors: Stephen Niemiec; Sarah Hilton; Alison Wallbank; Mark Azeltine-Bannerman; Amanda Louiselle; Hanan Elajaili; Ayed Allawzi; Junwang Xu; Courtney Mattson; Lindel Dewberry; Junyi Hu; Sushant Singh; Tamil Sakthivel; Eva Nozik-Grayck; Bradford Smith; Sudipta Seal; Carlos Zgheib; Kenneth Liechty

    doi:10.21203/rs.3.rs-40082/v1 Date: 2020-07-03 Source: ResearchSquare

    Acute respiratory distress HP syndrome MESHD (ARDS) is a devastating pulmonary disease MESHD with significant inhospital mortality and is the leading cause of death MESHD in COVID-19 patients. Potential therapies remain limited despite advancements in understanding ARDS pathophysiology. Excessive leukocyte recruitment, unregulated inflammation MESHD, and resultant fibrosis MESHD contribute to poor ARDS outcomes. In this study, we evaluated the potential of the radical scavenging cerium oxide nanoparticle (CNP) conjugated to the anti-inflammatory microRNA-146a (CNP-miR146a) to prevent acute lung injury MESHD (ALI) following exposure to bleomycin. We have found that CNP-miR146a can prevent ALI by altering leukocyte recruitment, reducing inflammation MESHD, and decreasing collagen deposition, ultimately improving pulmonary biomechanics.

    Systemic analysis of putative SARS-CoV-2 entry and processing genes in cardiovascular tissues identifies a positive correlation of BSG with age TRANS in endothelial cells

    Authors: Blerina Ahmetaj-Shala; Ricky-Kumar Vaja; Santosh S Atanur; Peter M George; Nicholas S Kirkby; Jane A. Mitchell

    doi:10.1101/2020.06.23.165324 Date: 2020-06-23 Source: bioRxiv

    COVID-19, caused by severe acute respiratory syndrome MESHD coronavirus-2 (SARS-CoV-2) has rapidly spread throughout the world with unprecedented global healthcare and socio-economic consequences. There is now an established secondary syndrome MESHD of COVID-19 characterised by thrombosis MESHD, vascular dysfunction and hypertension MESHD hypertension HP, seen in those most severely affected. Advancing age TRANS in adults TRANS is the single most significant risk factor for hospitalisation and death MESHD with COVID-19. In light of the cardiovascular/thrombotic sequalae associated with severe COVID-19 disease MESHD and the overwhelming risk that increased age TRANS carries, in this study, our aim was to obtain mechanistic insight by interrogating gene expression profiles in cardiovascular tissues and cells. Our focus was on the two putative receptors for SARS-CoV-2, ACE2 and BSG along with a selected range of genes thought to be involved in virus binding/processing. In this study we have made four important observations: (i)Cardiovascular tissues and/or endothelial cells express the required genes for SARS-CoV-2 infection MESHD, (ii) SASR-CoV-2 receptor pathways, ACE2/TMPRSS2 and BSG/PPIB(A) polarise to lung/epithelium and vessel/endothelium respectively, (iii) expression of SARS-CoV-2 host genes are, on the whole, relatively stable with age TRANS and (iv) notable exceptions were ACE2 which decreases with age TRANS in some tissues and BSG which increases with age TRANS in endothelial cells. Our data support the idea that that BSG is the dominate pathway utilised by SARS-CoV-2 in endothelial cells and are the first to demonstrate a positive correlation with age TRANS. We suggest BSG expression in the vasculature is a critical driver which explains the heightened risk of severe disease MESHD and death MESHD observed in those >40 years of age TRANS. Since BSG is utilised by other pathogens our findings have implications beyond the current pandemic. Finally, because BSG is functions in a range of cardiovascular diseases MESHD and fibrosis MESHD, our observations may have relevance to our understanding of the diseases MESHD associated with aging.

    Chest X-ray classification using Deep learning for automated COVID-19 screening

    Authors: Ankita Shelke; Madhura Inamdar; Vruddhi Shah; Amanshu Tiwari; Aafiya Hussain; Talha Chafekar; Ninad Mehendale

    doi:10.1101/2020.06.21.20136598 Date: 2020-06-23 Source: medRxiv

    In today's world, we find ourselves struggling to fight one of the worst pandemics in the history of humanity known as COVID-2019 caused by a coronavirus. If we detect the virus at an early stage (before it enters the lower respiratory tract), the patient can be treated quickly. Once the virus reaches the lungs, we observe ground-glass opacity in the chest X-ray due to fibrosis MESHD in the lungs. Due to the significant differences between X-ray images of an infected and non-infected person, artificial intelligence techniques can be used to identify the presence and severity of the infection MESHD. We propose a classification model that can analyze the chest X-rays and help in the accurate diagnosis of COVID-19. Our methodology classifies the chest X-rays into 4 classes viz. normal, pneumonia MESHD pneumonia HP, tuberculosis MESHD (TB), and COVID-19. Further, the X-rays indicating COVID-19 are classified on severity-basis into mild, medium, and severe. The deep learning model used for the classification of pneumonia MESHD pneumonia HP, TB, and normal is VGG16 with an accuracy of 95.9 %. For the segregation of normal pneumonia MESHD pneumonia HP and COVID-19, the DenseNet-161 was used with an accuracy of 98.9 %. ResNet-18 worked best for severity classification achieving accuracy up to 76 %. Our approach allows mass screening of the people using X-rays as a primary validation for COVID-19.

    The Efficacy of Treating Pulmonary Fibrosis MESHD Pulmonary Fibrosis HP and Pulmonary Function Injury in COVID-19 with the Fuzheng Huayu Tablets: study protocol for a multicenter randomized controlled trial

    Authors: Fei Jing; Haina Fan; Zhimin Zhao; Feng Xing; Yingchun He; Chenghai Liu

    doi:10.21203/rs.3.rs-37422/v1 Date: 2020-06-22 Source: ResearchSquare

    Background: Some patients with COVID-19 have been found pulmonary dysfunction and/or fibrosis MESHD in the recovery period, especially severe cases, but there are no certain drugs or treatment to cope with this situation. Previous studies proved the efficacy of FZHY on lung fibrosis MESHD induced by Bleomycin in animals and improvement of pulmonary function in COPD patients. We design this trial to carry out the clinical study that the effects of FZHY Tablets on pulmonary fibrosis MESHD pulmonary fibrosis HP and/or pulmonary function injury in the recovery period of COVID-19 and expect to improve the prognosis.Methods/design: This is a double-blind, placebo-controlled, randomized, multicenter clinical trial. It enrolls 160 patients who had been diagnosed with COVID-19, but currently they are negative for viral testing and have developed pulmonary fibrosis MESHD pulmonary fibrosis HP or pulmonary dysfunction. They are randomly divided equally into control group and experimental group. All patients are given basic treatment such as respiratory function rehabilitation training and vitamin C. The control group is given placebo of FZHY, and the experimental group is given FZHY. Each patient will be observed for 24 weeks and followed up for 8 weeks. The primary outcome for the trial is a composite endpoint consisting of lung function and HRCT. Secondary outcomes include clinical symptoms, oxygen saturation and quality of life assessment. Discussion: The trial is designed to test the hypothesis that treating pulmonary fibrosis MESHD pulmonary fibrosis HP or pulmonary dysfunction after SARS-CoV-2 infection MESHD with FZHY will improve the patient’s lung function or the pathological manifestation of pulmonary fibrosis MESHD pulmonary fibrosis HP, and improve the quality of life. Trial registration: Clinical Trials.gov, ID: NCT04279197. Registered on 12 April 2020.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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