Corpus overview


MeSH Disease

Human Phenotype


    displaying 1 - 10 records in total 34
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    LOX-1+ immature neutrophils predict severe COVID-19 patients at risk of thrombotic MESHD complications

    Authors: Behazine Combadiere; Lucille Adam; Paul Quentric; Pierre Rosenbaum; Karim Dorgham; Olivia Bonduelle; Christophe Parizot; Delphine Sauce; Julien Mayaux; Charles-Edouard Luyt; Alexandre Boissonnas; Zahir Amoura; Valerie Pourcher; Makoto Miyara; Guy Gorochov; Amelie Guihot; Christophe Combadiere; Duraipandian Thavaselvam; Devendra Kumar Dubey; Paul Lin; Hila Shaim; Sean G Yates; David Marin; Indreshpal Kaur; Sheetal Rao; Duncan Mak; Angelique Lin; Qi Miao; Jinzhuang Dou; Ken Chen; Richard Champlin; Elizabeth J Shpall; Katayoun Rezvani

    doi:10.1101/2020.09.15.293100 Date: 2020-09-15 Source: bioRxiv

    Rational: Lymphopenia HP Lymphopenia MESHD and neutrophil/lymphocyte ratio may have prognostic value in coronavirus disease MESHD 2019 (COVID-19) severity. Objective: We sought to investigate the representation of neutrophil subsets in severe and critical COVID-19 patients based on Intensive Care Units (ICU) and non-ICU admission. Methods: We developed a multi-parametric neutrophil profiling strategy based on known neutrophil markers to distinguish COVID-19 phenotypes in critical and severe patients. Results: Our results showed that 80 percent of ICU patients develop strong myelemia with CD10-CD64+ immature neutrophils. Cellular profiling revealed two distinct neutrophil subsets expressing either the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) or the Interleukin-3 receptor alpha (CD123), both significantly overrepresented in ICU patients compared to non-ICU patients. The proportion of LOX-1-expressing immature neutrophils positively correlated with clinical severity, with the cytokine storm (IL-1{beta}, IL-6, IL-8, TNF), and with intravascular coagulation MESHD. Importantly, high proportions of LOX-1+-immature neutrophils are associated with high risks of severe thrombosis MESHD. Conclusions: Together these data suggest that point of care enumeration of LOX-1-immature neutrophils might help distinguish patients at risk of thrombosis MESHD complication and most likely to benefit from intensified anticoagulant therapy.

    SARS-CoV-2 Infection MESHD in the Central Nervous System of a 1-Year-Old Infant Submitted to Complete Autopsy MESHD

    Authors: Ismael Carlos Gomes; Karina Karmirian; Julia Oliveira; Carolina Pedrosa; Fernando Colonna Rosman; Leila Chimelli; Stevens Rehen

    id:10.20944/preprints202009.0297.v1 Date: 2020-09-13 Source:

    Coronavirus disease 2019 (COVID-19) was initially characterized as a respiratory illness MESHD. Neurological manifestations were reported mostly in severely affected patients. Routes for brain infection MESHD and the presence of virus particles in situ have not been well described, raising controversy about how the virus causes neurological symptoms. Here, we report the autopsy findings of a 1-year old infant with COVID-19. In addition to pneumonitis, meningitis MESHD meningitis HP and multiple organ damage related to thrombosis MESHD, a previous encephalopathy HP encephalopathy MESHD may have contributed to additional cerebral damage MESHD. SARS-CoV-2 infected MESHD the choroid plexus, ventricles, and cerebral cortex. This is the first evidence of SARS-CoV-2 detection in an infant post-mortem brain.

    Tracheal tube obstruction MESHD due to hemoptysis HP associated with pulmonary infarction MESHD in a patient with severe COVID-19 pneumonia HP pneumonia MESHD: A case report.

    Authors: Takaaki Maruhashi; Yutaro Kurihara; Tatsuhiko Wada; Mayuko Osada; Marina Oi; Tomonari Masuda; Kunihiro Yamaoka; Yasushi Asari

    doi:10.21203/ Date: 2020-09-11 Source: ResearchSquare

    Background: The incidence of thrombotic complications MESHD is extremely high among severe coronavirus disease MESHD 2019(COVID-19) patients in the intensive care unit. Various factors such as a cytokine storm due to an excessive immune response to inflammation MESHD, hypoxemia HP hypoxemia MESHD, and disseminated intravascular coagulation HP intravascular coagulation MESHD are considered predisposing factors for thrombotic complications MESHD.Case presentation: A 55-year-old Japanese man intubated 8 days previously was referred to our hospital because of a severe COVID-19 pneumonia HP pneumonia MESHD diagnosis after his pharyngeal swab tested positive for severe acute respiratory syndrome MESHD coronavirus 2 using reverse transcription-polymerase chain reaction. The patient continued to remain hypoxic (PaO2/FiO2 ratio <100 mmHg) at the referring hospital. On admission, we initiated veno-venous extracorporeal membrane oxygenation (VV-ECMO). Unfractionated heparin and nafamostat mesylate were used as anticoagulants during VV-ECMO. Despite the adequate anticoagulant therapy, he developed pulmonary infarction MESHD due to pulmonary embolism HP pulmonary embolism MESHD followed by hemoptysis HP. On day 10 following admission, his oxygen saturation dropped from 95% to 88%, with a marked decrease in his ventilator tidal volume, accompanied by an inability to ventilate the patient. Thereafter, we increased the VV-ECMO flow and exchanged his endotracheal tube. The lumen of the removed tracheal tube was found to be occluded by a large-sized blood SERO coagulum. There was no further episode of tube occlusion MESHD. The patient was discharged in a walkable state on day 39 following admission. Conclusions: Endotracheal tube obstruction MESHD secondary to hemoptysis HP should be suggested in patients with COVID-19 requiring ventilator support, as they are not able to perform frequent endotracheal tube suctions owing to the risk of infection TRANS risk of infection TRANS infection MESHD.

    Plasma SERO tissue plasminogen activator and plasminogen activator inhibitor-1 in hospitalized COVID-19 patients

    Authors: Yu Zuo; Mark Warnock; Alyssa Harbaugh; Srilakshmi Yalavarthi; Kelsey Gockman; Melanie Zuo; Jacqueline A. Madison; Jason S. Knight; Yogendra Kanthi; Daniel A. Lawrence; Laura Vanessa Montes Fontalvo; Roger Hernandez; Carolin Chavez; Francisco Eduardo Campos; Fadia Uribe; Olguita del Aguila; JORGE ALBERTO RIOS AIDA; Andrea Parra Buitrago; Lina Maria Betancur Londono; Leon Felipe Mendoza Vega; Carolina Almeida Hernandez; Michela Sali; JULIAN HIGUITA PALACIO; Jessica Gomez-Vargas; Adriana Yock Corrales; Danilo Buonsenso

    doi:10.1101/2020.08.29.20184358 Date: 2020-09-02 Source: medRxiv

    Background: Patients with coronavirus disease MESHD 19 (COVID-19) are at high risk for thrombotic arterial and venous occlusions MESHD venous occlusions HP, while lung histopathology often reveals fibrin-based occlusion of small vessels in patients who succumb to the disease. At the same time, bleeding MESHD complications have been observed in some patients. Better understanding the balance between coagulation and fibrinolysis will help inform optimal approaches to thrombosis MESHD prophylaxis and potential utility of fibrinolytic-targeted therapies. Objective: To evaluate fibrinolysis among a large cohort of hospitalized COVID-19 patients. Patients and methods: 118 hospitalized COVID-19 patients and 30 healthy controls were included in the study. We measured plasma SERO antigen levels of tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) and performed spontaneous clot lysis assays. Results: We found markedly elevated levels of tPA and PAI-1 among patients hospitalized with COVID-19. Both factors demonstrated a strong correlation with neutrophil counts and markers of neutrophil activation, but not with D-dimer. High levels of tPA and PAI-1 were associated with worse respiratory status. High levels of tPA, in particular, were also strongly correlated with mortality and with a significant enhancement in spontaneous ex vivo clot lysis. Conclusion: While both tPA and PAI-1 are elevated among COVID-19 patients, extremely high levels of tPA enhance spontaneous fibrinolysis and are significantly associated with mortality in some patients. These data indicate that fibrinolytic homeostasis in COVID-19 is complex with a subset of patients expressing a balance of factors that may favor fibrinolysis and suggests that further study of tPA as a potential biomarker is warranted.

    The Potential Role of Extracellular Vesicles in COVID-19 Associated Endothelial injury and Pro-inflammation MESHD

    Authors: Balaji Krishnamachary; Christine Cook; Leslie Spikes; Prabhakar Chalise; Navneet K Dhillon; Yuhang Pan; Tanakao Takana; Peiyu Xie; Zhaoguang Wang; Shuocen Liu; George Fu Gao; Guojun He; Maigeng Zhou

    doi:10.1101/2020.08.27.20182808 Date: 2020-09-01 Source: medRxiv

    COVID-19 infection caused by the novel severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2) has resulted in a global pandemic with the number of deaths growing exponentially. Early evidence points to significant endothelial dysfunction, micro-thromboses, pro- inflammation MESHD as well as a dysregulated immune response in the pathogenesis of this disease. In this study, we analyzed the cargo of EVs isolated from the plasma SERO of patients with COVID-19 for the identification of potential biomarkers of disease severity and to explore their role in disease pathogenesis. Plasma SERO-derived EVs were isolated from 53 hospitalized patients with COVID infection MESHD and compared according to the severity of the disease. Analysis of inflammatory and cardiovascular protein cargo of large EVs revealed significantly differentially expressed proteins for each disease sub-group. Notably, members of the TNF superfamily and IL-6 family were up-regulated in patients on oxygen support with severe and moderate disease. EVs from the severe group were also enhanced with pro- thrombotic MESHD/endothelial injury factors (TF, t-PA, vWF) and proteins associated with cardiovascular pathology (MB, PRSS8, REN, HGF). Significantly higher levels of TF, CD163, and EN-RAGE were observed in EVs from severe patients when compared to patients with a moderate disease requiring supplemental O2. Importantly, we also observed increased caspase 3/7 activity and decreased cell survival in human pulmonary microvascular endothelial cells exposed to EVs from the plasma SERO of patients with severe disease compared to healthy controls. In conclusion, our findings indicate alterations in pro-inflammatory, coagulopathy MESHD, and endothelial injury MESHD protein cargo in large EVs in response to SARS-CoV-2 infection MESHD that may be a causative agent in severe illness.

    Eosinophil and Anticoagulation in COVID-19 Patients

    Authors: Selma Ari; Veysi Can; Ömer Furkan Demir; Hasan Ari; Fahriye Vatansever Ağca; Mehmet Melek; Sencer Çamcı; Özlem Şengören Dikiş; Kağan Huysal; Tamer Türk

    doi:10.21203/ Date: 2020-08-22 Source: ResearchSquare

    Introduction: Despite prophylactic anticoagulant treatments, thrombotic complications MESHD may develop in patients with Coronavirus disease MESHD 2019 (COVID-19). This study aimed to evaluate anti-Factor Xa levels to determine the anticoagulant activity of low molecular weight heparin (LMWH) in COVID-19 patients.Materials and methods: We prospectively evaluated 80 COVID-19 patients, diagnosed using polymerase-chain-reaction test, who were admitted to our clinic and administered LMWH; enoxaparin was applied according to the weight, D-dimer levels, and clinical condition of patients. Anti-Factor Xa levels in blood SERO, drawn 4h after the 3rd dose of LMWH, were measured and a level of <0.2IU/ml was considered subprophylactic. Patients were followed up clinically and anti-Factor Xa levels were re-examined before discharge.Results: Groups 1 and 2 included 13 and 67 patients with subprophylactic (0.18±0.06) and prophylactic (0.43±0.23) anti-Factor Xa levels, respectively. The proportion of eosinophils in patients was significantly higher in group 1 than in group 2 (2.96±2.55 vs 0.90±1.28;p=0.001). At the time of discharge the eosinophilic proportion of patients was significantly higher (3.06±1.49 vs 2.07±1.92;p=0.001) but the activated partial thromboplastin time MESHD was significantly lower (22.34±1.38 vs 24.38±3.58; p=0.01) in group 1 than in group 2. Of 14 patients with eosinophil content >4%, 6 were in group 1 ((6/13) 46.2%) while 8 were in group 2 ((8/63) 11.9%); (p=0.009), and all had a D-dimer level <1µg/mL (p=0.03). ROC analysis for the presence of anticoagulation at subprophylactic level revealed an area under curve of 0.79 (95% CI:0.64-0.93); p=0.001).Conclusions: In COVID-19 patients, eosinophil levels could be considered for determining effective prophylactic anticoagulant administration. (NCT04507282)

    IP-10 and MCP-1 as biomarkers predicting disease severity of COVID-19

    Authors: Yu Chen; Jinglan Wang; Chenxi Liu; Longxiang Su; Dong Zhang; Junping Fan; Yanli Yang; Meng Xiao; Jing Xie; Yingchun Xu; Yongzhe Li; Shuyang Zhang

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

    Background: COVID-19 is a viral respiratory disease MESHD caused by the severe acute respiratory syndrome-Coronavirus type 2 MESHD (SARS-CoV-2). Patients with this disease may be more prone to venous or arterial thrombosis MESHD arterial thrombosis HP because of the activation of many factors involved in it, including inflammation MESHD, platelet activation and endothelial dysfunction. Therefore, this study focused on coagulation and thrombosis MESHD-related indicators (IP-10, MCP-1 and MIP1a) in COVID-19, with the hope to find biomarkers that can predict patients’ outcome.Methods: This is a retrospective single-center study involving 74 severe and critically ill COVID-19 patients recruited from the ICU department of the Tongji Hospital in Wuhan, China. The patients were divided into two groups: severe patients and critically ill MESHD patients. The serum SERO IP-10, MCP-1 and MIP1a level in both groups was detected using the enzyme-linked immunosorbent assay SERO ( ELISA SERO) kit. The clinical symptoms, laboratory test results and the outcome of COVID-19 patients were retrospectively analyzed.Results: The serum SERO IP-10 and MCP-1 level in critically ill patients was significantly higher than that in severe patients (P < 0.001). However, no statistical difference in MIP1a between the two groups was found. The analysis of dynamic changes showed that these indicators remarkably increased in patients with poor prognosis. Since the selected patients were severe or critically ill, no significant difference was observed between survival and death MESHD.Conclusions: IP-10 and MCP-1 are biomarkers predicting the severity of COVID-19 disease and could be related to the risk of death in COVID-19 patients. In addition, anti-IP-10 antibody SERO treatment may represent a new approach in COVID-19 patients, especially the ones with thrombotic MESHD events.

    Association Between Antecedent Statin Use and Decreased Mortality in Hospitalized Patients with COVID-19

    Authors: Aakriti Gupta; Mahesh V. Madhavan; Timothy J. Poterucha; Ersilia M. DeFilippis; Jessica A. Hennessey; Bjorn Redfors; Christina Eckhardt; Behnood Bikdeli; Jonathan Platt; Ani Nalbandian; Pierre Elias; Matthew J. Cummings; Shayan N. Nouri; Matthew Lawlor; Lauren S. Ranard; Jianhua Li; Claudia Boyle; Raymond Givens; Daniel Brodie; Harlan M. Krumholz; Gregg W. Stone; Sanjum S. Sethi; Daniel Burkhoff; Nir Uriel; Allan Schwartz; Martin B. Leon; Ajay J. Kirtane; Elaine Y. Wan; Sahil A. Parikh

    doi:10.21203/ Date: 2020-08-09 Source: ResearchSquare

    The coronavirus disease MESHD 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), can result in a hyperinflammatory state, leading to acute respiratory distress HP respiratory distress MESHD syndrome ( ARDS MESHD), myocardial injury MESHD, and thrombotic complications MESHD, among other sequelae. Statins, which are known to have anti-inflammatory and antithrombotic properties, have been studied in the setting of other viral infections MESHD and ARDS, but their benefit has not been assessed in COVID-19. Thus, we sought to determine whether antecedent statin use is associated with lower in-hospital mortality in patients hospitalized for COVID-19. This is a retrospective analysis of patients admitted with COVID-19 from February 1st through May 12th, 2020 with study period ending on June 11th, 2020. Antecedent statin use was assessed using medication information available in the electronic medical record. We constructed a multivariable logistic regression model to predict the propensity of receiving statins, adjusting for baseline socio-demographic and clinical characteristics, and outpatient medications. The primary endpoint included in-hospital mortality within 30 days. A total of 2626 patients were admitted during the study period, of whom 951 (36.2%) were antecedent statin users. Among 1296 patients (648 statin users, 648 non-statin users) identified with 1:1 propensity-score matching, demographic, baseline, and outpatient medication information were well balanced. Statin use was significantly associated with lower odds of the primary endpoint in the propensity-matched cohort (OR 0.48, 95% CI 0.36 – 0.64, p<0.001). We conclude that antecedent statin use in patients hospitalized with COVID-19 was associated with lower inpatient mortality. Randomized clinical trials evaluating the utility of statin therapy in patients with COVID-19 are needed.

    COVID-19 induces a hyperactive MESHD phenotype in circulating platelets

    Authors: Shane P Comer; Sarah Cullivan; Paulina B Szklanna; Luisa Weiss; Steven Cullen; Sarah Kelliher; Albert Smolenski; Niamh Moran; Claire Murphy; Haidar Altaie; John Curran; Katherine O'Reilly; Aoife G Cotter; Brian Marsh; Sean Gaine; Patrick Mallon; Brian McCullagh; Fionnuala Ní Áinle; Barry Kevane; Patricia B Maguire

    doi:10.1101/2020.07.24.20156240 Date: 2020-07-26 Source: medRxiv

    Background Coronavirus disease MESHD 2019 (COVID-19), caused by novel coronavirus SARS-CoV-2 MESHD, has to date affected over 13.3 million globally. Although high rates of venous thromboembolism MESHD thromboembolism HP and evidence of COVID-19-induced endothelial dysfunction have been reported, the precise aetiology of the increased thrombotic MESHD risk associated with COVID-19 infection MESHD remains to be fully elucidated. Objectives Here, we assessed clinical platelet parameters and circulating platelet activity in patients with severe and non-severe COVID-19. Methods An assessment of clinical blood SERO parameters in patients with severe COVID-19 disease MESHD (requiring intensive care), patients with non-severe disease (not requiring intensive care), general medical in-patients without COVID-19 and healthy donors was undertaken. Platelet function and activity were also assessed by secretion and specific marker analysis. Results We show that routine clinical blood SERO parameters including increased MPV and decreased platelet:neutrophil ratio are associated with disease severity in COVID-19 upon hospitalisation and intensive care unit admission. Strikingly, agonist-induced ADP release was dramatically higher in COVID-19 patients compared with non-COVID-19 hospitalized patients and circulating levels of PF4, sP-selectin and TPO were also significantly elevated in COVID-19. Conclusion Distinct differences exist in routine full blood SERO count and other clinical laboratory parameters between patients with severe and non-severe COVID-19. Moreover, we have determined that COVID-19 patients possess hyperactive circulating platelets. These data suggest that abnormal platelet reactivity may contribute to hypercoagulability HP hypercoagulability MESHD in COVID-19. Further investigation of platelet function in COVID-19 may provide additional insights into the aetiology of thrombotic risk in this disease and may contribute to the optimisation of thrombosis MESHD prevention and treatment strategies.

    Severe COVID-19 is associated with elevated serum SERO IgA and antiphospholipid IgA- antibodies SERO

    Authors: Omar Hasan Ali; David Bomze; Lorenz Risch; Silvio D Brugger; Matthias Paprotny; Myriam Weber; Sarah Thiel; Lukas Kern; Werner C Albrich; Philipp Kohler; Christian R Kahlert; Pietro Vernazza; Philipp K Buehler; Reto A Schuepbach; Alejandro Gomez-Mejia; Alexandra M Popa; Andreas Bergthaler; Josef M Penninger; Lukas Flatz

    doi:10.1101/2020.07.21.20159244 Date: 2020-07-24 Source: medRxiv

    Background: While the pathogenesis of coronavirus disease MESHD 2019 (COVID-19) is becoming increasingly clear, there is little data on IgA response, the first line of bronchial immune defense. Objective: To determine, whether COVID-19 is associated with a vigorous total IgA response and whether IgA autoantibodies are associated with complications of severe illness. Since thrombotic MESHD events are frequent in severe COVID-19 and resemble hypercoagulation of antiphospholipid syndrome MESHD ( APS MESHD), our approach focused on antiphospholipid antibodies SERO (aPL). Materials and methods: In this retrospective cohort study we compared clinical data and aPL from 64 patients with COVID-19 from three independent centers (two in Switzerland, one in Liechtenstein). Samples were collected from April 9, 2020 to May 1, 2020. Total IgA and aPL were measured with FDA-approved commercially available clinical diagnostic kits. Results: Clinical records of the 64 patients with COVID-19 were reviewed and divided into a cohort with mild illness (mCOVID, n=26 [41%]), a discovery cohort with severe illness (sdCOVD, n=14 [22%]) and a confirmation cohort with severe illness (scCOVID, n=24 [38%]). Severe illness MESHD was significantly associated with increased total IgA (sdCOVID, P=0.01; scCOVID, P<0.001). Total IgG levels were similar in both cohorts. Among aPL, both cohorts with severe illness significantly correlated with elevated anti-Cardiolipin IgA (sdCOVID and scCOVID, P<0.001), anti-Cardiolipin IgM (sdCOVID, P=0.003; scCOVID, P<0.001), and anti-Beta2 Glycoprotein-1 IgA (sdCOVID and scCOVID, P<0.001). Systemic lupus erythematosus HP Systemic lupus erythematosus MESHD was excluded from all patients as a potential confounder of APS MESHD. Conclusions: Higher total IgA and IgA-aPL were consistently associated with severe illness. These novel data strongly suggest that a vigorous antiviral IgA-response triggered in the bronchial mucosa induces systemic autoimmunity MESHD autoimmunity HP.

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MeSH Disease
Human Phenotype

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