Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study

The aim of this study was to analyze the clinical data, discharge rate, and fatality rate of COVID-19 patients for clinical help. The clinical data of COVID-19 patients from December 2019 to February 2020 were retrieved from four databases. We statistically analyzed the clinical symptoms and laboratory results of COVID-19 patients and explained the discharge rate and fatality rate with a single-arm meta-analysis. The available data of 1994 patients in 10 literatures were included in our study. The main clinical symptoms of COVID-19 patients were fever (88.5%), cough (68.6%), myalgia or fatigue (35.8%), expectoration (28.2%), and dyspnea (21.9%). Minor symptoms include headache or dizziness (12.1%), diarrhea (4.8%), nausea and vomiting (3.9%). The results of the laboratory showed that the lymphocytopenia (64.5%), increase of C-reactive protein (44.3%), increase of lactic dehydrogenase (28.3%), and leukocytopenia (29.4%) were more common. The results of single-arm meta-analysis showed that the male took a larger percentage in the gender distribution of COVID-19 patients 60% (95% CI [0.54, 0.65]), the discharge rate of COVID-19 patients was 52% (95% CI [0.34,0.70]), and the fatality rate was 5% (95% CI [0.01,0.11]).

https://onlinelibrary.wiley.com/doi/epdf/10.1002/jmv.25757

COVID-19 patients' clinical characteristics, discharge rate, and fatality rate of meta-analysis.

We have read Char's comment1. Thanks for readers’ attention and valuable feedback on our article. Following was our response to Char's question about data overlap.Firstly, the meta‐analysis reprocessed the existing data about COVID‐19 patients in published articles, and involved no other information outside of the article.This article is protected by copyright. All rights reserved.

/pdf/response-to-char-s-comment-comment-on-li-et-al-covid-19-56zja6cvi9.pdf

Response to Char's comment: Comment on Li et al: COVID-19 patients' clinical characteristics, discharge rate, and fatality rate of meta-analysis.

Particulate matter 2.5 (PM2.5)-induced pulmonary inflammation has become a public concern in recent years. In which, the activation of the NLRP3/caspase-1 pathway was closely related to the inflammatory response of various diseases. However, the promotion effect of the NLRP3/caspase-1 pathway on PM2.5-induced pulmonary inflammation remains largely unclear. Here, our data showed that PM2.5 exposure caused lung injury in the mice by which inflammatory cell infiltration occurred in lung and alveolar structure disorder. Meanwhile, the exposure of human bronchial epithelial cells (16HBE) to PM2.5 resulted in suppressed cell viability, as well as elevated cell apoptosis. Moreover, a higher level of inflammatory cytokine and activation of the NLRP3/caspase-1 pathway in PM2.5-induced inflammation mice models and 16HBE cells. Mechanistically, pretreatment with MCC950, a NLRP3/caspase-1 pathway inhibitor, prevented PM2.5-induced lung injury, inflammatory response, and the number of inflammatory cells in BALFs, as well as promoted cell viability and decreased inflammatory cytokine secretion. Collectively, our findings indicated that the NLRP3/caspase-1 pathway serves a vital role in the pathological changes of pulmonary inflammation caused by PM2.5 exposure. MCC950 was expected to be the therapeutic target of PM2.5 inhalation mediated inflammatory diseases.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/tox.23035

PM2.5-induced pulmonary inflammation via activating of the NLRP3/caspase-1 signaling pathway.

Central nervous system (CNS) trauma, including traumatic brain injury (TBI) and spinal cord injury (SCI), remains a leading cause for morbidity and mortality worldwide. Past research has shown that cell death plays a critical role in the pathophysiology of CNS injuries. More recently, pyroptosis has been identified as a form of programmed inflammatory cell death, and it is a unique form of cell death in various aspects. Mechanistically, pyroptosis can be categorized into canonical (mediated by caspase-1) and non-canonical (mediated by caspase-4/5/11). In canonical pyroptosis, Nod-like receptors (NLRs) inflammasomes play a critical role, and their activation promotes the maturation and secretion of the inflammatory cytokines interleukin-1β/18 (IL-1β/18), cleavage of gasdermin D (GSDMD), and ultimately pyroptotic cell death. Despite a plethora of new knowledge regarding pyroptosis, detailed understanding of how pyroptosis is involved in CNS injuries and possible ways to improve clinical outcomes following CNS injuries remain elusive. This review discusses the current knowledge on how pyroptosis is involved in CNS injuries, focusing on new discoveries regarding how pyroptosis activation occurs, differences between CNS cell types following injury, time-course of inflammatory responses, and key regulatory steps of pyroptosis. In addition, we highlight various investigational agents that are capable of regulating key steps in pyroptotic cell death, and we discuss how these agents may be used as therapies to improve outcomes following CNS trauma.

/pdf/role-of-pyroptosis-in-traumatic-brain-and-spinal-cord-1gfzon7260.pdf

Role of Pyroptosis in Traumatic Brain and Spinal Cord Injuries.

Background: Pulmonary fat embolism (PFE) is one of the important causes of acute lung injury (ALI), but its pathogenesis is unclear. In recent years, it has been found that the NLRP3 inflammasome is closely related to inflammatory response. However, there are no reports about the involvement of NLRP3 in PFE- associated ALI. Glibenclamide is a kind of hypoglycaemic drug with anti-inflammatory effect. It has been reported to have the anti-inflammatory effect related to inhibiting NLRP3. Objective: To determine whether NLRP3 inflammasome was involved in ALI induced by PFE or whether glibenclamide had therapeutic effects on such lung injury, we designed this experiment. Materials and methods: The rat model of intravenous injection of oleic acid (OA) was used to simulate PFE. Rats were divided into three groups: control, OA and glibenclamide treatment group. Blood free fatty acid (FFA) concentration was determined by ACS-ACOD. Histopathological examinations were taken to assess the severity of lung injury. The expression of NLRP3 pathway and its downstream products were analyzed by IHC, WB, qPCR and ELISA. Results: Four hours after intravenous OA injection, the typical pathological manifestations of ALI accompanied by elevated levels of plasma FFAs were found. The activity of NLRP3 inflammasomes increased in OA group, too. Pretreatment with glibenclamide partly inhibited the increase in NLRP3, caspase-1 and IL-1β expression induced by OA, simultaneously attenuated the lung injury. But it has little effect on the expression of Toll-like receptor 4 (TLR4) expression in this experiment. Conclusion: NLRP3 inflammasome, one of the main components of innate immune response, involved in ALI induced by OA. Glibenclamide can alleviate this kind of ALI by inhibiting rather the NLRP3/caspase-1/IL-1β signaling pathway than the levels of FFAs or TLR4 pathway.

/pdf/glibenclamide-alleviates-inflammation-in-oleic-acid-model-of-2uphk9t0m4.pdf

Glibenclamide alleviates inflammation in oleic acid model of acute lung injury through NLRP3 inflammasome signaling pathway.

Introduction

Since February 2013, a novel reassortant H7N9 virus associated with human deaths, but no apparent outbreaks in poultry and wild birds has emerged in eastern China.



Objectives

The potential reemergence of H7N9 during next year's influenza season demand a further understanding of this important disease.



Methods

Between March 1 and April 30, 2013, we obtained and analyzed clinical, epidemiologic and radiologic features, and virologic data from three laboratory-confirmed patients of A H7N9 infection admitted in Shanghai Ruijin Hospital.



Results

All patients were middle to old aged (mean age 62 years) and overweight (mean body mass index 31) patients. Two patients were exposed to poultry directly or indirectly in food market. They presented with fever and rapidly progressive pneumonia that did not respond to antibiotics. Time between onset of symptoms and onset of respiratory failure (days) were 7–11 days. Two patients presented secondary invasive bacterial infections. All patients died on day 7 to day 86 after the onset of symptoms.



Conclusions

Cross species poultry-to-person transmission of this new reassortant avian influenza H7N9 virus can result in severe and fatal respiratory disease like acute respiratory distress syndrome (ARDS) in humans. Reduplicate chest imaging examination is suggested for risky patients with fever and dyspnea. Secondary invasive bacterial infections and pneumothorax can cause severe and fatal consequence. Old age, obesity and presence of comorbidity may be associated with increased mortality. Pulmonary fibrosis can be seen at late stage of the disease.

Clinical features of three avian influenza H7N9 virus-infected patients in Shanghai.

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Glibenclamide alleviates inflammation in oleic acid model of acute lung injury through NLRP3 inflammasome signaling pathway.

Clinical features of three avian influenza H7N9 virus-infected patients in Shanghai.