Analysis of Career-Advancement for Medical School Graduates During the COVID-19 Pandemic at a Chinese Teaching Hospital.

The COVID-19 pandemic has led to widespread social and economic disruptions in the balance of labor market. Our study aims to analyze the career-advancement of medical school graduates during the COVID-19 pandemic and the associated influencing factors. We collected and compared the career-advancement data of medical school graduates at a Chinese teaching hospital from 2016 to 2020. A self-designed 20-element medical graduates employment questionnaire and a Chinese adaptation of the General self-efficacy scale were distributed by the Questionnaire Star platform. Univariate analysis (Pearson's Chi-square-test and Fisher's exact-test) and subsequent binary logistic regression were used. Findings demonstrated that the career-advancement rate of medical graduate students in 2020 is 71.3%, which is significantly lower than that for the preceding 4 years from 2016 to 2019 (p < 0.001). Of the 251 employed medical school graduates, 159 (63.3%) have signed an employment agreement or contract, 83 (33.1%) are pursuing continued education domestically, and 9 (3.6%) have offers from foreign institutions. Univariate analysis revealed statistical differences of medical graduates' employment among various specialties, oral defense completion, job search start date, CV submission times, participation in a probationary period, and self-efficacy. Significant predictors for successful employment were early job search and self-efficacy by logistic regression model (χ2 = 12.719, p < 0.001). Most medical graduates assumed that the COVID-19 pandemic had a major (40.6%) or moderate (48%) impact on career-advancement. The COVID-19 pandemic has profoundly impacted the career-advancement of medical school graduates in 2020. We should make adaptive changes to improve the career-advancement of medical graduates.

Overexpression of the SARS-CoV-2 receptor ACE2 is induced by cigarette smoke in bronchial and alveolar epithelia.

Angiotensin-converting enzyme 2 (ACE2) has been identified as the functional receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and a target for disease prevention. However, the relationship between ACE2 expression and its clinical implications in SARS-CoV-2 pathogenesis remains unknown. Here, we explored the location and expression of ACE2, and its correlation with gender, age, and cigarette smoke (CS), in a CS-exposed mouse model and 224 non-malignant lung tissues (125 non-smokers, 81 current smokers, and 18 ex-smokers) by immunohistochemistry. Moreover, the correlations of ACE2 with CS-induced oxidative stress-related markers, hypoxia-inducible factor-1α (HIF-1α), inducible nitric oxide synthase (iNOS), and 4-hydroxynonenal (4-HNE) were investigated. Chromatin immunoprecipitation and luciferase reporter assays identified the cause of ACE2 overexpression in human primary lung epithelial cells. We demonstrated that ACE2 was predominantly overexpressed on the apical surface of bronchial epithelium, while reduced in alveolar epithelium, owing to the dramatically decreased abundance of alveolar type II pneumocytes in CS-exposed mouse lungs. Consistent with this, ACE2 was primarily significantly overexpressed in human bronchial and alveolar epithelial cells in smokers regardless of age or gender. Decreased ACE2 expression was observed in bronchial epithelial cells from ex-smokers compared with current smokers, especially in those who had ceased smoking for more than 10 years. Moreover, ACE2 expression was positively correlated with the levels of HIF-1α, iNOS, and 4-HNE in both mouse and human bronchioles. The results were further validated using a publicly available dataset from The Cancer Genome Atlas (TCGA) and our previous integrated data from Affymetrix U133 Plus 2.0 microarray (AE-meta). Finally, our results showed that HIF-1α transcriptionally upregulates ACE2 expression. Our results indicate that smoking-induced ACE2 overexpression in the apical surface of bronchial epithelial cells provides a route by which SARS-CoV-2 enters host cells, which supports clinical relevance in attenuating the potential transmission risk of COVID-19 in smoking populations by smoking cessation. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Smoking increases the risk of infectious diseases: A narrative review.

Smoking is relevant to infectious diseases resulting in increased prevalence and mortality. In this article, we aim to provide an overview of the effects of smoking in various infections and to explain the potential mechanisms. We searched PubMed and other relevant databases for scientific studies that explored the relationship between smoking and infection. The mechanisms of susceptibility to infection in smokers may include alteration of the structural, functional and immunologic host defences. Smoking is one of the main risk factors for infections in the respiratory tract, digestive tract, reproductive tract, and other systems in humans, increasing the prevalence of HIV, tuberculosis, SARS-CoV, and the current SARS-CoV-2. Smoking cessation can reduce the risk of infection. Smoking increases the incidence of infections and aggravates the progress and prognosis of infectious diseases in a dose-dependent manner. Smoking cessation promotion and education are the most practical and economical preventive measures to reduce aggravation of disease infection owing to tobacco use.

Insight into 2019 novel coronavirus - An updated interim review and lessons from SARS-CoV and MERS-CoV.

BACKGROUND: The rapid spread of the coronavirus disease 2019 (COVID-19), caused by a zoonotic beta-coronavirus entitled 2019 novel coronavirus (2019-nCoV), has become a global threat. Awareness of the biological features of 2019-nCoV should be updated in time and needs to be comprehensively summarized to help optimize control measures and make therapeutic decisions. METHODS: Based on recently published literature, official documents and selected up-to-date preprint studies, we reviewed the virology and origin, epidemiology, clinical manifestations, pathology and treatment of 2019-nCoV infection, in comparison with severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) infection. RESULTS: The genome of 2019-nCoV partially resembled SARS-CoV and MERS-CoV, and indicated a bat origin. The COVID-19 generally had a high reproductive number, a long incubation period, a short serial interval and a low case fatality rate (much higher in patients with comorbidities) than SARS and MERS. Clinical presentation and pathology of COVID-19 greatly resembled SARS and MERS, with less upper respiratory and gastrointestinal symptoms, and more exudative lesions in post-mortems. Potential treatments included remdesivir, chloroquine, tocilizumab, convalescent plasma and vaccine immunization (when possible). CONCLUSION: The initial experience from the current pandemic and lessons from the previous two pandemics can help improve future preparedness plans and combat disease progression.