In the recent outbreak of novel coronavirus infection worldwide, the risk of thrombosis and bleeding should be concerned. We aimed to observe the dynamic changes of D-dimer levels during disease progression to evaluate their value for thrombosis. In this study, we report the clinical and laboratory results of 57 patients with confirmed COVID-19 pneumonia and 46 patients with confirmed community-acquired bacterial pneumonia (CAP). And their concentrations of D-dimer, infection-related biomarkers, and conventional coagulation were retrospectively analyzed. The Padua prediction score is used to identify patients at high risk for venous thromboembolism (VTE). The results found that, on admission, both in COVID-19 patients and CAP patients, D-dimer levels were significantly increased, and compared with CAP patients, D-dimer levels were higher in COVID-19 patients (P < 0.05). Besides, we found that in COVID-19 patients, D-dimer were related with markers of inflammation, especially with hsCRP (R = 0.426, P < 0.05). However, there was low correlation between VTE score and D-dimer levels (Spearman's R = 0.264, P > 0.05) weakened the role of D-dimer in the prediction of thrombosis. After treatments, D-dimer levels decreased which was synchronous with hsCRP levels in patients with good clinical prognosis, but there were still some patients with anomalous increasing D-dimer levels after therapy. In conclusion, elevated baseline D-dimer levels are associated with inflammation but not with VTE score in COVID-19 patients, suggesting that it is unreasonable to judge whether anticoagulation is needed only according to D-dimer levels. However, the abnormal changes of D-dimer and inflammatory factors suggest that anticoagulant therapy might be needed. Keywords D-dimer • COVID-19 • Bacterial pneumonia • Retrospective analysis Highlights• After COVID-19 outbreaks, the risk of thrombosis and bleeding has attracted much attention. • It has been reported that abnormal D-dimer levels are associated with poor prognosis.• D-dimer levels were higher in COVID-19 patients and were related with markers of inflammation, and after treatments, D-dimer levels decreased which was synchronous with hsCRP levels in patients with good clinical prognosis. Also, the low correlation between Padua VTE score and D-dimer levels weakened the role of D-dimer in the prediction of thrombosis. • The abnormal changes of D-dimer and inflammatory factors suggest that aggressive anticoagulant therapy might be needed.

Obesity is the most common nutritional disorder worldwide and is associated with dyslipidemia and atherosclerotic cardiovascular disease. The hallmark of dyslipidemia in obesity is low high density lipoprotein (HDL) cholesterol (HDL-C) levels. Moreover, the quality of HDL is also changed in the obese setting. However, there are still some disputes on the explanations for this phenomenon. There is increasing evidence that adipose tissue, as an energy storage tissue, participates in several metabolism activities, such as hormone secretion and cholesterol efflux. It can influence overall reverse cholesterol transport and plasma HDL-C level. In obesity individuals, the changes in morphology and function of adipose tissue affect plasma HDL-C levels and HDL function, thus, adipose tissue should be the main target for the treatment of HDL metabolism in obesity. In this review, we will summarize the cross-talk between adipocytes and HDL related to cardiovascular disease and focus on the new insights of the potential mechanism underlying obesity and HDL dysfunction.

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IntroductionPrevious observational studies have indicated that gut microbiota and metabolites may contribute to heart failure and its risk factors. However, with the limitation of reverse causality and confounder in observational studies, such relationship remains unclear. This study aims to reveal the causal effect of gut microbiota and metabolites on heart failure and its risk factors.MethodsThis study collected summary statistics regarding gut microbiota and metabolites, heart failure, diabetes, hypertension, chronic kidney disease, myocardial infarction, atrial fibrillation, hypertrophic cardiomyopathy, dilated cardiomyopathy, coronary heart disease, valvular heart disease, and myocarditis. Two-sample Mendelian randomization analysis was performed using MR-Egger, inverse variance weighted (IVW), MR-PRESSO, maximum likelihood, and weighted median.ResultsResults from gene prediction showed that among all gut microbiota, candida, shigella, and campylobacter were not associated with higher incidence of heart failure. However, genetic prediction suggested that for every 1 unit increase in shigella concentration, the relative risk increased by 38.1% for myocarditis and 13.3% for hypertrophic cardiomyopathy. Besides, for every 1 unit increased in candida concentration, the relative risk of chronic kidney disease increased by 7.1%. As for intestinal metabolites, genetic prediction results suggested that for every 1 unit increase in betaine, the relative risk of heart failure and myocardial infarction increased by 1.4% and 1.7%, separately.ConclusionsThis study suggested new evidence of the relationship between gut microbiota and heart failure and its risk factors, which may shed light on designing microbiome- and microbiome-dependent metabolite interventions on heart failure and its risk factors in clinical trials in the future.

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Small nucleolar RNA host gene 3 (SNHG3) is a long noncoding RNA (lncRNA), which is known to promote oncogenesis in many cancers but its role in human papillary thyroid carcinoma (PTC) remains poorly understood. We therefore assessed SNHG3 expression in PTC tissues via quantitative reverse transcription polymerase chain reaction. We additionally knocked down SNHG3 in PTC cells using short-hairpin RNAs (shRNAs) to explore its functional roles in PTC. The ability of SNHG3 to bind to specific microRNAs (miRNAs) was predicted using a bioinformatics tool, and this binding was confirmed via dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. We then used a tumor xenograft model to assess the relevance of SNHG3 in vivo. We determined SNHG3 expression to be elevated in PTC tissues relative to controls, with advanced tumor-node-metastasis stage and lymph node metastasis being associated with this expression. Knocking down SNHG3 significantly reduced in vitro PTC cell migration, invasion, proliferation, and colony formation, and it further slowed the growth of tumors in vivo. We found that SNHG3 could bind to miR-214-3p as a competing endogenous RNA (ceRNA) for this miRNA, thereby regulating proteasome 26S subunit non-ATPase 10 (PSMD10) expression, a miR-214-3p target. These results thus indicate that SNHG3 is an oncogenic lncRNA in PTC, acting at least in part via the miR-214-3p/PSMD10 axis.

Objective: To investigate how physical exercise (PE) would affect brain-derived neurotrophic factor (BDNF) in randomized controlled trials (RCTs) of healthy subjects. Methods:Seven databases (PubMed, Web of Science, Cochrane, Embase, PsycINFO, CINAHL, SPORTDiscus) were searched for RCTs assessing the effects of PE on serum and/or plasma BDNF until December 18, 2021. Meta-analysis was performed by random-effects method with standardized mean difference (SMD) and 95% confidence intervals (CIs). Subgroup analysis and meta-regression analysis were conducted to investigate the potential source of heterogeneity. Trim and fill method, and leave-oneout cross-validation were conducted.Results: Eventually, 21 articles, involving 809 participants, were included in the metaanalysis. Overall, both acute (5 trials, SMD: 1.20, 95% CI: 0.36 to 2.04, p = .005) and long-term (17 trials, SMD: 0.68, 95% CI: 0.27 to 1.08, p = .001) PE had significant positive effects on BDNF levels. Via subgroup analysis, studies of long-term PE with larger sample sizes, female participants, participants older than 60 years, and aerobic exercise contributed to a more pronounced improvement on BDNF levels than that found when all studies were combined. Conclusion:Both acute and long-term PE had significant positive effects on circulating BDNF in healthy subjects. This review suggests that acute exercise and long-term aerobic exercise are powerful forms of PE to enhance neurotrophic effect, especially for female subjects or subjects over 60 years.