Background: Cardiac arrest (CA) is a serious threat to human health. Cardiopulmonary resuscitation (CPR) is an effective treatment for CA. Early and high-quality CPR is closely related to the survival rate of patients with CA. But manual chest compression has a lot of defects. To solve the defects and improve the quality of CPR, mechanical CPR device was invented. However, it has still controversy whether manual chest compression or mechanical chest compression is better. This systematic review was aimed to investigate the difference in clinical outcomes between manual chest compression and Lund University Cardiac Assist System (LUCAS) assisted CPR in patients with out-hospital CA.Methods: Original research studies, conducted on adult out-of-hospital CA, were included. PubMed/Medline, EMBASE, Scopus, Cochrane Library, CNKI, and Wanfang database were searched from the setting to February 21, 2019. Odds ratio (OR) with 95% confidence interval (CI) was selected as effect scale index for evaluation of the difference in return of spontaneous circulation (ROSC), survival to hospital admission, survival to hospital discharge, and survival to 30 days. Random effects model was used in this study to estimate overall mean effects.Results: A total of 6 articles, including 4 randomized controlled trials and 2 nonrandomized controlled trials, were selected. And 8501 subjects were involved to analyze the clinical outcomes of LUCAS and manual chest compression for patients with outhospital CA. Comparisons of ROSC (33.3% vs 33.

Background: Recent studies have found that adropin is associated with coronary artery disease (CAD). This meta-analysis sought to assess the relationship between serum adropin level and CAD. Methods: Online databases including the Cochrane Library, PubMed, EMbase, Ovid, CBM, CNKI, VIP and WanFang Data were electronically searched for the clinical study concerning the relationship between serum adropin levels and CAD, including acute myocardial infarction (AMI), unstable angina pectoris (UAP), and stable angina pectoris (SAP). Two reviewers independently screened literature, extracted data and assessed methodological quality of included studies. Standard mean difference (SMD) with its 95% confidence interval (CI) was used as the effect size in this study. Then meta-analysis was performed using RevMan 5.2 software. Results: A total of seven articles involved 945 participants were included. The results indicated that serum adropin level in CAD group was lower than healthy control group (SMD =−2.44, P=0.0008). In the subgroup analysis, the levels of serum adropin in AMI group (SMD =−2.96, P<0.00001), UAP group (SMD =−2.09, P=0.0001) and SAP group (SMD =−1.23, P=0.007) were also lower than that of healthy control. Conclusions: Serum adropin level in patients with CAD was lower than healthy individuals, indicating that the decrease of adropin concentration might play an important role in the development of CAD.

Endothelial dysfunction, and the differentiation of smooth muscle cells (SMCs) into proliferative, secretory phenotypes, are two major pathophysiological processes in atherosclerosis. SMCs have the potential to recruit macrophages in atherosclerotic plaques, in which macrophages drive inflammatory responses. In this study, we found that microRNA-503-5p (miR-503-5p) was enriched in either extracellular vesicles (EVs), secreted by oxidized low-density lipoprotein-treated macrophages, or the EVs from peripheral blood mononuclear cells of atherosclerosis patients. miR-503-5p was transferred intercellularly from macrophages to the co-cultured human coronary artery endothelial cells (HCAECs) and HCASMCs via EVs, thus reducing the proliferative and angiogenic abilities of HCAECs and accelerating the proliferative and migrating abilities of HCASMCs. Smad family members 1, 2 and 7 were negatively regulated by miR-503-5p in HCAECs and HCASMCs. miR-503-5p was verified as an enhancer of inflammatory cytokines and adhesion molecules released by macrophages, in part via the down-regulation of smad family members 1, 2 and 7. The inhibition of miR-503-5p by lentivirus reduced atherosclerotic lesion formations in the aorta of atherosclerotic mice. Our work demonstrated a miR-503-5p- and EV-mediated mechanism for macrophage communication with HCAECs and HCASMCs in atherosclerosis. miR-503-5p is pro-atherosclerotic stimuli that may be a therapeutic target for atherosclerosis treatment.