mass index as well by a lower risk of LVH. Limitations include high prevalence of modest renal artery stenosis (≥50%); small sample of fibromuscular dysplasia; lack of randomized design of most studies.
  The aim of this study was to identify demographic and clinical risk factors for mortality in patients with antineutrophil cytoplasmic antibodies-associated vasculitides (AAVs) in a Peruvian tertiary referral hospital.
 
  Medical records of patients with AAV according to classification criteria or diagnosed by an experienced rheumatologist, covering the period between January 1990 and December 2018, were reviewed. Granulomatosis with polyangiitis, microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis, and renal-limited vasculitis were included. Potential predictors of mortality were demographic factors, clinical manifestations, antineutrophil cytoplasmic antibodies status, diagnosis, disease categorization, the 2009 Five Factor Score (FFS), and treatment. Cox regression models were used to determine the risk factors for mortality. Univariable and multivariable analyses using a backward selection method were performed.
 
  One hundred ninety-six patients were included; female-to-male ratio was nts.
 Ocular involvement was protective, whereas 2009 FFS ≥ 1 and renal and lung involvement were predictive factors of mortality in Peruvian AAV patients.
  Previous investigations showed inconsistent results for comparison in clinical outcomes between patients with 3-vessel disease (3VD) treated with percutaneous coronary intervention (PCI) and coronary artery bypass graft (CABG) surgery.  https://www.selleckchem.com/products/cpi-0610.html  A systematic review and meta-analysis is essential to compare the clinical outcomes of PCI with CABG surgery for patients with 3VD.
 
  We systematically searched on PubMed and Web of Science for articles which compared PCI with CABG for patients with 3VD and published from January 1989 to January 2020. We computed the hazard ratios (HRs) and 95% confidence intervals (CIs) for individual clinical outcomes.
 
  This study indicated that the PCI group was associated with a 1.51-fold higher risk of all-cause mortality compared with the CABG group in patients with 3VD (HR 1.51, 95% CI 1.38-1.65). In addition, the PCI group showed a 3.08-fold and 2.94-fold higher risk compared with the CABG group in risks of myocardial infarction (MI) and target-vessel revascularization (TVR), respectively (MI HR 3.08, 95% CI 2.61-3.63; TVR HR 2.94, 95% CI 1.94-4.46).
 
  In conclusion, in patients with 3VD, PCI was consistently associated with higher rates of all-cause mortality, MI, and TVR, compared with CABG.
 In conclusion, in patients with 3VD, PCI was consistently associated with higher rates of all-cause mortality, MI, and TVR, compared with CABG.Chemokine (C-C motif) ligand 6 (CCL6), one of the small cytokines in the CC chemokine family, has been reported to involve in renal ischemia-reperfusion (I/R) injury. However, the role of CCL-6 in myocardial I/R injury is nonelucidated. In this study, we used in vitro H9c2 cell model to investigate the overall contributions of CCL6 to myocardial I/R injury. We found the elevated level of CCL6 from the reanalysis of data set GSE-4105 and in hypoxia-reoxygenation (H/R)-injured H9c2 cells. CCL6 silencing attenuated the cardiomyocyte apoptosis induced by H/R injury, whereas exogenous CCL6 treatment aggravated the apoptosis of H/R-injured H9c2 cells. During CCL6 administration, the expression of numerous long noncoding RNAs was differentially regulated. Quantitative RT-Polymerase chain reaction assay demonstrated that insulin-like growth factor 2 (IGF2)-Antisense (AS) had the highest induction by CCL6 addition. IGF2-AS silencing alleviated the apoptosis of H/R-injured H9c2 cells. Collectively, we have identified a potential mechanism by which high expression of CCL6 contributes to the H/R-induced apoptosis in H9c2 cells through enhancing the expression of IGF2-AS. These findings also give evidence of the feasibility of CCL6 or long noncoding RNA IGF2-AS as a potential target for modulation or therapeutic intervention in myocardial I/R injury.Emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) are related to the pathogenesis of atherosclerosis (AS). We aimed to investigate the roles and molecular mechanisms of myocardial infarction-associated transcript (MIAT) in the proliferation, migration and invasion of oxidized low-density lipoprotein (ox-LDL)-induced vascular smooth muscle cells (VSMCs). Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the levels of MIAT, microRNA490-3p (miR-490-3p) and Intercellular Adhesion Molecule 1 (ICAM1). Cell Counting Kit-8 (CCK-8) assay was carried out to assess cell proliferation. Transwell assay was employed to evaluate cell migration and invasion. Western blot assay was performed to measure the protein levels of proliferating cell nuclear antigen (PCNA), N-cadherin, matrix metalloprotein-9 (MMP9) and ICAM1. Dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays were conducted to verify the relationship between miR-490-3p and MIAT or ICAM1. MIAT was elevated in AS patients' serum and ox-LDL-induced VSMCs. MIAT knockdown suppressed cell proliferation, migration and invasion in ox-LDL-stimulated VSMCs. MIAT acted as a sponge of miR-490-3p and miR-490-3p deficiency overturned the inhibition of MIAT knockdown on VSMC proliferation, migration and invasion. ICAM1 was a direct target of miR-490-3p and ICAM1 silencing repressed the proliferation, migration and invasion of ox-LDL-stimulated VSMCs. Moreover, ICAM1 overexpression reversed the impacts of MIAT knockdown on ox-LDL-induced VSMC proliferation, migration and invasion. MIAT knockdown could depress cell proliferation, migration and invasion via miR-490-3p/ICAM1 axis in ox-LDL-induced VSMCs.Resveratrol is well known to exhibit vascular relaxant and antihypertensive effects. In this study, we determined the effects of resveratrol on the modulation of cytosolic [Ca] level and adenosine 5'-triphosphate-induced Ca release from the sarcoplasmic reticulum (SR) in rat aortic smooth muscle cells (ASMCs) and explored its underlying mechanisms. In this article, cytosolic [Ca] and SR [Ca] in ASMCs were determined by Fluo-4/acetoxymethyl and Mag-Fluo-4/acetoxymethyl respectively. Resveratrol (20, 50, and 100 µM) caused a rapid and substantial reduction in cytosolic [Ca] in ASMCs bathed in normal Hank's Balanced Salt Solution or Ca-free Hank's Balanced Salt Solution. Pretreatment with resveratrol reduced adenosine 5'-triphosphate-induced SR Ca release and SR Ca content. In the cells bathed in Na-free physiological saline, which favors the reverse mode of the Na-Ca exchanger (NCX), resveratrol induced an increase in cytosolic [Ca] and SR [Ca]. However, its effect on cytosolic [Ca] was inhibited by the selective NCX inhibitor, SEA0400.