Aim: Omentin-1, a novel adipokine expressed in visceral adipose tissue, is negatively correlated with insulin resistance and obesity. Decreased omentin-1 expression has been found in many chronic inflammatory diseases. However, the role of omentin-1 in coronary artery disease (CAD) has not been elucidated. The aim of the present study was to determine whether serum concentration of omentin-1 was independently associated with CAD. Methods: One hundred and fifty five patients with CAD were divided into two groups: acute coronary syndrome (ACS) and stable angina pectoris (SAP). A total of 52 healthy participants served as controls. Serum concentrations of omentin-1 and interleukin-6 (IL-6) were measured using ELISA. The association of omentin-1 with CAD and cardiovascular disease risk factors was evaluated. Results: Serum omentin-1 levels were lower in patients with ACS or SAP compared with controls (ACS, 113.08±61.43 ng/mL; SAP, 155.41±66.89 ng/mL; control, 254.00±72.9 ng/mL; P<0.01). Patients with ACS also had lower serum concentrations of omentin-1 compared with patients with SAP (P<0.01). Serum concentration of omentin-1 was negatively correlated with body mass index (r=-0.17, P<0.05) and serum IL-6 concentration (r=-0.19, P<0.05). Furthermore, multiple logistic regression analysis showed that serum omentin-1 concentrations were independently correlated with CAD. Conclusion: The findings suggest that serum concentrations of omentin-1 are related to CAD.

No abstract

Despite the growing recognition of the impact psychosocial distress has on the quality of life of patients with cancer, the implementation of the NCCN Distress Management Guidelines and the mandate of evidence-based policy for routine distress screening continue to lag. To speed adoption of the guideline, The American Psychosocial Oncology Society (APOS) and Yale School of Nursing (YSN) launched the Screening for Psychosocial Distress Program in 2014. The program resulted in the development of five steps necessary to carry out routine psychosocial distress screening. The steps are consistent with the NCCN Distress Management Guidelines and the new criterion for accreditation by the American College of Surgeons (ACS) Commission on Cancer as of 2015. These five steps are: (1) screen, (2) evaluation, (3) referral, (4) follow-up and (5) documentation & quality improvement. The purpose of this article is to summarize the detailed procedure of the five steps for cancer care professionals-including oncologists, nurses, psychiatrists, psychologists, and social workers-so they can manage psychosocial distress efficiently in their own clinical environments.

The voltage-gated sodium channel 1.5 (Nav1.5), encoded by the SCN5A gene, is responsible for the rising phase of the action potential of cardiomyocytes. The sodium current mediated by Nav1.5 consists of peak and late components (I and I). Mutant Nav1.5 causes alterations in the peak and late sodium current and is associated with an increasingly wide range of congenital arrhythmias. More than 400 mutations have been identified in the SCN5A gene. Although the mechanisms of SCN5A mutations leading to a variety of arrhythmias can be classified according to the alteration of I and I as gain-of-function, loss-of-function and both, few researchers have summarized the mechanisms in this way before. In this review article, we aim to review the mechanisms underlying dysfunctional Nav1.5 due to SCN5A mutations and to provide some new insights into further approaches in the treatment of arrhythmias. Impact statement The field of ion channelopathy caused by dysfunctional Nav1.5 due to SCN5A mutations is rapidly evolving as novel technologies of electrophysiology are introduced and our understanding of the mechanisms of various arrhythmias develops. In this review, we focus on the dysfunctional Nav1.5 related to arrhythmias and the underlying mechanisms. We update SCN5A mutations in a precise way since 2013 and presents novel classifications of SCN5A mutations responsible for the dysfunction of the peak (I) and late (I) sodium channels based on their phenotypes, including loss-, gain-, and coexistence of gain- and loss-of function mutations in I, I, respectively. We hope this review will provide a new comprehensive way to better understand the electrophysiological mechanisms underlying arrhythmias from cell to bedside, promoting the management of various arrhythmias in practice.

No abstract

SUMMARYBackground: Only limited data of the long-term effect of levosimendan on renal dysfunction in patients with decompensated heart failure (DHF) have been published previously. To date, there has been no similar study carried out in a Chinese population. Design and Methods: A prospective, randomized, placebo-controlled, and double-blind study was performed to investigate the effect of levosimendan on estimated glomerular filtration rate (eGFR) in DHF patients with renal dysfunction during a 30-day period. Sixty-six patients with left ventricular ejection fraction (LVEF) 40% and eGFR 15-89 mL/min/1.73 m 2 were randomized in a 1:1 ratio to receive a 24-h infusion with levosimendan or placebo. The B-type natriuretic peptide (BNP) and eGFR were determined at baseline and day 1, 3, 7, 14, 30 after the start of treatment. Results: The eGFR levels were obviously enhanced following levosimendan, peaked at 3 days, sustained for at least 14 days, and returned to baseline by day 30 after starting infusion. In contrast, placebo did not induce any significant changes in eGFR levels during the follow-up. In addition, levosimendan resulted in a distinct decrease in BNP levels in comparison with placebo, and the beneficial effect returned to baseline by day 14 and remained so at day 30 postinfusion. Conclusions: A 24-h infusion with levosimendan transiently improved the renal dysfunction compared with placebo in patients with DHF, and its beneficial effects persisted for at least 14 days after the initiation of treatment.

Patients with chronic kidney disease (CKD) have a high risk of fatal arrhythmias. The extended severe corrected QT (QTc) interval is a hallmark of ventricular arrhythmias and sudden cardiac death. The objective of this study was to evaluate the prevalence of acquired long QT syndrome (aLQTS) in hospitalized patients with CKD and search for potential risk factors to improve clinical risk stratification in patients with CKD. Information about patients with CKD was retrospectively collected in our hospital between January 2013 and June 2017. The prevalence of aLQTS in different stages of CKD was evaluated. The common risk factors for QTc prolongation in patients with CKD were compiled, and multivariable logistic regression analysis was used to evaluate how each factor was related to aLQTS in CKD. A total of 804 patients with CKD (299 females, 37.2%) participated in our study. The prevalence of aLQTS among all 804 patients was 56.97%, and the prevalence of QTc prolongation (>500 ms) was 10.07%. Among the elderly, impaired kidney function, hemodialysis, low serum potassium and low left ventricular ejection fraction (LVEF) were associated with QTc prolongation in patients with CKD. The prevalence of aLQTS is much higher and increases with the decline of kidney function in hospitalized patients with CKD, which is related to older age, impaired kidney function, hemodialysis, serum potassium and low LVEF.

UCBT demonstrated a good therapeutic effect on severe viral hepatitis and no obvious side effects. Umbilical cord blood can attenuate the liver lesions and reproduce hepatocyte. The treatment of UCBT combined with PE was much better than that of single plasma exchange, thus UCBT can enhance the therapeutic effect of plasma exchange on severe viral hepatitis.