Background:Infections caused by strains with multi-drug resistance are difficult to treat with standard antibiotics. Garlic is a powerful remedy to protect against infections of many bacteria, fungi and viruses. However, little is known about the potentials of fresh garlic extract (FGE) to improve the sensitivity of multi-drug resistant strains to antibiotics.Objectives:In this study, we used the disk diffusion method to investigate the antimicrobial activities of FGE and the combination of antibiotics with FGE, on methicillin-resistant Staphylococcus aureus (MRSA), Pseudomonas aeruginosa and Candida albicans, to evaluate the interactions between antibiotics and FGE.Materials and Methods:Clinical isolates were isolated from clinical specimens obtained from the inpatients at the First Affiliated Hospital of Xi’an Jiaotong University Health Science Center. The isolates consisted of MRSA, (n = 30), C. albicans (n = 30) and P. aeruginosa (n = 30). Quality control for CLSI (Clinical and Laboratory Standards Institute) disk diffusion was performed using S. aureus ATCC®25923, C. albicans ATCC®90028 and P. aeruginosa ATCC®27853. The 93 microorganisms were divided into four groups in a factorial design: control (deionized water), FGE, antibiotics without FGE, and antibiotics with FGE. Next, antibacterial activity was evaluated by measuring the diameter of inhibition zones according to performance standards for antimicrobial susceptibility testing of the Clinical and Laboratory Standards Institute (CLSI, formerly NCCLS).Results:Fresh garlic extract displayed evident inhibition properties against C. albicans and MRSA, yet weak inhibition properties against P. aeruginosa. Additionally, FGE showed the potential to improve the effect of antibiotics on antibiotic resistant pathogens. The synergism of fluconazole and itraconazole with FGE on C. albicans yielded larger sized inhibition zones compared with fluconazole and itraconazole without FGE (P < 0.01). The factorial analysis represents intense positive interaction effects (P < 0.01). The synergism of cefotaxime and ceftriaxone with FGE on P. aeruginosa yielded larger sized inhibition zones than cefotaxime and ceftriaxone without FGE (P < 0.01). The factorial analysis represents intense positive interaction effects (P < 0.01).Conclusions:The results suggest that FGE can improve the antibiotic sensitivity of these pathogens to some antibiotics.

Atrial fibrillation (AF) is the most common cardiac arrhythmia whose incidence is on the rise globally. However, the pathophysiologic mechanism of AF remains poorly understood and there has been a lack of circulatory markers to diagnose and predict prognosis of AF. In the present study, by measuring metabolic profile and analyzing plasma amino acid levels in AF patients, we sought to determine whether amino acid metabolism was correlated to the occurrence of AF. Consecutive patients admitted to hospital for AF were enrolled. Plasma samples were obtained after overnight fast and a profile of 61 amino acids was then measured using gas chromatography/mass spectrometry (GC/MS). Twenty-three AF and thirty-seven control patients were enrolled in the study. A number of plasma amino acids were altered in AF, which showed significant prediction value for AF. Intriguingly, circulating 4-hydroxypyrrolidine-2-carboxylic was gradually lowered with the persistence of AF. Plasma amino acid levels were more strongly correlated with each other in AF as compared with control. By utilizing non-target metabolic profile surveys, we have found a number of altered amino acids, which exhibit diagnostic value for AF. Enhanced amino acids correlation network further identified AF as a metabolism disorder.

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.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in chronic kidney disease (CKD) patients. QT interval prolongation is a congenital or acquired condition that is associated with an increased risk of torsade de pointes (TdP), sudden cardiac death (SCD), and all-cause mortality in the general population. The prevalence of acquired long QT syndrome (aLQTS) is high, and various acquired conditions contribute to the prolonged QT interval in patients with CKD. More notably, the prolonged QT interval in CKD is an independent risk factor for SCD and all-cause mortality. In this review, we focus on the epidemiological characteristics, risk factors, underlying mechanisms and treatments of aLQTS in CKD, promoting the management of aLQTS in CKD patients.