a-simple-efficient-method-for-vivo-cardiac-specific-gene-manipulation

A Simple and Efficient Method for <em>In Vivo</em> Cardiac-specific Gene Manipulation by Intramyocardial Injection in Mice

Gene manipulation specifically in the heart significantly potentiate the investigation of cardiac disease pathomechanisms and their therapeutic potential. ...

The First Affiliated Hospital of Bengbu Medical College

To explore the clinical effect of internal fixation treatment of intra-articular calcaneal fractures with titanium plate, we used open reduction and internal fixation with titanium plate to 48 treated feet from 42 patients with intra-articular calcaneal fractures. The efficacy of surgical treatment was evaluated based on assessment of pain, function, and line of force aspects according to the American Orthopedic Foot and Ankle Society scoring system. Our data show that internal fixation with titanium plate is an effective treatment for calcaneal fractures. It provides satisfactory reduction, reliable fixation, and early rehabilitation. 

Clinical Analysis of Internal Fixation Treatment of Intra-articular Calcaneal Fractures with Titanium Plate.

The aim of this paper is to observe the change of mitochondrial aldehyde dehydrogenase 2 (ALDH2) when diabetes mellitus (DM) rat heart was subjected to ischemia/reperfusion (I/R) intervention and analyze its underlying mechanisms. DM rat hearts were subjected to 30 min regional ischemia and 120 min reperfusion in vitro and pretreated with ALDH2 activator ethanol (EtOH); cardiomyocyte in high glucose (HG) condition was pretreated with ALDH2 activator Alda-1. In control I/R group, myocardial tissue structure collapse appeared. Compared with control I/R group, left ventricular parameters, SOD activity, the level of Bcl-2/Bax mRNA, ALDH2 mRNA, and protein expressions were decreased and LDH and MDA contents were increased, meanwhile the aggravation of myocardial structure injury in DM I/R group. When DM I/R rats were pretreated with EtOH, left ventricular parameters, SOD, Bcl-2/Bax, and ALDH2 expression were increased; LDH, MDA, and myocardial structure injury were attenuated. Compared with DM + EtOH I/R group, cyanamide (ALDH2 nonspecific blocker), atractyloside (mitoPTP opener), and wortmannin (PI3K inhibitor) groups all decreased left ventricular parameters, SOD, Bcl-2/Bax, and ALDH2 and increased LDH, MDA, and myocardial injury. When cardiomyocyte was under HG condition, CCK-8 activity and ALDH2 protein expression were decreased. Alda-1 increased CCK-8 and ALDH2. Our findings suggested enhanced ALDH2 expression in diabetic I/R rats played the cardioprotective role, maybe through activating PI3K and inhibiting mitoPTP opening.

Activation of ALDH2 with Low Concentration of Ethanol Attenuates Myocardial Ischemia/Reperfusion Injury in Diabetes Rat Model.

MicroRNA (miR)‑138 serves an important role in the proliferation, differentiation and apoptosis of human pulmonary artery smooth muscle cells (HPASMCs), indi-cating the involvement of miR‑138 in the development and progression of pulmonary artery hypertension (PAH). Potassium channel subfamily K member 3 (TASK‑1), a two‑pore domain K+ channel, is expressed in HPASMCs and is associated with hypoxic PAH. However, whether miR‑138 mediates PAH through targeting TASK‑1 is not known. In the present study, HPASMCs were transfected with miR‑138 mimic to establish a PAH model in vitro, and the effects of a miR‑138 inhibitor and a TASK‑1 inhibitor (A293) were examined. Cell proliferation and mitochondrial membrane potential (MMP) were measured by CCK‑8 assay and flow cytometry, respectively. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to examine the expression of miR‑138, TASK‑1, Bcl‑2, caspase‑3 and activation of extracellular signal‑regulated kinase 1/2 (ERK1/2). A dual‑luciferase reporter assay was also used to analyse the expression level of TASK‑1 in HPASMCs. The results of the present study demonstrated that the miR‑138 mimic promoted proliferation and MMP level, which was similar to the effect of A293 treatment on HPASMCs. However, the miR‑138 inhibitor inhibited the effects induced by miR‑138 mimic or A293 treatment, as demonstrated by a decrease in proliferation and MMP level in HPASMCs, accompanied by a decrease of Bcl‑2 and an increase of caspase‑3 expression levels, as well as ERK1/2 activation. The dual‑luciferase reporter assay indicated that TASK‑1 expression was negatively regulated by miR‑138. The results of the present study suggested that miR‑138 promoted proliferation and suppressed mitochondrial depolarization of HPASMCs by targeting TASK‑1.

MicroRNA‑138 promotes proliferation and suppresses mitochondrial depolarization in human pulmonary artery smooth muscle cells through targeting TASK‑1.

Heng Zhang

Department of Cardiology

The First Affiliated Hospital of Bengbu Medical College

A Simple and Efficient Method for In Vivo Cardiac-specific Gene Manipulation by Intramyocardial Injection in Mice

Heng Zhang

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Cardiology

The First Affiliated Hospital of Bengbu Medical College

A Simple and Efficient Method for In Vivo Cardiac-specific Gene Manipulation by Intramyocardial Injection in Mice

Department of Cardiology