Intracardiac echocardiography Chinese expert consensus.

In recent years, percutaneous catheter interventions have continuously evolved, becoming an essential strategy for interventional diagnosis and treatment of many structural heart diseases and arrhythmias. Along with the increasing complexity of cardiac interventions comes ever more complex demands for intraoperative imaging. Intracardiac echocardiography (ICE) is well-suited for these requirements with real-time imaging, real-time monitoring for intraoperative complications, and a well-tolerated procedure. As a result, ICE is increasingly used many types of cardiac interventions. Given the lack of relevant guidelines at home and abroad and to promote and standardize the clinical applications of ICE, the members of this panel extensively evaluated relevant research findings, and they developed this consensus document after discussions and correlation with front-line clinical work experience, aiming to provide guidance for clinicians and to further improve interventional cardiovascular diagnosis and treatment procedures.

Oxidative stress and mitogen-activated protein kinase pathways involved in cadmium-induced BRL 3A cell apoptosis.

In this study, BRL 3A cells were treated with different Cd concentrations (0, 10, 20, and 40 µmol/L) for 12 h and preincubated with or without N-acetyl-L-cysteine (NAC) (2 mmol/L) for 30 min, and cells were treated with Cd (0 and 20 µmol/L), pretreated with p38 inhibitor (SB203580), JNK (c-Jun NH2-terminal kinases) inhibitor (SP600125), and extracellular signal-regulated kinase (ERK) inhibitor (U0126) for 30 min, and then treated with 20 µmol/L Cd for 12 h. Cd decreased cell viability, SOD, and GSH-Px activity in a concentration-dependent manner. Increased MDA level, ROS generation, nuclear condensation, shrinkage, and fragmentation in cell morphology were inhibited by NAC. Cd-induced apoptosis was attenuated by pretreatment with SB203580, SP600125, and U0126. The results of western blot showed that NAC preincubation affected Cd-activated MAPK pathways, p38 and ERK phosphorylation. Cd treatment elevated the mRNA levels of Bax and decreased the mRNA levels of Bcl-2, respectively. The same effect was found in their protein expression levels. These results suggest that oxidative stress and MAPK pathways participate in Cd-induced apoptosis and that the balance between pro- and antiapoptotic genes (Bax and Bcl-2) is important in Cd-induced apoptosis.