Objective To investigate the effect of positive acceleration (+Gz) on monophasic action potential duration of 90%repolarization( MAPD90 ) and transmural dispersion of repolarization ( TDR) in ventricles of rabbits and to explore the cellular electrophysiologic mechanism of tachyarrhythmia induced by positive acceleration .Methods Twenty-four healthy, male New Zealand white rabbits were randomly and equally divided into control group and +Gz group.The +Gz group rabbits were given +8 Gz exposure, 1 min a time, 3 times a day,and a total of 7 days.The two groups were subjec-ted to Holter monitoring at the same time to observe the incidence of tachyarrhythmia .Using the monophasic action potential ( MAP) recording technology , the MAP of the left ventricle was recorded while MAPD 90 and TDR were measured .By using Burst stimulation method , the right ventricular anterior wall of the rabbits was stimulated , and the incidence of tachya-rrhythmia was observed .Results The Holter record showed that the incidence of tachyarrhythmias in +Gz group was 55%(6/11), but the control group did not have any case of tachyarrhythmias .Compared with the control group ,MAPD90 of en-docardial and epicardial cells was significantly decreased in the +Gz group, while MAPD90 of middle myocardial cells did not change significantly ,but TDR was increased obviously .Four rabbits in +Gz group suffered from tachyarrhythmias dur-ing Burst stimulation ,and the incidence of tachyarrhythmias was 40% ( 4/10 ) .Conclusion +Gz exposure can increase the incidence of tachyarrhythmias .The shortened MAPD90 of ventricular muscle cells and the increased TDR may be the cell electrophysiological mechanisms of tachyarrhythmias induced by +Gz.

BACKGROUNDOne of mechanisms of carcinogenesis is suppression of cell apoptosis which leads to accumulation of aberrant cells. The aim of this study is to investigate cell apoptosis and COX-2 protein expression in non-small cell lung cancer (NSCLC).

METHODSCell apoptosis, expression of COX-2 and microvessel density (MVD) were detcted in 111 NSCLC samples by TdT-mediated dUTP nick end labeling (TUNEL) technique and immunohistochemical staining.

RESULTSThe positive rate of COX-2 protein expression was 67.6% (75/111), and there were 53 patients with high level cell apoptosis (47.7%). Expression of COX-2 protien was significantly related to TNM stages (P=0.025) and lymph node metastasis (P=0.018). The MVD in NSCLC tissues with positive COX-2 expression was significantly higher than that in negative expression ones (P=0.000). COX model showed that lymph node metastasis (P=0.006) and positive expression of COX-2 protein (P=0.000) were independent prognostic factors of NSCLC.

CONCLUSIONSThe expression of COX-2 protein may suppress cell apoptosis of tumor, and it may serve as a potential marker of prognosis for NSCLC.

In vitro studies have established the prevalent theory that the mitochondrial kinase PINK1 protects neurodegeneration by removing damaged mitochondria in Parkinson's disease (PD). However, difficulty in detecting endogenous PINK1 protein in rodent brains and cell lines has prevented the rigorous investigation of the in vivo role of PINK1. Here we report that PINK1 kinase form is selectively expressed in the human and monkey brains. CRISPR/Cas9-mediated deficiency of PINK1 causes similar neurodegeneration in the brains of fetal and adult monkeys as well as cultured monkey neurons without affecting mitochondrial protein expression and morphology. Importantly, PINK1 mutations in the primate brain and human cells reduce protein phosphorylation that is important for neuronal function and survival. Our findings suggest that PINK1 kinase activity rather than its mitochondrial function is essential for the neuronal survival in the primate brains and that its kinase dysfunction could be involved in the pathogenesis of PD.