Objective To analyze the changes of heart rate turbulence (HRT) and heart rate variability (HRV) in coronary heart disease (CHD), and evaluate the relationship between CHD and coronary artery disease (CAD) and two parameters of HRT and HRV, and investigate the correlation between the 2 parameters.Methods We performed coronary angiography in all 103 patients with CHD (group A), who were classified into 3 subgroups: 35 patients of stable angina pectoris ( group A1 ), 28 patients of unstable angina pectoris ( group A2 ) and 40 patients of AMI ( group A3 ), and 30 structurally normal patients with ventricular premature contraction who were included in healthy control group ( group B).The 24-hour ambulatory electrocardiogram was performed in all the patients, and the parameters of HRT and HRV were obtained.Results The value of the TO onset of group A was significantly higher than that of group B( -4.17± 2.75, - 3.16 ± 3.18, - 0.96 ± 2.92; - 6.30 ± 3.47 ), the value of TS of group A was lower than that of groupB(6.81±3.18,5.12±3.31,3.20±1.71;9.52±3.85) (P ＜0.05 orP ＜0.01).The values of SDNN, PNN50, and HF of group A were significantly lower than those of group B (P＜ 0.05).TO was positively correlated with Gensinies score, while TS, SDNN, PNN50 and HF were negatively correlated with Gensinies score, and TS showed the strongest negative correlation with Gensini score (r=-0.45).TO was negatively correlated with SDNN, PNN50, and HF, while TS was positively correlated with SDNN, PNN50 and HF, and TS showed much stronger correlation with HF (r=0.47).Conclusions HRT was dramatically blunted and HRV in patients with CHD was significantly lower;.HRT and HRV of group A1 were significantly correlated with Gensini score, and TS had the strongest correlation with Gensini score.TO and TS were correlated with SDNN, PNN50 and HF, and TS had much stronger relationship with HF.

Objective To analyze the apoptosis mechanisms of K562 cells in a PI3K-AKT-dependent manner.Methods K562 cells were cultured in vitro for experiments below:the proliferation assay of K562 cells detected by MTT,the analysis of apoptosis rate and cell cycle of K562 cells measured by flow cytometry(FCM),the construction of chronic myeloid leukemia(CML) animal model through the subcutaneous inoculation of K562 cells to 12 BALB/c-nu/nu nude mice,the early apoptosis changes of K562 cells detected by TdT-mediated dUTP nick end labeling(TUNEL) and the in vitro and in vivo changes of N-ras,PI3K,AKT1,IKK-?,NF-?B1 at transcription level detected by RT-PCR.Results Simvastatin inhibited the proliferation of K562 cells and induced their G0/G1 arrest and significant apoptosis.N-ras and most genes of PI3K-AKT signal pathway were expressed differentially in vitro.K562 cells on nude mice could be induced to apoptosis by simvastatin and the apoptotic index increased with the dose accumulation of simvastatin(P=0.000).The differential mRNA expression changes of N-Ras and most genes of PI3K-AKT signal pathway in K562 cells were observed after treatment of simvastatin at different doses(P=0.000 or P=0.003).However,mRNA expres-sion of the genes in PI3K-AKT pathway in vitro differed to that in vivo.Conclusion The differential expression at transcription levels of N-ras and the most genes in PI3K-AKT pathway that are involved in anti-apoptosis in K562 cells,to some degree,indicates that simvastatin can induce the apoptosis of K562 cells in a PI3K-AKT pathway-dependent fashion in vitro.The animal experiments confirm that there are different mechanisms of simvastatin in inducing the apoptosis of K562 cells in vitro and in vivo.