Objective To explore the clinical significance of sinus heart rate turbulence (HRT)and heart rate variability (HRV) in patients with chronic obstructive pulmonary disease(COPD).Methods The 59 moderate to severe COPD patients and 30 healthy subjects were enrolled in this study. The 24-hour holter monitor was used to screen the HRT onset (TO), turbulence slope (TS)and HRV. Pulmonary function tests and echocardiographic examination were performed for measuring left ventricular ejection fraction (LVEF), right atrial dimension (RAD), right ventricular dimension (RVD), right ventricular wall thickness (RVWT). Then all the parameters were compared between NC group and COPD group, and the relationship between HRT and HRV was investigated. Results Compared with control group, TO was significantly increased [(-0.2±1.1) % vs.(-3.8±2.8) %, t=6. 830,P＜0.01] and TS was decreased [(7.0±3.6) ms/RR vs. (11.7±6.1) ms/RR, t =3. 866, P＜0.01] in COPD group. In time domain HRV parameters, normal RR intervallerinin standart deviation(SDNN), standard deviation of normal-to-normal beats index (SDNNi), standard deviation of the averages of normal sinus to normal sinus (SDANN), mean squared differences of the successive RR intervals (rMSDD), fraction of consecutive normal sinus intervals that differ by more than 50 ms (PNN50) were significantly lower in COPD group than in control group(P＜0. 05). TO was negatively correlated with SDANN and rMSDD (r=-0. 369, P＜0. 05; r=-0.472, P＜0.01).TS was positively correlated with SDNN, SDANN and PNN50 (all P＜0.05), but had no correlation with rMSDD (P＞0. 05). Conclusions HRT and HRV are dramatically blunted in COPD patients.Combination of HRV and prognosis. and HRT may be simple and elegant ways for evaluating cardiac autonomic functions.

AIM: To establish an animal model of experimental autoimmune myocarditis (EAM) in BALB/c mice and to investigate the expression and significance of Toll-like receptor 3 in mouse EAM. METHODS: BALB/c mice were immunized with cardiac myosin extracted from porcine ventricular myocardium covered by complete freund's adjuvant (CFA) on 0 d and 7 d, then divided into immunized with CFA only. Serum and myocardium samples were collected at 14 d and 21 d after the first immunization. HE staining was used to identify the areas of inflammation. The myosin IgG antibody was examined by indirect ELISA assay. The changes of TLR3 protein and mRNA expression in myocardial tissue were measured by immunohistochemistry and real time-PCR. RESULTS: Compared to control group, immunohistochemistry results showed that there was positive expression of TLR3 in the myocardium of mice with EAM and the mRNA of TLR3 were more than 20 times (P<0.05). The expression of interferon beta mRNA in EAM group was more than 14 times as many as basal expression, that of tumor necrosis factor alpha was more than 18 times (P<0.05). CONCLUSION: The expression of Toll-like receptor 3 in myocardium is up-regulated in experimental autoimmune myocarditis. The inflammatory response to cardiac myosin may associate with the TLR3 signal transduction pathway.

Objective To investigate the effect of YTH domain family protein 2(YTHDF2)on an-giotensin Ⅱ(Ang Ⅱ)-induced hypertrophy and apoptosis of primary neonatal rat cardiomyocytes.Methods The expression level of YTHDF2 was detected in the primary neonatal rat cardiomyo-cytes with or without Ang Ⅱ stimulation(AngⅡ group and normal group).The cells were divid-ed into blank group(transfected with siRNA+PBS),siYTHDF2 group(transfected with siYTHDF2+PBS),model group(siRNA+Ang Ⅱ)and experimental group(siYTHDF2+Ang Ⅱ)to investi-gate the effects of silencing YTHDF2 on the hypertrophy and apoptosis of cardiomyocytes.West-ern blotting and RT-qPCR were used to detect the expression of YTHDF2 at protein and mRNA levels,and RT-qPCR was employed to measure the mRNA levels of myocardial hypertrophic related genes atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP)and beta-myosin heavy chain(β-MHC),and cardiomyocyte apoptosis related genes Bax and B lymphocytoma 2 gene(Bcl-2).The surface area of cardiomyocytes was observed by α-actin immunofluorescence staining.Cardiomyocyte apoptosis was observed by TUNEL staining,and the binding relationship between YTHDF2 and Bcl-2 was verified by immunoprecipitation.Results The expression of YTHDF2 at protein and mRNA levels were significantly higher in the AngⅡ group than the nor-mal group(1.49±0.03 vs 0.97±0.09,1.50±0.08 vs 1.00±0.07,P＜0.05).Compared with the blank group,the surface area of cardiomyocytes was notably enlarged,apoptotic rate was obvi-ously increased,the mRNA levels of ANP,BNP,β-MHC and Bax were significantly increased,and that of Bcl-2 was remarkably decreased in the model group(P＜0.05).The experimental group obtained decreased surface area and apoptotic rate of cardiomyocytes,lower mRNA levels of ANP,BNP,β-MHC and Bax,and increased mRNA expression of Bcl-2(P＜0.05).Conclusion Silencing YTHDF2 can alleviate Ang Ⅱ-induced hypertrophy and apoptosis in primary neonatal rat cardiomyocyte,and YTHDF2 inhibits the expression of Bcl-2 by binding to it.