1.Effect of different doses of perindopril on myocardial energy expenditure in patients with heart failure following myocardial infarction.
Jianqiu LIANG ; Shuchang BAI ; Dingli XU ; Zhou CHENG
Journal of Southern Medical University 2012;32(12):1816-1832
OBJECTIVETo investigate the changes of myocardial energy expenditure in patients with heart failure following myocardial infarction after treatment with different doses of perindopril.
METHODSSixty-three patients with heart failure after myocardial infarction were treated with perindopril for 12 months at the doses of 4 mg (group N) and 8 mg (group H). Doppler imaging was used to measure the structural and systolic functional parameters before and after the treatment, and the circumferential end-systolic wall stress (cESS) and myocardial energy expenditure (MEE) were calculated. The biochemical indicators including serum creatinine and plasma NT-proBNP were detected before and after the treatment.
RESULTSThe two groups had similar measurements before treatment. After 12 months of perindopril treatment, the patients in group N showed higher LA, LV, RA, RV, LVIDs, AD, cESS, lgNT-proBNP, and MEE with lower LVFS and LVEF than those in group H. Compared to those before treatment, LVFS and LVEF were increased and LA, LV, RA, RV, AD, LVIDs, LVMI, lgNT-proBNP and MEEm lowered after the 12-month treatment in group H. Significant changes were also found in the measured parameters except for PWTs, LVET, LVSV and LVFS in group N after the treatment. Bivariate analysis showed a significant positive correlation between MEE and lgNT-proBNP (r=0.513, P<0.01).
CONCLUSIONA 12-month treatment with perindopril can suppress myocardial remodeling, improve left ventricular systolic function, and lower NT-proBNP and myocardial energy expenditure in patients with heart failure after myocardial infarction, and a higher dose can produce better results.
Aged ; Energy Metabolism ; Female ; Heart Failure ; drug therapy ; etiology ; metabolism ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; complications ; drug therapy ; Myocardium ; metabolism ; Perindopril ; administration & dosage ; therapeutic use ; Treatment Outcome ; Ventricular Function, Left ; Ventricular Remodeling
2.Changes of exercise and the clinical effects among eldly non-small cell lung cancer survivors.
Hongyan YING ; Yuzhou WANG ; Xiaohong NING ; Jianfeng ZHOU ; Lin ZHAO ; Yajuan SHAO ; Chunmei BAI ; Shuchang CHEN
Chinese Journal of Lung Cancer 2010;13(1):64-68
BACKGROUND AND OBJECTIVEExercise can improve circulation, muscular strength and happiness of cancer survivors. But more data were needed to demonstrate both the exercise ability of cancer suivivors after pulmonary lobectomy and the influences of exercise on their survivals. The aim of this study was to examine changes of exercise and its clinical effects among eldly non-small cell lung cancer survivors.
METHODSElderly non-small cell lung cancer survivors who had progression-free disease after surgery, chemotherapy, radiation therapy or tyrosine kinase inhibitors were included. Their exercises and participation rates per week before cancer diagnosis, after 3 months anticancer therapy and 1 year after diagnosis as well as their exercise motivations and prevalences were investigated retrospectively.
RESULTSForty-eight elderly non-small cell lung cancer survivors were selected. Moderate-vigorous intensity exercise had by the elderly progressin-free non-small cell lung cancer survivors after diagnosis decreased, but the participation rate of light intensity exercise was higher in 1 year after diagnosis than before diagnosis. 75.9% (14/58) patients had exercise up to the standard and the cancer recurrence rate was 20.0% (7/35). The recurrence rate of the other group was 35.7% (5/14), and the risk ratio of recurrence was 2.14 (95% CI: 0.81-5.68, P = 0.26). The most common motivations of exercise were improving health, increasing physical activity, maintaining healthy life style and improving immunity. And the main disturbances were fatigue, discomfort and lack of motivation.
CONCLUSIONThe exercise participation rate during anticancer treatment among the elderly non-small cell lung cancer survivors decreased and did not return to prediagnosis levels after treatments were completed. The relationship between exercise and recurrence of cancer was not clear and needed further work.
Aged ; Aged, 80 and over ; Carcinoma, Non-Small-Cell Lung ; pathology ; Female ; Humans ; Male ; Motor Activity ; physiology ; Retrospective Studies ; Survivors ; statistics & numerical data
3.Construction and identification of conditional islet βcell DEPTOR knockout mice
Shuchang LAI ; Hong QIU ; Xiao WANG ; Daoyan PAN ; Zhenyu WANG ; Kai LI ; Xiaochun BAI ; Jie SHEN
The Journal of Practical Medicine 2018;34(4):552-555
Objective To study the function of Deptor gene on the regulation of diabetes mellitus in suc-cessfully constructed and identified islet β-cell conditionally DEPTOR knockout mice model. Method By cross-breeding Deptorflox/floxmice with Cre mice expressed conditional specifically in pancreatic β-cell,Deptorflox/+Cre+/-mice were acquired and their genotypic identification was then performed. As the mice model of this study, Deptorflox/floxCre+/-mice were generated by crossing Deptorflox/+Cre+/-mice with Deptorflox/floxmice.Genotypic identifica-tion was performed by PCR at the age of 3 weeks. Tamoxifen was administered through intraperitoneal injection to induce the activation of the Cre recombination in islet beta cells of 8 weeks mice.Double immunofluorescence label-ing was then applied to identify the knockout effect of DEPTOR gene. Results Ten Islets Deptor knockout mice models were successfully acquired after 10-month cross-breeding. Validated genotype by PCR analysis were Deptorflox/floxCre+/- and double immunofluorescence labeling showed a significant difference between knockout mice and rodent controls. Conclusion Our study successfully constructs the islets conditionally Deptor deleted mice model by using Cre-loxp recombination system,providing a promising appliable animal model for study of dia-betes mellitus pathogenetic mechanism.