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1.
Chinese Medical Journal ; (24): 1794-1801, 2006.
Article in English | WPRIM | ID: wpr-335528

ABSTRACT

<p><b>BACKGROUND</b>Estrogen might play an important role in type 2 diabetes mellitus pathogenesis. A number of polymorphisms have been reported in the estrogen receptor alpha (ERalpha) gene (also named ESR1), including the XbaI and PvuII restriction enzyme polymorphisms of ESR1, which may be involved in disease pathogenesis. The aim of this study was to determine whether ERX gene polymorphisms are associated with type 2 diabetes mellitus and serum lipid level.</p><p><b>METHODS</b>Two hundred and ninety-nine patients with type 2 diabetes mellitus were compared with three hundred and forty-one health controls of Guangzhou in China, both were male and postmenopausal female residents at 51 - 70 years. ESR1 genotyping was performed using polymerase chain reaction (PCR) and PvuII and XbaI restriction fragment length polymorphism (PCR-RFLP) analysis.</p><p><b>RESULTS</b>ESR1 allelic frequencies of P, p and X, x alleles were 0.408, 0.592; 0.360, 0.640 in the type 2 diabetes mellitus group and 0.318, 0.682; 0.328, 0.672 in the control group, respectively. In case-control study, there was significant difference in PvuII, but not XbaI, allele frequency between the type 2 diabetes mellitus and control groups (P = 0.001 and P = 0.122). When the group was separated into men and women, the difference was significant in women (P < 0.001) but not in men (P = 0.854) with the PvuII genotype, and the effect of PvuII variant on the development of type 2 diabetes mellitus was improved with aging. In addition, PvuII genotype was associated with blood glucose [fasting blood glucose (FBG), postprandial blood glucose (PBG)] and serum lipid [total cholesterol (TC) and low density lipoprotein (LDL)-c] concentration in healthy women.</p><p><b>CONCLUSIONS</b>PvuII polymorphism of ESR1 increases susceptibility to type 2 diabetes mellitus in Chinese Guangzhou women. ESR1 variants may also impact serum lipid metabolism, which might provide a mechanism connecting ESR1 to type 2 diabetes.</p>


Subject(s)
Aged , Female , Humans , Middle Aged , Blood Glucose , Cholesterol, LDL , Blood , Diabetes Mellitus, Type 2 , Blood , Genetics , Estrogen Receptor alpha , Genetics , Genotype , Lipids , Blood , Logistic Models , Polymorphism, Genetic
2.
Chinese Journal of Medical Education Research ; (12)2006.
Article in Chinese | WPRIM | ID: wpr-686791

ABSTRACT

Virtual experiment is the application of virtual reality technology in experiment sciences.In the physiology teaching, virtual reality modules are made up of experiment theory module,experiment process module,virtual reality module,review mod- ule and experiment report module.We set up a virtual physiology experiment system by author ware and other software.

3.
Acta Physiologica Sinica ; (6): 379-383, 2004.
Article in Chinese | WPRIM | ID: wpr-352764

ABSTRACT

The aim of the present study was to investigate the role of caveolin-1 in the inhibition of endothelin-1 induced proliferation of vascular smooth muscle cells (VSMCs) by 17beta-estradiol. In the cultured rat thoracic aortic VSMCs, proliferation of VSMCs was determined by using [(3)H]-thymidine incorporation and the expression of caveolin-1 protein was measured by immunofluorescence assays and Western blotting. The measurement demonstate VSMCs exposed to various concentrations of endothelin-1 (1-100 nmol/L) for 24 h induced an increase in [(3)H]-thymidine incorporation. Pretreament with various concentrations of 17beta-estradiol (0.1-10 nmol/L) for 24 h inhibited the proliferation effect of endothelin-1. Immunofluorescence assays showed that after 24 h treatment of VSMCs with endothelin-1 (100 nmol/L), the expression of caveolin-1 in VSMCs was significantly increased, whereas pretreament with 17beta-estradiol (10 nmol/L) for 24 h inhibited the effect. Western blotting results further proved that endothelin-1 inhibited and 17beta-estradiol increased the expression of caveolin-1 in VSMCs. These results demonstrate that 17beta-estradiol inhibits the VSMCs proliferation induced by endothelin-1, and that the effect of estradiol is probably mediated by caveolin-1.


Subject(s)
Animals , Rats , Aorta, Thoracic , Cell Biology , Caveolin 1 , Physiology , Cell Division , Cells, Cultured , Endothelin-1 , Physiology , Estradiol , Pharmacology , Muscle, Smooth, Vascular , Cell Biology , Rats, Sprague-Dawley
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