1.The role of social capital in three levels prevention of stroke
Chinese Journal of Behavioral Medicine and Brain Science 2017;26(6):573-576
Social capital is an invisible capital form that promotes the efficient allocation and utilization of resources.It plays an active role in the prevention and control of chronic diseases.The purpose of this study is to investigate the effect of social capital on the three levels prevention of stroke by means of document retrieval.Social capital is associated with both morbidity and mortality of stroke.Social participation and social support at a high level can promote the rehabilitation of stroke patients,and have a beneficial effect on improving the quality of life and the ability of daily life.Social capital is correlated with stroke related behavioral factors,such as smoking,drinking,obesity,diet and physical activity.People with high social capital stock are more likely to choose healthy behavior patterns,thus reducing the risk of stroke.We should take full account of the social capital factors,and make more comprehensive and effective completion of the three levels of stroke prevention.
4.Curative effects of salmetorel xinafoate and fluticasone propionate powder inhalation on 140 children with asth- ma
zhi-jian, YANG ; yang-jing, ZHENG ; mei-yu, SU ; qiang-zhi, ZHUO
Journal of Applied Clinical Pediatrics 2004;0(12):-
Objective To observe the effects of asthmatic children treated by inhaled salmeterol xinafoate and fluticasone propi-onate powder. Methods One hundred and fourty cases of moderate and severe asthmatic children were treated in non- acute period aged from 4 to 14 years by inhaling salmeterol xinafoate and fluticasone propionate powder, compared with control group treated by flu-ticasone propionate in 106 cases, and the pulmonary function was monitored simultaneously. Results The total effective rate of the treatment group and control group were 99. 3 % , 99. 1 % , respectively.The pulmonary function indexes such as the first one second expiration volume(FEV1), flow velocity of 50 % expiration vital capacity(FEF50%), peak expiration velocity(PEF1) after being treated 4 months was improved significantly compared with those before treatment.The difference between them was statistically significant (P
5.Expression and Role of Brain-derived Neurotrophic Factor in Intestinal Tract
Shujuan JING ; Shiwei YANG ; Zhi LI ; Junning LIU
Chinese Journal of Gastroenterology 2014;(5):312-314
Brain-derived neurotrophic factor (BDNF)is both a neurotrophic substance and a neurotransmitter.BDNF and its receptors are highly expressed in enteric nervous system,intestinal mucosal epithelium and intestinal muscularis, which play an important role in regulating intestinal sensitivity and motility.This article reviewed the expression and role of BDNF in intestinal tract.
6.Effects of astragaloside on proliferation and apoptosis of keloid fibroblasts
Yu FU ; Liang ZHANG ; Na CHEN ; Zhi YAN ; Jing YANG
Chongqing Medicine 2017;46(6):746-748
Objective To study the effect of astragaloside on proliferation and apoptosis in human keloid fibroblasts.Methods The human keloid fibroblast ceils were treated with different concentration of astragaloside(10、20、40 ng/mL).Cell proliferation was detected by MTT,the gene expreesion levels and protein levels of apoptosis-related proteins,survivin,p53 and Bcl-2.were determined by real-time PCR and Western blot,respectively.Results Comparecl with control group(treated with 0 ng/mL astragaloside),the absorbance values (A490 nm) of each concentration group were significantly reduced,which suggest that the proliferation of all keloid fibroblast were markably inhibited in a dose-dependent way (P<0.05).The gene expreesion levels and protein levels of apoptosis-related proteins,survivin、Bcl-2 were largely suppressed and P53 werelargely promoted in a dose-dependent.Conclusion The keloid fibroblasts cells proliferation and apoptosis could be regulated by astragaloside.
7.Effect of leptin on proliferation and apoptosis of human breast cancer cell MCF-7
Yang ZHI ; Lili DU ; Jiexian JING ; Xianwen ZHAO ; Cunzhi HAN
Cancer Research and Clinic 2012;24(3):161-164
Objective To observe the effect of leptin on proliferation and apoptosis of breast cancer MCF-7 cell line,and to explore the effect of leptin on occurrence and development of breast cancer.Method The MCF-7 cell line was treated with different concentration of leptin in vitro.Cell proliferation was evaluated by MTT assay. Distribution of cell cycle was determined by flow cytomery, meanwhile the rates of apoptosis were estimated on the basis of Annexin V-FITC/PI apoptosis detection. Results When treated with different concentration of leptin for 24 h, 48 h and 72 h, they could significantly induce the proliferation of MCF-7 cells by MTT method.There was not interaction between concentration of leptin and time course (F=0.919,P=0.523).The main effect of concentration of leptin and time course was statistically significant (F=12.699,P=0.000;F=647.881, P=0.000). Compared 200 ng/ml and 400 ng/ml with the control group, we found the difference was statistically significant by multiple comparison (P=0.007,P=0.000,respectively).The difference was also statistically significant among time course by multiple comparison (P=0.000,respectively).By the flow cytometry analysis,it was found that the 100 ng/ml and 400 ng/ml leptin groups could change the distribution of cell cycle of MCF-7 cell line after 48 h. Compared with control group, the cell number decreased by 14.42 % in G0/G1 phase (F=10.464, P=0.044),but increased by 7.57 % and 22.19 % respectively in S phase (F=47.361,P=0.005).The difference was not statistically significant in G2/M phase (F=1.77, P=0.311).However, the effect of apoptosis inhibition was not obvious. Conclusions Leptin could stimulate the proliferation of MCF-7 cell line and change the distribution of cell cycle.But leptin could not inhibit apoptosis of MCF-7 cell line.It suggested that leptin may serve as a risk factor of breast cancer development.
8.Effect of different sex and gonadal function on soman-induced hypothermia in rats.
Yong-Lu YANG ; Zhi-Min JING ; Yu-Shan LI
Chinese Journal of Applied Physiology 2006;22(2):157-158
Animals
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Female
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Gonads
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physiopathology
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Hypothermia
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chemically induced
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physiopathology
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Male
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Rats
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Rats, Wistar
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Sex Factors
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Soman
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adverse effects
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pharmacology
9.Effect of human placental extracton the lipoprotein-cholesterol metabolism
Wen-Ji CUI ; Jing-Wen YANG ; Zhong-Zhi LV ;
Chinese Journal of Clinical Pharmacology and Therapeutics 2000;0(02):-
Aim The effect and mechanism of human placental extract(HPE) on the lipoprotein-cholesterol metabolism, peroxidation and the function of platelet aggregation in hyperlipaemia rats were abserved.Methods Wistar rat with hyperlipaemia models were given each HPE 0.4 ml (100 g)-1?d-1 through lavage for 12 days.The serum levels of TG,TC,LDL-C,HDL-C and HDL2-C in its subgroup were measured.The activies of LPO and SOD in both blood and liver tissue were determined .The effect of HPE on lipidosis of liver were abserved by fat dyeing.The levels of 6-keto-PGF1?,TXB2 in plasma and maximum platelet aggregation rate were measured by ELASA. Result The levels of HDL-C and HDL2-C were increased (P
10.Expression and Function Analysis of Cholinergic Components nAChRα7 in Preadipocytes
Jing WU ; Huiling LU ; Xiufen HU ; Xiaoyan LIANG ; Hanhua LIN ; Hongwei WANG ; Yang YANG ; Zhi XIA
Chinese Journal of Biochemistry and Molecular Biology 2008;24(9):803-809
The non-neuronal cholinergic system, widely exists in prokaryotic, eukarytic, and even plant cells, however, it has not been investigated in preadipocytes and adipocytes. To search for evidence its existence in preadipocytes and adipocytes, the nicotinic acetylcholine receptor (nAChR) α7 subunit, acetyicholinesterase (ACHE) and choline acetyltransferase (CHAT) in 3T3-L1 cells were examined using immunohistochemical staining and Western blotting. The choline-regulated visfatin expression in 3T3-L1 preadipocytes was also tested by reverse transcriptase-PCR. Incubation with methyilycaconitine (10-6 to 10-4mol/L) for 12, 24 and 36 hours dose-dependently increased visfatin expression from 1.3- to 1.55-folds (P <0.01) with maximal induction at 24 hours with 10-4mol/L methyllycaconitine. Nicotine treatments (10-6 to 10-4 mol/L) for 12, 24 and 36 hours decreased visfatin expression; choline chloride (10-4 mol/L))suppressed visfatin expression in 3T3-L1 preadipocytes at 36 hours by 1.64 to 2.03 fold (P < 0.05) which was more effective as compared with nicotine. It was concluded that α7 nAChR was expressed in 3T3-L1 preadipocytes and involved in visfatin expression.