1.Allergy--challenge and opportunity.
Chinese Journal of Pediatrics 2009;47(11):801-803
2.Penicillin skin test: status quo.
Chinese Journal of Pediatrics 2003;41(9):712-714
6.The role of eNOS on the regulatory effects of EPO on mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia
Chuan QIN ; Lin CHEN ; Yinbing XIAO
Chongqing Medicine 2015;(16):2167-2169,2173
Objective To explore the role of endothelial nitric oxide synthase(eNOS) in the regulatory effects of erythropoie‐tin (EPO) on mitochondiral biogenesis in cardiomyocytes exposed to chronic hypoxia .Methods H9c2 cardiomyocytes were cultured in the environment of hypoxia for 1 week(94% N2 ,5% O2 ) ,establishing the chronic hypoxic cardiomyocyte model .All the cells were divided into 3 groups :HC(chronic hypoxic control) ,HE[treated with chronic hypoxia and 20 U/mL recombinant human EPO (rhEPO) ]and HR(cells transfected with eNOS shRNA plasmid and treated with 20 U/mL rhEPO and chronic hypoxia) .Fluores‐cent probe was used to detect the changes of mitochondial number .Mitochondial DNA (mtDNA) relative express level was assayed by RT‐PCR .The expression and phosphorylation of eNOS protein were analyzed with Western blot .Results rhEPO significantly increased the phosphorylation of eNOS and elavated the mitochondialt number and mtDNA (P< 0 .05) .shRNA interference on eNOS significantly blocked all the above changes induced by rhEPO (P<0 .05) .Conclusion Phosphory lation of eNOS is the im‐portant signalling pathway for the enhanced mitochondrial biogenesis in cardiomyocytes exposed to chronic hypoxia by EPO .
7.Effect of Anti-Epileplic Drugs on Immunological Function
min, ZHANG ; xiao-chuan, WANG ; yi, WANG
Journal of Applied Clinical Pediatrics 2004;0(09):-
Epilepsy is a common nervous system disease,with a morbidity of 4.8‰-11.2‰,so there has been about 50 million patients globally.Drug treatment is a major mean to treat epileptic patients.Recently,researches illustrated that cellular immunity disorder and humoral immunity disorder were coexist in epleptic patients,but there was no consensus on whether it was induced by anti-epileptic drugs(AEDs) or epilepsy itself up to now.This article is aimed to explain the impact of AEDs on immunity through review recent literature internal and abroad.
8.Study of EPO pretreatment's effect on expression of TNF-? gene in cultured cardiac myocytes with hypoxia/reoxygenation injury and the possible mechanism
Chuan QIN ; Yingbin XIAO ; Qianjin ZHONG
Chinese Journal of Thoracic and Cardiovascular Surgery 2003;0(03):-
Objective The present study is to investigate the effect of EPO pretreatment on TNF-? expression in cultured cardiac myocytes with H/R and to explore the possible NF-?B signal transduction mechanism. Methods The model of cultured cardiac myocytes with H/R was established and the cardiac myocytes were divided into 4 groups, including EPO group (treat with EPO 10?U/ml 24?h before H/R), EPO+PDTC group (treat with EPO 10?U/mL and PDTC 5??g/ml 24?h before H/R), PDTC group (treat with PDTC 5??g /ml 24h before H/R) and control group. Change of TNF-? gene expression before and after H/R in cardiac myocytes was detected with RT-PCR and western blot. Change of NF-?B activity before and after H/R in cardiac myocytes was assayed with EMSA. Results Before H/R, there was no significant difference in TNF-? mRNA and protein expression between the 4 groups and after H/R, TNF-? mRNA and protein expression increased significantly in the 4 groups compared to control group before H/R. After H/R, TNF-? mRNA and protein expression was lower in EPO group than in the other 3 groups. Before H/R, NF-?B activity was higher in EPO group than in the other groups. After H/R, NF-?B activity increased significantly in all the 4 groups compared to the control before H/R and NF-?B activity was lower in EPO group than in the other groups. Conclusion EPO pretreatment inhibited the upregulation of TNF-? gene expression after H/R in cardiac myocytes, which might be related to the inhibition of NF-?B activation; EPO pretreatment might inhibit the activation of NF-?B after H/R through the negative feed-back mechanism of NF-?B activation.
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