The National Institute of Health (NIH), the biggest and most influential biomedical research institute and subsidy management agent in America and the world at large, provides financial aids to the scientific research and academic career development of post-doctors through various ways,ushering them into the field of professional research. Over the past two decades, China's postdoctoral system enjoys great prosperity but leaves much to be desired in its subsidy system. The present article gives a detailed portrayal of the subsidy system in the National Institute of Health and presents the author's suggestions over issues in China, such as the combination of post-doctors and scientific research program, postdoctoral payment and welfare, postdoctoral funding, policy support of key subjects such as medicine mattering to the national welfare and national strategy.

Objective To assess the effect of peroxisome proliferator-activated receptor γ (PPARγ) agonist on prostate epithelial cells in vitro.Methods The expression of peroxisome proliferator-activated receptor γ(PPARγ) was studied by immunocytochemistry and immunofluorescence study.The RWPE-1 human prostate epithelial cell line was treated with PPARγ agonist rosiglitazone 100 μmol/L for 48 h.Analysis of apoptosis was performed by Caspase 3/7 activity assay.Mitochondria depolarization was measured by using the potential-sensitive color,JC-1.The expression of apoptosis-related proteins-Bax was investigated by immunohistochemistry.Results PPARγ mainly located in nucleus and perinucleus.RWPE-1 cell line treated with PPARγ agonist rosiglitazone showed higher Caspase 3/7 activity (10636±1032 RLU) than in control (5936±620 RLU),P＜0.01 and significantly upregulated Bax level (8250±694 vs.6017±563)than in control group,P＜0.01.In addition,mitochondrial membrane potential was depolarized in rosiglitazone treated cells.Conclusions PPARmay play important roles in the pathophysiology of BPH.The mechanism might be that PPARγ regulates cell apoptosis.It is suggested that the mitochondrial and Bax pathway might be involved in signaling PPARγ induced cell apoptosis.