ABSTRACT
At an early stage of its foundation, new China became clear about the nature of public welfare and quickly developed medical and health services, which was well received by the World Health Organization. The marketization and the reduction of input into medical and health services from the 1980s created severe adverse consequences. After the SARS' outbreak in 2003, China started to give serious consideration to its medical and health system, and to work at developing medical and health services. The new healthcare reform launched in 2009 re-emphasizes fairness and public welfare, and China's achievements have been remarkable. Of course, there are still many problems to be solved in the reform, which also paves the way for increasing the reform in future.
Subject(s)
Financing, Government , Health Care Rationing/ethics , Health Care Reform/ethics , Health Care Sector , Health Services Needs and Demand , Health Services , China/epidemiology , Disease Outbreaks , Financing, Government/economics , Financing, Government/ethics , Health Care Rationing/economics , Health Care Sector/economics , Health Care Sector/ethics , Health Services/economics , Health Services/ethics , Health Services Needs and Demand/economics , Health Services Needs and Demand/ethics , Humans , Insurance, Health , Severe Acute Respiratory SyndromeABSTRACT
Dehydroepiandrosterone (DHEA) is an endogenous steroid that is metabolized to androgens and/or estrogens in the human prostate. DHEA levels decline with age, and use of DHEA supplements to retard the aging process is of unproved effectiveness and safety. In this study, rat ventral prostatic epithelial cells were used to determine whether DHEA-modulated proliferation and prostate-specific antigen (PSA listed as KLKB1 in the MGI Database) production were mediated via the androgen receptor (AR) and its potential mechanism. We demonstrated that proliferation of prostatic epithelial cells and increase of PSA expression induced by DHEA were neutralized by Casodex or Ar siRNA, two specific AR blockers. DHEA stimulated Nfkb DNA binding activity, with this effect being blunted by Casodex or Ar siRNA. Moreover, the inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT nullified the effects of DHEA on NFKB activation. These findings suggested that DHEA stimulated normal prostatic epithelial cell proliferation, and AR is involved in DHEA-induced PSA expression in normal prostatic epithelial cells. This stimulation effect induced by DHEA is mediated by the activation of NFKB via PI3K/AKT pathway.