Specifically, we found significant alterations in the transcript level of the two opposing members, bcl-2 and bax, in astrocytes after 48 h of exposure to 1950-MHz TD-SCDMA. The down-regulation of bcl-2 mRNA levels was accompanied by the up-regulation of bax transcript levels after same time of exposure. The protein expression of caspase-3 was also augmented after 48 h of exposure. These results were in accordance with the apoptosis ratio of astrocytes examined by Annexin V/PI assay. In contrast, no significant effect on the gene and protein expression profile was observed in C6 cells after the same treatment. Thus our results demonstrated that the apoptosis of astrocytes induced by RF exposure was mediated by caspase-3 related pathway with the involvement of both bax and bcl-2. Therefore, the present study showed that 1950-MHz TDSCDMA phone emissions exerted differential effects on normal astroglial and transformed glial cells. Because both cells were cultured in an attached manner, and the density of cells was adjusted to ensure the two cell types to be passaged at the same time. Although the culture media for two kinds of cells were slightly different, we anticipated that the media should contribute minimally to this change. To our knowledge, tumor cells showed a stronger ability to proliferate and repair the damages caused by environment. Therefore, it was possible that C6 cells have a stronger inner resistance to EMF exposure. In summary, this study firstly examined the effects of 1950-MHz TD-SCDMA emissions from a calibrated standard dipole on the biological features of normal or transformed cells of glial origin. Our results confirmed that the 1950-MH TD-SCDMA EMF exhibited no significant effect on cancer promotion, progression, or carcinogenesis of rat astrocytes and C6 cells at the exposure time from 12 to 48 h. However, 48 h of exposure damaged the mitochondria of astrocytes and induced apoptosis through caspase-3-dependent pathway involving bax and bcl-2. These results are important for properly understanding the mode of action of 1950-MHz TD-SCDMA RF radiation on living organisms, especially in the case of adverse effects. However, further studies are needed to ascertain the effect of EMF exposure on other related cell types and at longer exposure time. Percutaneous coronary intervention is a common strategy to treat coronary artery disease but, neointimal hyperplasia with resultant restenosis following interventional procedure remains the major limitation. Although the magnitude of intimal hyperplasia and late luminal loss have been significantly reduced by BAY-60-7550 implantation of drug eluting stents, late stent thrombosis requiring longer periods of anti-platelet therapy is a potentially fatal complication. Neointimal hyperplasia, a cell proliferation and differentiation process, is the predominant mechanism in the development of in-stent restenosis and anti-proliferative drugs in DES suppress tissue re-growth. Inflammatory mediators in the atheromatous tissue potentiate the underlying cellular response in the development of restenosis. Indeed, the inflammatory reaction is more prominent after stent implantation compared to balloon angioplasty. Tumor necrosis factor, a pluripotent pro-inflammatory cytokine, plays a pivotal role in restenosis after coronary intervention. There is marked increase in tissue expression of TNF-a due to arterial injury following balloon angioplasty. Vitamin D is a secosteroid which functions through vitamin D receptor, a transcription factor, and directly or indirectly controls more than 200 heterogeneous genes including the genes for the regulation of cellular differentiation, proliferation, and angiogenesis.