YAG (Yttrium Aluminum Garnet, Y3Al5O12) has excellent plasma resistance and recently has been used as an alternative to Y2O3 as a chamber coating material in the semiconductor process. However, due to the presence of an impurity phase and difficulties in synthesis and densification, many studies on YAG are being conducted. In this study, YAG powder is synthesized by an organic-inorganic complex solution synthesis method using PVA polymer. The PVA solution is added to the sol in which the metal nitrate salts are dissolved, and the precursor is calcined into a porous and soft YAG powder. By controlling the molecular weight and the amount of PVA polymer, the effect on the particle size and particle shape of the synthesized YAG powder is evaluated. The sintering behavior of the YAG powder compact according to PVA type and grinding time is studied through an examination of its microstructure. Single phase YAG is synthesized at relatively low temperature of 1,000 ℃ and can be pulverized to sub-micron size by ball milling. In addition, sintered YAG with a relative density of about 98 % is obtained by sintering at 1,650 ℃.

Bcl-2 protects tumor cells from the apoptotic effects of various anti-neoplastic agents. Increased expression of Bcl-2 has been associated with a poor response to chemotherapy in various malignancies, including leukemia. Hence, bypassing the resistance conferred by anti-apoptotic factors such as Bcl-2 represents an attractive therapeutic strategy against cancer cells, including leukemic cells. This study was undertaken to examine whether the anticancer drug, cisplatin and the synthetic chenodeoxycholic acid (CDCA) derivative, HS-1200 show anti-tumor activity in U937 and U937/Bcl-2 cells. Viability assays revealed that HS-1200 overcomes the resistance conferred by Bcl-2 in human leukemic U937 cells. Various apoptosis assessment assays further demonstrated that HS-1200 overcomes the resistance conferred by Bcl-2 in human leukemic U937 cells by inducing apoptosis. In addition HS-1200, but not cisplatin, overcomes the anti-apoptotic effects of Bcl-2 in Bcl-2 over-expressing human leukemic cells (U937/Bcl-2 cells). Notably, we observed that the HS-1200-induced formation of mature promyelocytic leukemia (PML) nuclear bodies (NBs) correlates with a suppression of the anti-apoptotic effects of Bcl-2 in human leukemic cells over-expressing this protein (U937/Bcl-2 cells). Furthermore, HS-1200 was found to induce the association between PML and SUMO-1, Daxx, Sp100, p53 or CBP in the aggregated PML-NBs of U937/Bcl-2 cells. Thus, PML protein and the formation of mature PML-NBs could be considered as therapeutic targets that may help to bypass the resistance to apoptosis conferred by Bcl-2. Elucidating the exact mechanism by which PML regulates Bcl-2 will require further work.