The aim of this study was to evaluate the association between postmenopausal osteoporosis and kidney-vacuity syndrome. Eighty-one postmenopausal women were enrolled; their age were between 40 to 65 years old. The mean ages of the non-osteoporosis group and osteoporosis group were 54.0 +/- 4.8 and 58.9 +/- 5.9 years old, respectively. Bone density examination was performed by DEXA technique and the diagnosis of osteoporosis was made by finding 2.5 standard deviations below the bone density of healthy youths. Kidney-vacuity syndrome was deduced according to the diagnostic criteria developed in the National Congress on Chinese Medicine and Sino-Western Combined Geriatric Medicine held in the People's Republic of China in 1986. The results showed that patients with kidney-qi-vacuity and kidney-yin-vacuity were more likely to have osteoporosis than those who were not. No significant difference in the rates of osteoporosis between the kidney-yang-vacuity group and non-kidney-yang-vacuity group was found. The kidney-qi-yin-vacuity group had a higher probability of developing osteoporosis than the kidney-qi-vacuity or kidney-yin-vacuity group. By logistic regression analysis, patients with kidney-qi-vacuity or kidney-yin-vacuity were more likely to develop osteoporosis than those who were not. In conclusion, a marked association between kidney-vacuity syndrome and postmenopausal osteoporosis was observed. Patients with kidney-qi-yin-vacuity syndrome were more likely to get osteoporosis than those with kidney-qi-vacuity syndrome or kidney-yin-vacuity syndrome.

Abstract. The natural antioxidant gallic acid (GA) has demonstrated a significant inhibition of cell proliferation and induction of apoptosis in a series of cancer cell lines. However, there is no available information to show whether GA induces apoptosis in human skin cancer cells. In the present study, we report GA-induced apoptosis in A375.S2 human melanoma cells. GA affected morphological changes, decreased the percentage of viable cells and induced apoptosis in A375.S2 cells in a dose-and time-dependent manner. Observation of the molecular mechanism of apoptosis in A375.S2 cells showed that GA up-regulated the proapoptotic proteins such as Bax, and induced caspase cascade activity, but down-regulated antiapoptotic proteins such as Bcl-2. GA induced reactive oxygen species (ROS) and intracellular Ca 2+ productions and decreased the level of mitochondrial membrane potential (Δae m ) in A375.S2 cells in a timedependent manner. GA triggered cytosolic release of apoptotic molecules, cytochrome c, promoted activation of caspase-9 and caspase-3, and ultimately apoptotic cell death. In addition, GA also promoted cytosolic release of apoptosisinducing factor (AIF) and endonuclease G (Endo G). Therefore, GA may also induce apoptosis through a caspaseindependent pathway. Our results suggest that GA might be a potential anticancer compound; however, in depth in vivo studies are needed to elucidate the exact mechanism.