http://ntur.lib.ntu.edu.tw/handle/246246/48123 Search the Channel s http://ntur.lib.ntu.edu.tw//simple-search http://ntur.lib.ntu.edu.tw/handle/246246/170307 title: Diosgenin Induces Hypoxia-Inducible Factor-1 Activation and Angiogenesis through Estrogen Receptor-Related Phosphatidylinositol 3-Kinase/Akt and P 38 Mitogen-Activated Protein Kinase Pathways in Osteoblasts abstract: Diosgenin, extracted from the root of wild yam (Dioscorea villosa), has been reported to demonstrate an opportunity for medical application. Vascular endothelial growth factor- A (VEGF-A) plays an important role in bone-related angiogenesis, a critical process occurring during bone formation and fracture healing. In this study, we examine whether diosgenin is able to induce VEGF-A expression and to promote angiogenesis in osteoblasts. For murine MC3T3-E1 preosteoblast-like cells, VEGF-A mRNA and protein expression seemed to be significantly elevated in response to diosgenin in a concentration-dependent fashion. Conditioned media prepared from cells treated with diosgenin induced strong angiogenic activity in either in vitro or ex vivo angiogenesis assay. Furthermore, diosgenin treatment increased the stability and activity of HIF-1 protein. Inhibition of HIF-1 activity by transfection with DN-HIF-1 significantly diminished diosgenin-mediated VEGF-A up- regulation. The use of pharmacological inhibitors or genetic inhibition revealed that both the phosphatidylinositol 3- kinase (PI3K)/Akt and p38 signaling pathways were potentially required for diosgenin-induced HIF-1 activation and subsequent VEGF-A up-regulation. It is noteworthy that an estrogen receptor binding assay revealed that diosgenin has the strong ability to replace [3H] estradiol bound to estrogen receptor (IC50, 10 nM). In addition, the specific estrogen receptor antagonists ICI 182,780 (faslodex) and tamoxifen were noted to be able to strongly inhibit diosgenin-induced, src kinase-dependent Akt and p38 MAPK activation. Taken together, such results provide evidence that diosgenin up-regulates VEGF-A and promotes angiogenesis in preosteoblast-like cells by a hypoxia-inducible factor-1 - dependent mechanism involving the activation of src kinase, p38 MAPK, and Akt signaling pathways via estrogen receptor. <br> Tue, 13 Oct 2009 13:24:58 GMT http://ntur.lib.ntu.edu.tw/handle/246246/170305 title: Risk Factors for Ovarian Cancer in Taiwan:A Case-Control Study in a Low Incidence Population Tue, 13 Oct 2009 13:23:38 GMT http://ntur.lib.ntu.edu.tw/handle/246246/170300 title: Effects of Alendronate on Osteopenic Postmenopausal Chinese Women abstract: To evaluate the effects of alendronate on postmenopausal Chinese women with osteopenia, we treated 46 subjects daily with either 10 mg alendronate (N = 24) or placebo plus 500 mg calcium supplement (N = 22), and measured their bone mineral density (BMD) at the lumbar spine and hip, and urinary bone resorption markers before, during, and after the 1 year treatment period. The bone markers included N- telopeptide of type I collagen (NTx) and deoxypyridinoline ( Dpd); both were corrected by the concentration of creatinine in the same sample (NTx/Cr and Dpd/Cr). Both NTx/ Cr and Dpd/Cr decreased significantly by 44% and 28%, respectively (p < 0.05 for both), in 1 month in the active treatment group but did not change in the placebo group. BMD at the spine, femoral neck, trochanter, and Ward's triangle increased significantly by 6 months and showed a further increase through month 12 at the spine in the alendronate- treated group. Relative to the placebo group, BMD changes at various sites in the alendronate-treated group were higher at 12 months by 6%-11%. Thus, our data suggest that 10 mg alendronate daily resulted in significant increases in spine and hip BMD, and decreases of urinary resorption markers in the osteopenic postmenopausal Chinese women studied. The amplitude of responses was higher than in previous reports in the USA and Europe. <br> Tue, 13 Oct 2009 13:22:00 GMT http://ntur.lib.ntu.edu.tw/handle/246246/170298 title: Multilineage Differentiation and Characterization of the Human Fetal Osteoblastic 1.19 Cell Line: A Possible in Vitro Model of Human Mesenchymal Progenitors Tue, 13 Oct 2009 13:18:58 GMT