\n\nA total of 406 women participated in this study (mean age = 22, SD = 2.9). There were 211 participants in the gain condition and 195 in the loss condition.\n\nAn analysis of covariance found a main DMH1 effect for framing (F(1, 402) = 6.3; P < 0.01) after controlling for existing attitudes towards oocyte donation and pre-message intentions to donate. Specifically, participants in the gain-framed condition were significantly more likely to report higher post-message intentions to donate oocytes than participants in the loss condition. However, the framing effect was only observed with British populations and not with women from South
East Asia. Further, structural equation modelling analyses revealed lower levels of ‘perceived behavioural control’ (beta = -0.420, P < 0.03) and positive attitudes towards ‘the importance of genetic ties between parent and child’ (beta = 0.70, P < 0.001) were direct predictors of post-message intentions in the gain (but not loss) frame condition.\n\nFindings obtained from this study indicate that oocyte donation campaigns should consider using gain-framed messages in recruitment appeals and message
frames this website should be matched to the target populations’ perceived level of behavioural control.”
“NAD(P)H:quinone oxidoreductase 1 (NQO1) has been known to protect cells against stressors, including the diabetogenic reagent streptozotocin (STZ). The present study demonstrated that NQO1 deficiency resulted in increased pancreatic beta-cell death induced by multiple low dose of STZ (MLDS) injections. NQO1 knockout (KO) mice showed hyperglycemia,
body weight loss, impaired glucose clearance rate and a lower plasma insulin level after MLDS treatment. Moreover, beta-cell mass and pancreatic insulin content were significantly lower in KO mice than in wild-type (WT) mice after MLDS treatment. Five days after the first STZ treatment, the islets of KO mice had substantially more TUNEL-positive beta-cells than those of WT mice, but there was no difference in the 5-Fluoracil research buy regeneration of beta-cells between KO mice and WT mice. At the same time, MLDS-treated KO mice showed significantly increased apoptotic markers in beta-cells, including cleaved caspase 3, Smac/DIABLO and AIF (apoptosis inducing factor) in the cytoplasm. These results suggest that mice deficient in NQO1 are vulnerable to MLDS-induced beta-cell destruction and diabetes, caused by increase of beta-cell apoptosis in pancreas. (C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Bone diseases such as rickets and osteoporosis cause significant reduction in bone quantity and quality, which leads to mechanical abnormalities.