Factors Influencing Self-Identity and Menopausal Symptoms on Level of Depression in Middle Aged Women

PURPOSE: The purpose of this study was to identify the factors influencing self-identity and menopausal symptoms their influence on level of depression in middle-aged woman. METHODS: Participants were 135 middle-aged women who were living in city B, were 45-60 years old, informed of study purpose, and agreed to participate. Data were collected from December, 2012 to January, 2013 using scales measuring depression, self-identity, and menopausal symptoms. Data were analyzed using t-test, ANOVA, Scheffe test, Pearson Correlation Coefficients, and Multiple Stepwise Regression. RESULTS: Level of depression was low, self-identity was slightly high, and menopausal symptoms were relatively low in these middle-aged women. There were significant differences in depression by perceived health status and perceived economic status. Depression had a moderate negative correlation with self-identity (r=-.49, p<.001) and a moderate positive correlation with menopausal symptoms (r=.57, p<.001). Menopausal psychological symptoms were the factor most affecting depression and explained 37% of the variance in depression. A total of 51% of variance in depression was explained by menopausal symptoms (psychological and physical), self-identity, and perceived economic status. CONCLUSION: Thus, an effort to improve self-identity, especially a plan to attenuate menopausal psychological symptoms is needed to reduce depression.

Coptidis rhizoma extract protects against cytokine-induced death of pancreatic beta-cells through suppression of NF-kappa B activation

We demonstrated previously that Coptidis rhizoma extract (CRE) prevented S-nitroso-N-acetylpenicillamine-induced apoptotic cell death via the inhibition of mitochondrial membrane potential disruption and cytochrome c release in RINm5F (RIN) rat insulinoma cells. In this study, the preventive effects of CRE against cytokine-induced beta-cell death was assessed. Cytokines generated by immune cells infiltrating pancreatic islets are crucial mediators of beta-cell destruction in insulin-dependent diabetes mellitus. The treatment of RIN cells with IL-1beta and IFN-gamma resulted in a reduction of cell viability. CRE completely protected IL-1beta and IFN-gamma-mediated cell death in a concentration-dependent manner. Incubation with CRE induced a significant suppression of IL-1beta and IFN-gamma-induced nitric oxide (NO) production, a finding which correlated well with reduced levels of the iNOS mRNA and protein. The molecular mechanism by which CRE inhibited iNOS gene expression appeared to involve the inhibition of NF-kappa B activation. The IL-1beta and IFN-gamma-stimulated RIN cells showed increases in NF-kappa B binding activity and p65 subunit levels in nucleus, and IkappaBalpha degradation in cytosol compared to unstimulated cells. Furthermore, the protective effects of CRE were verified via the observation of reduced NO generation and iNOS expression, and normal insulin-secretion responses to glucose in IL-1beta and IFN-gamma-treated islets.