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It is well established that intimate partner violence (IPV) against women adversely affects maternal morbidity and mortality. But a limited number of studies were found in the literature regarding the association between IPV and under-five child mortality. In this article, using Bangladesh Demographic and Health Survey (BDHS) 2007 data, we examined the effect of IPV on under-five child mortality. A product-limit approach was used for bivariate survival analysis, and Cox proportional hazard multiple regression models were used to investigate the effect of IPV controlling potential confounders. In bivariate analysis, the variables exposure to IPV, mother's age at birth, mother's education, residence type, division, number of children, wealth index, occupation, access to media, and decision autonomy were found to be potential risk factors for child mortality. Results indicated that women exposed to IPV were more likely to experience under-five child mortality compared with women not exposed. The unadjusted hazard ratio for IPV was 1.21 (95% confidence interval [CI] = [1.09, 1.35]) with p value < .01, whereas it was 1.16 (95% CI = [1.04, 1.29]) with p value < .01 and 1.13 (95% CI = [1.01, 1.26]) with p value < .05 in two adjusted models. These results implied that IPV against women is a problem not only for women but also for their children's survival.

The present study was designed to investigate the effect of the phosphodiesterase IV inhibitor rolipram on Th1 and Th2 immune responses in mice. Mice were immunized subcutaneously at the base of the tail with ovalbumin (OVA) emulsified with complete Freund's adjuvant (day 0) and were treated daily with oral administration of various doses of rolipram from days 0 to 20. On day 21, production of anti-OVA IgG and proliferative responses to the antigen were determined. Anti-OVA IgG2a and interferon-gamma (IFN-gamma), as indicators of Th1 responses, and anti-OVA IgG1 and interleukin-10 (IL-10), as indicators of Th2 responses, were also measured. The results showed that treatment with rolipram failed to affect the production of OVA-specific IgG but decreased the proliferation of spleen cells to the antigen. Its inhibitory effect on these immune responses was correlated with a marked decrease in IFN-gamma but not IL-10 production, although neither anti-OVA IgG2a nor IgG1 production was affected by rolipram. These results suggest that rolipram may preferentially inhibit Th1 responses more effectively than Th2 responses. Administration of rolipram resulted in suppression of antigen (OVA)-induced arthritis in mice. The suppression of joint inflammation by rolipram was associated with the inhibition of the OVA-specific proliferative responses of spleen cells and IFN-gamma secretion. These results indicate that rolipram may be effective in regulating Th1-mediated diseases such as rheumatoid arthritis.

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