Contraceptive Adoption and Changes in Empowerment in Kenya, Nigeria, and Senegal.

Women's empowerment and contraceptive use are critical to achieving gender equality. The positive association between more empowered women and higher rates of contraceptive use has been well-established by cross-sectional research. However, there remains a gap in understanding the longitudinal relationship between contraceptive adoption and changes to women's empowerment. This study represents a novel approach to understanding the relationship between contraceptive adoption and women's empowerment longitudinally, at the individual level. To the authors' knowledge, this is the first attempt to measure the relationship between contraceptive adoption and women's empowerment using more than one wave of panel data. We leverage the longitudinal design of the Urban Reproductive Health Initiative data to code empowerment items by change over time (e.g., more empowered, no change, less empowered). We use sparse principal component analysis to establish empowerment change domains and calculate individual scores standardized by country-level averages. We estimate mixed effects models on these change domains, to investigate the link between contraceptive adoption and empowerment. We find common themes in empowerment across contexts-but contraceptive adoption has both positive and negative effects on those domains, and this varies across context. We discuss the need for cohort studies to examine this relationship.

The Consequences of the Tajikistani Civil War for Abortion and Miscarriage.

Although a great deal of attention is paid to reproductive health during violent conflicts, the literature is sparse on the consequences of conflict for abortion and miscarriage. This research provides an analysis of a recent historical case: the 1992-1997 civil war in Tajikistan, using the female questionnaire of the 2007 Tajik Living Standards Survey to examine a subsample of 1,445 women surveyed who had reached menarche during or after the war and had been pregnant at least once by the time of the survey. The analysis leverages the uneven geographical scope of conflict events during the civil war to pinpoint women's exposure to violence, measured by the Uppsala Conflict Data Program. The results show that for women who had reached menarche during or after the civil war, exposure to conflict events increases the likelihood of ever experiencing miscarriage, but not abortion. Including a spatial lag operator reveals that there were also spillover effects for abortion, in which women who were in a broader region of uncertainty were more likely to induce an abortion. These findings highlight the role of institutional changes in affecting pregnancy loss during and after civil war.

Disruption and decline: the gendered consequences of civil war and political transition for education in Tajikistan.

The sweeping political transition from the Soviet Union to independence in Tajikistan was accompanied by a devastating civil war. Social, economic, and demographic change followed. This research examines a critical indicator of human welfare and stability at the micro- and macro-levels: educational attainment and mobility. Using the 2007 Tajik Living Standards Survey, I compare cohorts educated before, during, and after the civil war. I examine the impact of the war and the political transition on educational attainment and mobility. The findings suggest that the consequences of civil war and political transition in Tajikistan were gendered: boys' attainment was disrupted when they lived in a conflict-affected area and were 16-to-17 years old when the war began; girls' attainment decline was more widespread. This research contributes to our understanding of the long-term consequences of political events on human capital accumulation over the life course.

Migration as an adaptive response to ethnic nationalism in Russia.

In this paper, I argue that migration responses to push factors can differ along ethnic lines. To arrive at migration as an adaptive response in which minorities engage, two processes are necessary. First, an individual making the decision to migrate must interpret ethnic tensions as a threat to her life chances, and she must evaluate her future prospects in this ethnically charged framework. Second, the option of migration must be a viable one. That is, an individual must consider them self the plausible target of the threat of diminishing life chances, conclude that an adaptive response is required, and determine that the benefits of migrating outweigh the costs. In order to explain these processes, the relational theory of ethnic politics (Hale 2008) and demographic theories of migration are employed. To test this hypothesis, an event history model is estimated using regional, household, and individual-level data from Russian censuses and the Russia Longitudinal Monitoring Survey. The relationship between out-migration and regional nationalist vote share is examined as well as regional hate crimes. The findings suggest that political push factors affect minority groups differently from the ethnic majority, supporting the hypothesis that the success of ethno nationalist politics in a region signals vulnerability to ethnic minorities, influencing migration decisions.

Role of oxidative stress in peroxisome proliferator-mediated carcinogenesis.

In this review, the evidence about the role of oxidative stress in the induction of hepatocellular carcinomas by peroxisome proliferators is examined. The activation of PPAR-alpha by peroxisome proliferators in rats and mice may produce oxidative stress, due to the induction of enzymes like fatty acyl coenzyme A (CoA) oxidase (AOX) and cytochrome P-450 4A1. The effect of peroxisome proliferators on the antioxidant defense system is reviewed, as is the effect on endpoints resulting from oxidative stress that may be important in carcinogenesis, such as lipid peroxidation, oxidative DNA damage, and transcription factor activation. Peroxisome proliferators clearly inhibit several enzymes in the antioxidant defense system, but studies examining effects on lipid peroxidation and oxidative DNA damage are conflicting. There is a profound species difference in the induction of hepatocellular carcinomas by peroxisome proliferators, with rats and mice being sensitive, whereas species such as nonhuman primates and guinea pigs are not susceptible to the effects of peroxisome proliferators. The possible role of oxidative stress in these species differences is also reviewed. Overall, peroxisome proliferators produce changes in oxidative stress, but whether these changes are important in the carcinogenic process is not clear at this time.

Peroxisome proliferators do not activate the transcription factors AP-1, early growth response-1, or heat shock factors 1 and 2 in rats or hamsters.

Peroxisome proliferators (PPs) cause hepatomegaly, peroxisome proliferation, and hepatocarcinogenesis in rats and mice, whereas hamsters are less responsive to these compounds. PPs increase peroxisomal beta-oxidation and P4504A subfamily activity, which have been hypothesized to result in oxidative stress. Work in our laboratory indicated that differential modulation of the redox-sensitive transcription factor NF-kappaB may contribute to the resulting difference in species susceptibility following PP administration. Therefore, we hypothesized that other redox-sensitive transcription factors such as AP-1, early growth response gene 1 (Egr-1), and heat-shock factors 1 and 2 (HSF1/2) may also be alternatively activated in differentially susceptible species. Accordingly, we measured the activation of these transcription factors using gel mobility shift assays, with hepatic nuclear extracts derived from rats and Syrian hamsters fed two doses of three peroxisome proliferators (dibutyl-phthalate [DBP], gemfibrozil and Wy-14,643) for 6, 34, or 90 days. Although changes were observed at various time points, no consistent, dose-responsive changes were observed in the DNA binding activities of these transcription factors following PP treatment. The lack of increased binding of AP-1, Egr-1, and HSFs suggests that these factors are not involved in increased cell proliferation following PP administration, although we cannot rule out that these factors are activated at earlier time points than those examined in this study.