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Child marriage remains common even where female schooling and employment opportunities have grown. We experimentally evaluate a financial incentive to delay marriage alongside a girls' empowerment program in Bangladesh. While girls eligible for two years of incentive are 19 percent less likely to marry underage, the empowerment program failed to decrease adolescent marriage. We show that these results are consistent with a signaling model in which bride type is imperfectly observed but preferred types (socially conservative girls) have lower returns to delaying marriage. Consistent with our theoretical prediction, we observe substantial spillovers of the incentive on untreated nonpreferred types. (JEL C93, D91, J12, J13, J16, 012)

Background: Different locations and study periods were used in the assessment of the relationships between heatwaves and mortality. However, little is known about the comparability and consistency of the previous effect estimates in the literature. This study assessed the heatwave—mortality relationship using different study periods in the three largest Australian cities (Brisbane, Melbourne and Sydney). Methods: Daily data on climatic variables and mortality for the three cities were obtained from relevant government agencies between 1988 and 2011. A consistent definition of heatwaves was used for these cities. Poisson generalised additive model was fitted to assess the impact of heatwaves on mortality. Results: Non-accidental and circulatory mortality significantly increased during heatwaves across the three cities even with different heatwave definitions and study periods. Using the summer data resulted in the largest increase in effect estimates compared to those using the warm season or the whole year data. Conclusion: The findings may have implications for developing standard approaches to evaluating the heatwave-mortality relationship and advancing heat health warning systems. It also provides an impetus to methodological advance for assessing climate change-related health consequences.

Abstract
Abdominal aortic aneurysm (AAA) is a common but life-threatening vascular condition in men at an advanced age. However, the underlying mechanisms of age-increased incidence and mortality of AAA remain elusive. Here, we performed RNA sequencing (RNA-seq) of mouse aortas from males (young: 3-month, n = 4 vs old: 23-month, n = 4) and integrated with the data sets of human aortas (young: 20–39, n = 47 vs old: 60–79 years, n = 92) from GTEx project and the data set (GSE183464) for AAA to search for age-shifted aortic aneurysm genes, their relevant biological processes, and signaling pathways. Angiotensin II-induced AAA in mice was used to verify the critical findings. We found 1 001 genes transcriptionally changed with ages in both mouse and human. Most age-increased genes were enriched intracellularly and the relevant biological processes included mitochondrial function and translational controls, whereas the age-decreased genes were largely localized in extracellular regions and cell periphery and the involved biological processes were associated with extracellular matrix (ECM). Fifty-one were known genes for AAA and found dominantly in extracellular region. The common age-shifted vascular genes and known aortic aneurysm genes had shared functional influences on ECM organization, apoptosis, and angiogenesis. Aorta with angiotensin II-induced AAA exhibited similar phenotypic changes in ECM to that in old mice. Together, we present a conserved transcriptional signature for aortic aging and provide evidence that mitochondrial dysfunction and the imbalanced ribosomal homeostasis act likely as driven-forces for aortic aging and age-disturbed ECM is the substrate for developing AAA.