We hypothesize that black women experience accelerated biological aging in response to repeated or prolonged adaptation to subjective and objective stressors. Drawing on stress physiology and ethnographic, social science, and public health literature, we lay out the rationale for this hypothesis. We also perform a first population-based test of its plausibility, focusing on telomere length, a biomeasure of aging that may be shortened by stressors. Analyzing data from the Study of Women's Health Across the Nation (SWAN), we estimate that at ages 49-55, black women are 7.5 years biologically "older" than white women. Indicators of perceived stress and poverty account for 27% of this difference. Data limitations preclude assessing objective stressors and also result in imprecise estimates, limiting our ability to draw firm inferences. Further investigation of black-white differences in telomere length using large-population-based samples of broad age range and with detailed measures of environmental stressors is merited.Correspondence to: Arline T. Geronimus, arline@umich.edu. NIH Public Access Author ManuscriptHum Nat. Author manuscript; available in PMC 2011 March 10. Despite overall gains in active life expectancy and efforts to reduce health disparities in the United States, black-white and socioeconomic inequalities in life expectancy and the prevalence of chronic disease persist (Flegal et al. 2002;Geronimus et al. 1996;Levine et al. 2001;Mokdad et al. 2001;Wong et al. 2002). These health disadvantages are severe among African Americans. More troubling still, some evidence suggests that black health disadvantages worsened after the early 1990s, especially among women. In some high-poverty localities, excess mortality rates increased among black women residents between 1990 and 2000, largely due to deaths attributed to chronic disease (Geronimus et al. 2008). Yet another example, estimates using data from the National Health and Nutrition Examination Surveys III (1988 and IV (1999IV ( -2002 show that hypertension prevalence rates grew in nonelderly black adults nationwide between the two survey waves, both absolutely and relative to whites (Geronimus et al. 2007). The entrenchment and, in some cases, worsening of black health disadvantages occurred across a wide range of health outcomes and during a period when the reduction or elimination of health disparities was identified as a high-priority national health objective. The clear failure to meet this objective suggests that future success may require new conceptual models and deepening understandings of the sources and mechanisms leading to health disparities. 1 The age dimension of black-white health disadvantages may provide key insights. For example, in the case cited above, black women in young through middle adulthood experienced the steepest increase with age in the probability of being hypertensive, even net of excess obesity rates among US black relative to white women. More broadly, the most pronounced differences in health between US bla...

Prion diseases are caused by conversion of a normally folded, non-pathogenic isoform of the prion protein (PrPC) to a misfolded, pathogenic isoform (PrPSc). Prion inoculation experiments in mice expressing homologous PrPC molecules on different genetic backgrounds displayed different incubation times, indicating that the conversion reaction may be influenced by other gene products. To identify genes that contribute to prion pathogenesis, we analysed incubation times of prions in mice in which the gene product was inactivated, knocked out or overexpressed. We tested 20 candidate genes, because their products either colocalize with PrP, are associated with Alzheimer's disease, are elevated during prion disease, or function in PrP-mediated signalling, PrP glycosylation, or protein maintenance. Whereas some of the candidates tested may have a role in the normal function of PrPC, our data show that many genes previously implicated in prion replication have no discernible effect on the pathogenesis of prion disease. While most genes tested did not significantly affect survival times, ablation of the amyloid beta (A4) precursor protein (App) or interleukin-1 receptor, type I (Il1r1), and transgenic overexpression of human superoxide dismutase 1 (SOD1) prolonged incubation times by 13, 16 and 19 %, respectively.

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DNA profiles have been obtained from fingerprints, but there is limited knowledge regarding DNA analysis from archived latent fingerprints-touch DNA "sandwiched" between adhesive and paper. Thus, this study sought to comparatively analyze a variety of collection and analytical methods in an effort to seek an optimized workflow for this specific sample type. Untreated and treated archived latent fingerprints were utilized to compare different biological sampling techniques, swab diluents, DNA extraction systems, DNA concentration practices, and post-amplification purification methods. Archived latent fingerprints disassembled and sampled via direct cutting, followed by DNA extracted using the QIAampâ DNA Investigator Kit, and concentration with Centri-Sep TM columns increased the odds of obtaining an STR profile. Using the recommended DNA workflow, 9 of the 10 samples provided STR profiles, which included 7-100% of the expected STR alleles and two full profiles. Thus, with carefully selected procedures, archived latent fingerprints can be a viable DNA source for criminal investigations including cold/postconviction cases.