The statistical properties of turbulence at upper levels in the atmosphere [upper troposphere and lower stratosphere (UTLS)] are still not well known, partly because of the lack of adequate routine observations. This is despite the obvious benefit that such observations would have for alerting aircraft of potentially hazardous conditions, either in real time or for route planning. To address this deficiency, a research project sponsored by the Federal Aviation Administration has developed a software package that automatically estimates and reports atmospheric turbulence intensity levels (as EDR ≡ ε1/3, where ε is the energy or eddy dissipation rate). The package has been tested and evaluated on commercial aircraft. The amount of turbulence data gathered from these in situ reports is unprecedented. As of January 2014, there are ~200 aircraft outfitted with this system, contributing to over 137 million archived records of EDR values through 2013, most of which were taken at cruise levels of commercial aircraft, that is, in the UTLS. In this paper, techniques used for estimating EDR are outlined and comparisons with pilot reports from the same or nearby aircraft are presented. These reports allow calibration of EDR in terms of traditionally reported intensity categories (“light,” “moderate,” or “severe”). The results of some statistical analyses of EDR values are also presented. These analyses are restricted to the United States for now, but, as this program is expanded to international carriers, such data will begin to become available over other areas of the globe.
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...
Residents of distressed urban areas suffer early aging-related disease and excess mortality. Using a community-based participatory research approach in a collaboration between social researchers and cellular biologists, we collected a unique data set of 239 black, white, or Mexican adults from a stratified, multi-stage probability sample of three Detroit neighborhoods. We drew venous blood and measured Telomere Length (TL), an indicator of stress-mediated biological aging, linking respondents’ TL to their community survey responses. We regressed TL on socioeconomic, psychosocial, neighborhood, and behavioral stressors, hypothesizing and finding an interaction between poverty and racial/ethnic group. Poor whites had shorter TL than nonpoor whites; poor and nonpoor blacks had equivalent TL; poor Mexicans had longer TL than nonpoor Mexicans. Findings suggest unobserved heterogeneity bias is an important threat to the validity of estimates of TL differences by race/ethnicity. They point to health impacts of social identity as contingent, the products of structurally-rooted biopsychosocial processes.
Socioeconomic factors play an important but complex role in PTB disparities. The absence of Black-White disparities in PTB within certain socioeconomic subgroups, alongside substantial disparities within others, suggests that social factors moderate the disparity. Further research should explore social factors suggested by the literature-including life course socioeconomic experiences and racism-related stress, and the biological pathways through which they operate-as potential contributors to PTB among Black and White women with different levels of social advantage.
Objective To assess whether the cumulative impact of exposure to repeated or chronic stressors as measured by allostatic load, contributes to the “unhealthy assimilation” effects often observed for immigrants with time in the United States. Methods We analyzed data from the National Health and Nutrition Examination Survey, 1988–1994, to estimate multivariate logistic regression models of the odds of having a high allostatic load score among Mexican immigrants, stratified by adult age group, according to length of residence in US, controlling for demographic, socioeconomic, and health input covariates. Results Estimates indicate that 45–60 year old Mexican immigrants have lower allostatic load scores upon arrival than US-born Mexican Americans, non-Hispanic whites, and non-Hispanic Blacks, and that this health advantage is attenuated with duration of residence in the US. Conclusions The findings of our analysis are consistent with the hypothesis that repeated or chronic physiological adaptation to stressors is one contributor to the “unhealthy assimilation” effect observed for Mexican immigrants.
Current automated aviation turbulence forecast algorithms diagnose turbulence from numerical weather prediction (NWP) model output by identifying large values in computed horizontal or vertical spatial gradients of various atmospheric state variables (velocity; temperature) and thresholding these gradients empirically to indicate expected areas of “light,” “moderate,” and “severe” levels of aviation turbulence. This approach is obviously aircraft dependent and cannot accommodate the many different aircraft types that may be in the airspace. Therefore, it is proposed to provide forecasts of an atmospheric turbulence metric: the energy dissipation rate to the one-third power (EDR). A strategy is developed to statistically map automated turbulence forecast diagnostics or groups of diagnostics to EDR. The method assumes a lognormal distribution of EDR and uses climatological peak EDR data from in situ equipped aircraft in conjunction with the distribution of computed diagnostic values. These remapped values can then be combined to provide an ensemble mean EDR that is the final forecast. New mountain-wave-turbulence algorithms are presented, and the lognormal mapping is applied to them as well. The EDR forecasts are compared with aircraft in situ EDR observations and verbal pilot reports (converted to EDR) to obtain statistical performance metrics of the individual diagnostics and the ensemble mean. It is shown by one common performance metric, the area under the relative operating characteristics curve, that the ensemble mean provides better performance than forecasts from individual model diagnostics at all altitudes (low, mid-, and upper levels) and for two input NWP models.
Plasminogen activator inhibitor-2 (PAI-2), a member of the serpin gene family, is thought to serve as a primary regulator of plasminogen activation in the extravascular compartment. High levels of PAI-2 are found in keratinocytes, monocytes, and the human trophoblast, the latter suggesting a role in placental maintenance or embryo development. The primarily intracellular distribution of PAI-2 also may indicate a unique regulatory role in a protease-dependent cellular process such as apoptosis. To examine the potential functions of PAI-2 in vivo, we generated PAI-2-deficient mice by gene targeting in embryonic stem cells. Homozygous PAI-2-deficient mice exhibited normal development, survival, and fertility and were also indistinguishable from normal controls in response to a bacterial infectious challenge or endotoxin infusion. No differences in monocyte recruitment into the peritoneum were observed after thioglycollate injection. Epidermal wound healing was equivalent among PAI-2 ؊͞؊ null and control mice. Finally, crossing PAI-2 ؊͞؊ with PAI-1 ؊͞؊ mice to generate animals deficient in both plasminogen activator inhibitors failed to uncover an overlap in function between these two related proteins.
The extent to which socially-assigned and culturally mediated social identity affects health depends on contingencies of social identity that vary across and within populations in day-to-day life. These contingencies are structurally rooted and health damaging inasmuch as they activate physiological stress responses. They also have adverse effects on cognition and emotion, undermining self-confidence and diminishing academic performance. This impact reduces opportunities for social mobility, while ensuring those who "beat the odds" pay a physical price for their positive efforts. Recent applications of social identity theory toward closing racial, ethnic, and gender academic achievement gaps through changing features of educational settings, rather than individual students, have proved fruitful. We sought to integrate this evidence with growing social epidemiological evidence that structurally-rooted biopsychosocial processes have population health effects. We explicate an emergent framework, Jedi Public Health (JPH). JPH focuses on changing features of settings in everyday life, rather than individuals, to promote population health equity, a high priority, yet, elusive national public health objective. We call for an expansion and, in some ways, a re-orienting of efforts to eliminate population health inequity. Policies and interventions to remove and replace discrediting cues in everyday settings hold promise for disrupting the repeated physiological stress process activation that fuels population health inequities with potentially wide application.
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