The association between overall health, psychological distress, and occupational heat stress among a large national cohort of 40,913 Thai workers

BACKGROUND Occupational heat stress is a well-known problem, particularly in tropical countries, affecting workers, health and well-being. There are very few recent studies that have reported on the effect of heat stress on mental health, or overall health in workers, although socioeconomic development and rapid urbanization in tropical developing countries like Thailand create working conditions in which heat stress is likely. OBJECTIVE This study is aimed at identifying the relationship between self-reported heat stress and psychological distress, and overall health status in Thai workers. RESULTS 18% of our large national cohort (>40,000 subjects) often works under heat stress conditions and males are exposed to heat stress more often than females. Furthermore, working under heat stress conditions is associated with both worse overall health and psychological distress (adjusted odds ratios ranging from 1.49 to 1.84). CONCLUSIONS This association between occupational heat stress and worse health needs more public health attention and further development on occupational health interventions as climate change increases Thailand's temperatures.This study was supported by the International Collaborative Research Grants Scheme with joint grants from the Wellcome Trust UK (GR0587MA) and the Australian NHMRC (268055)

Contribution of time of day and the circadian clock to the heat stress responsive transcriptome in Arabidopsis.

In Arabidopsis, a large subset of heat responsive genes exhibits diurnal or circadian oscillations. However, to what extent the dimension of time and/or the circadian clock contribute to heat stress responses remains largely unknown. To determine the direct contribution of time of day and/or the clock to differential heat stress responses, we probed wild-type and mutants of the circadian clock genes CCA1, LHY, PRR7, and PRR9 following exposure to heat (37 °C) and moderate cold (10 °C) in the early morning (ZT1) and afternoon (ZT6). Thousands of genes were differentially expressed in response to temperature, time of day, and/or the clock mutation. Approximately 30% more genes were differentially expressed in the afternoon compared to the morning, and heat stress significantly perturbed the transcriptome. Of the DEGs (~3000) specifically responsive to heat stress, ~70% showed time of day (ZT1 or ZT6) occurrence of the transcriptional response. For the DEGs (~1400) that are shared between ZT1 and ZT6, we observed changes to the magnitude of the transcriptional response. In addition, ~2% of all DEGs showed differential responses to temperature stress in the clock mutants. The findings in this study highlight a significant role for time of day in the heat stress responsive transcriptome, and the clock through CCA1 and LHY, appears to have a more profound role than PRR7 and PRR9 in modulating heat stress responses during the day. Our results emphasize the importance of considering the dimension of time in studies on abiotic stress responses in Arabidopsis

Whole-body heat stress and exercise stimulate the appearance of platelet microvesicles in plasma with limited influence of vascular shear stress

Intense, large muscle mass exercise increases circulating microvesicles, but our understanding of microvesicle dynamics and mechanisms inducing their release remains limited. However, increased vascular shear stress is generally thought to be involved. Here, we manipulated exercise-independent and exercise-dependent shear stress using systemic heat stress with localized single-leg cooling (low shear) followed by single-leg knee extensor exercise with the cooled or heated leg (Study 1, n = 8) and whole-body passive heat stress followed by cycling (Study 2, n = 8). We quantified femoral artery shear rates (SRs) and arterial and venous platelet microvesicles (PMV-CD41+) and endothelial microvesicles (EMV-CD62E+). In Study 1, mild passive heat stress while one leg remained cooled did not affect [microvesicle] (P ≥ 0.05). Single-leg knee extensor exercise increased active leg SRs by ~12-fold and increased arterial and venous [PMVs] by two- to threefold, even in the nonexercising contralateral leg (P < 0.05). In Study 2, moderate whole-body passive heat stress increased arterial [PMV] compared with baseline (mean±SE, from 19.9 ± 1.5 to 35.5 ± 5.4 PMV.μL-1.103, P < 0.05), and cycling with heat stress increased [PMV] further in the venous circulation (from 27.5 ± 2.2 at baseline to 57.5 ± 7.2 PMV.μL-1.103 during cycling with heat stress, P < 0.05), with a tendency for increased appearance of PMV across exercising limbs. Taken together, these findings demonstrate that whole-body heat stress may increase arterial [PMV], and intense exercise engaging either large or small muscle mass promote PMV formation locally and systemically, with no influence upon [EMV]. Local shear stress, however, does not appear to be the major stimulus modulating PMV formation in healthy humans

Phenotypic evidence for local adaptation to heat stress in the marine snail Chlorostoma (formerly Tegula) funebralis

Southern California (USA) populations of the intertidal marine snail Chlorostoma (formerly Tegula) funebralis generally occupy warmer climates and are exposed to high air temperatures during low tides more often than northern California populations. Available genetic data suggest there is extensive gene flow across a broad range of C. funebralis populations, so it is unclear if populations can adapt to differences in local environments. To test for population-specific responses to heat stress, three phenotypic assays were performed on three northern and on three southern populations of C. funebralis, after acclimation to common-garden conditions in the laboratory. Thermal drop-down, heat stress mortality, and heat stress reattachment assays were designed to evaluate ecologically relevant phenotypic responses to heat stress; these assays assessed tolerance during, mortality following, and speed of recovery following heat stress. The latter two tests indicate that southern populations consistently suffer significantly lower mortality and recover significantly more quickly following heat stress compared to northern populations. Hierarchical cluster analysis of stress response data clearly identified northern California and southern California regional groupings of populations. Thus, these results indicate that southern populations have higher tolerance to heat stress than northern populations and suggest that adaptation to local environmental differences can evolve despite moderate potential for larval dispersal in this species. Accounting for intraspecific population variation in thermal tolerance may provide important insights for predicting how species distributions will respond to global warming. © 2013 Elsevier B.V

Impact of phenylpropanoid compounds on heat stress tolerance in carrot cell cultures

The phenylpropanoid and flavonoid families include thousands of specialized metabolites that influence a wide range of processes in plants, including seed dispersal, auxin transport, photoprotection, mechanical support and protection against insect herbivory. Such metabolites play a key role in the protection of plants against abiotic stress, in many cases through their well-known ability to inhibit the formation of reactive oxygen species (ROS). However, the precise role of specific phenylpropanoid and flavonoid molecules is unclear. We therefore investigated the role of specific anthocyanins (ACs) and other phenylpropanoids that accumulate in carrot cells cultivated in vitro, focusing on their supposed ability to protect cells from heat stress. First we characterized the effects of heat stress to identify quantifiable morphological traits as markers of heat stress susceptibility. We then fed the cultures with precursors to induce the targeted accumulation of specific compounds, and compared the impact of heat stress in these cultures and unfed controls. Data modeling based on Projection to Latent Structures (PLS) regression revealed that metabolites containing coumaric or caffeic acid, including ACs, correlate with less heat damage. Further experiments suggested that one of the cellular targets damaged by heat stress and protected by these metabolites is the actin microfilament cytoskeleton

On thermal stress failure of the SNAP-19A RTG heat shield

Results of a study on thermal stress problems in an amorphous graphite heat shield that is part of the launch-abort protect system for the SNAP-19A radio-isotope thermoelectric generators (RTG) that will be used on the Viking Mars Lander are presended. The first result is from a thermal stress analysis of a full-scale RTG heat source that failed to survive a suborbital entry flight test, possibly due to thermal stress failure. It was calculated that the maximum stress in the heat shield was only 50 percent of the ultimate strength of the material. To provide information on the stress failure criterion used for this calculation, some heat shield specimens were fractured under abort entry conditions in a plasma arc facility. It was found that in regions free of stress concentrations the POCO graphite heat shield material did fracture when the local stress reached the ultimate uniaxial stress of the material

Simplified method measures changes in tensile yield strength using least number of specimens

Simplified method determines yield strength due to heat treat, irradiation or mechanical treatment. Each specimen in a group of specimens is tested for yield stress point, subjected to heat treat or irradiation, and retested for new yield stress point which is a measure of change in material

The Skn7 Response Regulator of \u3ci\u3eSaccharomyces cerevisiae\u3c/i\u3e Interacts with Hsf1 In Vivo and Is Required for the Induction of Heat Shock Genes by Oxidative Stress

The Skn7 response regulator has previously been shown to play a role in the induction of stress-responsive genes in yeast, e.g., in the induction of the thioredoxin gene in response to hydrogen peroxide. The yeast Heat Shock Factor, Hsf1, is central to the induction of another set of stress-inducible genes, namely the heat shock genes. These two regulatory trans-activators, Hsf1 and Skn7, share certain structural homologies, particularly in their DNA-binding domains and the presence of adjacent regions of coiled-coil structure, which are known to mediate protein–protein interactions. Here, we provide evidence that Hsf1 and Skn7 interact in vitro and in vivo and we show that Skn7 can bind to the same regulatory sequences as Hsf1, namely heat shock elements. Furthermore, we demonstrate that a strain deleted for the SKN7 gene and containing a temperature-sensitive mutation in Hsf1 is hypersensitive to oxidative stress. Our data suggest that Skn7 and Hsf1 cooperate to achieve maximal induction of heat shock genes in response specifically to oxidative stress. We further show that, like Hsf1, Skn7 can interact with itself and is localized to the nucleus under normal growth conditions as well as during oxidative stress