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Migrating adult Pacific salmon (Oncorhynchus spp.) are sensitive to warm water (>18[degrees]C), with a range of consequences from decreased spawning success to early mortality. We examined the proportion of Yukon River Chinook salmon (O. tshawytscha) exhibiting evidence of heat stress to assess the potential that high temperatures contribute to freshwater adult mortality in a northern Pacific salmon population. Water temperatures greater than 18[degrees]C have occurred almost annually in the Yukon River and correspond with low population abundance since the 1990s. Using gene transcription products and heat shock protein 70 biomarkers validated by field experiment, we identified heat stress in half of Chinook salmon examined (54%, n = 477) across three mainstem locations and three tributaries in 2016-2017. Biomarkers tracked wide variation in water temperature (14-23[degrees]C) within a tributary. The proportion of salmon with heat stress differed between years at four of the six locations, with more prevalent heat stress in the warmer year. This work demonstrates that warming water temperatures are currently affecting northern populations of Pacific salmon. Les saumons du Pacifique (Oncorhynchus spp.) en migration sont sensibles a l'eau chaude (>18[degrees]C), les consequences pouvant aller d'une diminution du succes du frai a une mortalite precoce. Nous avons examine la proportion de saumons chinooks (O. tshawytscha) du fleuve Yukon qui presentent des indices de stress thermique afin d'evaluer la possibilite que des temperatures elevees jouent un role dans la mortalite en eau douce des adultes dans une population septentrionale de saumons de Pacifique. Des temperatures de l'eau superieures a 18[degrees]C se sont produites presque chaque annee dans le fleuve Yukon et correspondent a de faibles abondances de la population depuis les annees 1990. En utilisant des biomarqueurs de produits de transcription genique et de la proteine de choc thermique 70 valides par une experience de terrain, nous avons releve un stress thermique chez la moitie des saumons chinooks examines (54 %, n = 477) dans trois sites du cours principal et dans trois affluents, en 2016-2017. Les biomarqueurs temoignent de grandes variations de la temperature de l'eau (14-23[degrees]C) au sein d'un affluent. La proportion des saumons presentant un stress thermique differe entre les deux annees dans quatre des six sites, la prevalence du stress thermique etant plus grande durant l'annee plus chaude. Ces travaux demontrent que la hausse des temperatures de l'eau a actuellement une incidence sur les populations septentrionales de saumons du Pacifique. [Traduit par la Redaction], Introduction Air temperatures in the Arctic have warmed by more than 2[degrees]C since the late 19th century, disproportionally higher than the 0.8[degrees]C rise globally during the same time period (Post [...]

As much as 50% of cardiac output can be distributed to the skin in the hyperthermic human, and therefore the control of cutaneous vascular conductance (CVC) becomes critical for the maintenance of blood pressure. Little is known regarding the magnitude of cutaneous vasoconstriction in profoundly hypotensive individuals while heat stressed. This project investigated the hypothesis that leading up to and during syncopal symptoms associated with combined heat and orthostatic stress, reductions in CVC are inadequate to prevent syncope. Using a retrospective study design, we evaluated data from subjects who experienced syncopal symptoms during lower body negative pressure (N = 41) and head-up tilt (N = 5). Subjects were instrumented for measures of internal temperature, forearm skin blood flow, arterial pressure, and heart rate. CVC was calculated as skin blood flow/mean arterial pressure x 100. Data were obtained while subjects were normothermic, immediately before an orthostatic challenge while heat stressed, and at 5-s averages for the 2 min preceding the cessation of the orthostatic challenge due to syncopal symptoms. Whole body heat stress increased internal temperature (1.25 [+ or -] 0.3[degrees]C; P < 0.001) and CVC (29 [+ or -] 20 to 160 [+ or -] 58 CVC units; P < 0.001) without altering mean arterial pressure (83 [+ or -] 7 to 82 [+ or -] 6 mmHg). Mean arterial pressure was reduced to 57 [+ or -] 9 mmHg (P < 0.001) immediately before the termination of the orthostatic challenge. At test termination, CVC decreased to 138 [+ or -] 61 CVC units (P < 0.001) relative to before the orthostatic challenge but remained approximately fourfold greater than when subjects were normothermic. This negligible reduction in CVC during pronounced hypotension likely contributes to reduced orthostatic tolerance in heat-stressed humans. Given that lower body negative pressure and head-up tilt are models of acute hemorrhage, these findings have important implications with respect to mechanisms of compromised blood pressure control in the hemorrhagic individual who is also hyperthermic (e.g., military personnel, firefighters, etc.). skin blood flow; baroreceptors; hyperthermia; orthostasis doi: 10.1152/ajpheart.00290.2010.

Objectives. We compared the ability of several heat--health warning systems to predict days of heat-associated mortality using common data sets. Methods. Heat-health warning systems initiate emergency public health interventions once forecasts have identified weather conditions to breach predetermined trigger levels. We examined 4 commonly used trigger-setting approaches: (1) synoptic classification, (2) epidemiologic assessment of the temperature--mortality relationship, (3) temperature--humidity index, and (4) physiologic classification. We applied each approach in Chicago, Illinois; London, United Kingdom; Madrid, Spain; and Montreal, Canada, to identify days expected to be associated with the highest heat-related mortality. Results. We found little agreement across the approaches in which days were identified as most dangerous. In general, days identified by temperature-mortality assessment were associated with the highest excess mortality. Conclusions. Triggering of alert days and ultimately the initiation of emergency responses by a heat-health warning system varies significantly across approaches adopted to establish triggers. (Am J Public Health. 2010;100: 1137-1144. doi: 10.2105/AJPH.2009.169748)

Extreme heat during certain days of the summer renders pigs susceptible to severe heat stress, which negatively affects their growth performance. We hypothesized that such heat stress impaired the small intestinal mucosa, a site responsible for nutrient absorption. To simulate heat stress, Chinese experimental mini-pigs were treated with 5 h of continual 40[degrees]C temperature each day for 10 d in succession. Pigs were killed at 1, 3, 6 and 10 d after treatment, and small intestinal epithelia were sampled for histochemical examination and biochemical analyses. The duodenum and jejunum were seriously damaged within 3 d of initiation of treatment. Subsequent study of the process of jejunum recovery showed that the initiation of recovery started within 6 d following heat stress, Such damage was associated with the downregulation of epithelial growth factor signaling. In conclusion, heat stress induced short-term damage to the epithelium of porcine intestine, Because the intestinal epithelium is crucial for nutrient uptake, such damage should partially account for the impairment of growth performance of pigs under heat stress. Key words: epithelial growth factor, gene expression, heat stress, intestinal mucosa, swine

This study tested the hypothesis that passive heating impairs cerebral autoregulation. Transfer function analyses of resting arterial blood pressure and middle cerebral artery blood velocity (MCA [V.sub.mean]), as well as MCA [V.sub.mean] and blood pressure responses to rapid deflation of previously inflated thigh cuffs, were examined in nine healthy subjects under normothermic and passive heat stress (increase core temperature 1.1 [+ or -] 0.2[degrees]C, P < 0.001) conditions. Passive heating reduced MCA [V.sub.mean] [change ([DELTA]) of 8 [+ or -] 8 cm/s, P = 0.01], while blood pressure was maintained ([DELTA] - 1 [+ or -] 4 mmHg, P = 0.36). Coherence was decreased in the very-low-frequency range during heat stress (0.57 [+ or -] 0.13 to 0.26 [+ or -] 0.10, P = 0.001), but was >0.5 and similar between normothermia and heat stress in the low- (0.07-0.20 Hz, P = 0.40) and high-frequency (0.20-0.35 Hz, P = 0.12) ranges. Transfer gain was reduced during heat stress in the very-low-frequency (0.88 [+ or -] 0.38 to 0.59 [+ or -] 0.19 cm x [s.sup.-1] x [mmHg.sup.-1], P = 0.02) range, but was unaffected in the low-and high-frequency ranges. The magnitude of the decrease in blood pressure (normothermia: 20 [+ or -] 4 mmHg, heat stress: 19 [+ or -] 6 mmHg, P = 0.88) and MCA [V.sub.mean] (13 [+ or -] 4 to 12 [+ or -] 6 cm/s, P = 0.59) in response to cuff deflation was not affected by the thermal condition. Similarly, the rate of regulation of cerebrovascular conductance (CBVC) after cuff release (0.44 [+ or -] 0.22 to 0.38 [+ or -] 0.13 [DELTA]CBVC units/s, P = 0.16) and the time for MCA [V.sub.mean] to recover to precuff deflation baseline (10.0 [+ or -] 7.9 to 8.7 [+ or -] 4.9 s, P = 0.77) were not affected by heat stress. Counter to the proposed hypothesis, similar rate of regulation responses suggests that heat stress does not impair the ability to control cerebral perfusion after a rapid reduction in perfusion pressure, while reduced transfer function gain and coherence in the very-low-frequency range during heat stress suggest that dynamic cerebral autoregulation is improved during spontaneous oscillations in blood pressure within this frequency range. brain blood flow; heating; transfer function; blood pressure

During a whole body heat stress, stroke volume is either maintained or slightly elevated despite reduced ventricular filling pressures and central blood volume, suggestive of improved cardiac diastolic and/or systolic function. Heat stress improves cardiac systolic and diastolic function in patients with congestive heart failure, although it remains unknown whether similar responses occur in healthy individuals, which is the hypothesis to be tested. Nine male volunteers underwent a whole body heat stress. Echocardiographic indexes of diastolic and systolic function were performed following a supine resting period, and again following an increase in internal temperature of ~ 1.0[degrees]C via passive heat stress. Despite previous reports of heat stress-induced decreases in ventricular filling pressures and central blood volume, no changes in indexes of diastolic function were identified during heating [i.e., unchanged early diastolic mitral annular tissue velocity (E'), mitral inflow during the early diastolic phase (E), the E/E' ratio, and isovolumetric relaxation time]. Heat stress increased late diastolic septal (P = 0.03) and lateral (P = 0.0l) mitral annular tissue velocities (A'), mitral inflow velocity during atrial contraction (P < 0.001), and the relative contribution of atrial contraction to left ventricular filling during diastole (P = 0.01), all indicative of improved atrial systolic function. Furthermore, indexes of ventricular systolic function were increased by heat stress [i.e., increased septal (P = 0.001) and lateral (P = 0.01) mitral annular systolic velocities and isovolumic acceleration at the septal (P = 0.03) and lateral (P < 0.001) mitral annulus]. These data are suggestive of improved atrial and ventricular systolic function by the heat stress. Together these data support previous findings, which used the less precise measure of ejection fraction, that heat stress improves indexes of systolic function, while diastolic function is maintained. cardiac systolic function; stroke volume

Cotton (Gossypium hirsutum L.) seedlings are considered to be sensitive to temperature stress. The exposure of plants to high and low temperatures can result in the production of reactive oxygen species that contribute to diminished plant performance. Plants have mechanisms that metabolize oxidants into less harmful chemicals, and enhancement of antioxidant metabolism has been shown to be beneficial to plants exposed to acute oxidative stresses. Transgenic overexpression of glutathione reductase (GR) in cotton could result in faster seedling emergence at nonoptimal temperatures. Transgenic GR and 5 nontransgenic cotton lines were planted at four dates in the field in Lubbock, TX, and in constant temperature growth boxes. The temperatures in the field were typical for the cotton planting period in the region, and in growth boxes ranged from 15 to 45[degrees]C. Emergence rates were determined for all lines, and the activity of GR and the levels of malondialdehyde in the cotyledons were monitored to verify altered enzyme activity and to detect differences in oxidative damage, respectively. Enhancement of GR activity did not improve emergence or reduce oxidative damage. It is concluded that GR activity did not limit emergence.

The objectives of this study were 1) to investigate if there were differences in the relation between temperature and reproductive performance traits in 2 different sow lines, a Yorkshire line producing mainly in temperate climates and a Large White line producing mainly in warm climates, and 2) to determine the upper critical temperature (UCT) for the reproductive performance of these 2 lines. Sows are exposed to heat stress when temperature exceeds the UCT of the thermo-neutral zone. Data included 32,631 observations on reproductive performance from 11,935 sows on 20 farms in Spain, collected from 2003 to 2005. Sows belonged to 2 different purebred sow lines, named D (Yorkshire sow line, producing mainly in temperate climates) and I (Large White sow line, producing mainly in warm climates). Only first insemination records per parity were used and were combined with the maximum outside temperature at day of insemination. Upper critical temperatures were studied for 3 reproduction traits: farrowing rate (0 or 1), litter size (range from 1 to 25), and total number of piglets born per first insemination (combination of farrowing rate and litter size, range from 0 to 25). Data were corrected for fixed effects, which included parity, service sire, and an interaction between farm and year. Corrected data were used as observations in the models to study the effect of outside temperature on reproductive performance. Two models were compared for goodness of fit: a linear regression model and a plateau-linear model with the plateau representing the thermo-neutral zone and a linear decrease above that zone. Farrowing rate of I-line sows was not affected by temperature. For litter size and total number born per first insemination of I-line sows no UCT could be estimated. These traits were linearly affected by temperature. For all 3 reproduction traits of the D-line the best model was the plateau-linear model; the UCT for the D-line sows was estimated to be 19.2[degrees]C for farrowing rate, 21.7[degrees]C for litter size, and 19.6[degrees]C for total number born per first insemination. The decrease in reproductive performance of I-line sows with increasing outside temperature was less than in D-line sows. From this study it can be concluded that there are differences in heat stress tolerance between sow lines as measured by the differences in reproductive performance. These differences are an indication of genetic differences in heat stress tolerance in sow lines. Key words: heat stress, reproductive performance, sow, sow line, upper critical temperature

In plants, heat stress responses are controlled by heat stress transcription factors that are conserved among all eukaryotes and can be constitutively expressed or induced by heat. Heat-inducible transcription factors that are distinct from the 'classical' heat stress transcription factors have also been reported to contribute to heat tolerance. Here, we show that bZIP28, a gene encoding a putative membrane-tethered transcription factor, is up-regulated in response to heat and that a bZIP28 null mutant has a striking heat-sensitive phenotype. The heat-inducible expression of genes that encode BiP2, an endoplasmic reticulum (ER) chaperone, and HSP26.5-P, a small heat shock protein, is attenuated in the bZIP28 null mutant. An estradiol-inducible bZIP28 transgene induces a variety of heat and ER stress-inducible genes. Moreover, heat stress appears to induce the proteolytic release of the predicted transcription factor domain of bZIP28 from the ER membrane, thereby causing its redistribution to the nucleus. These findings indicate that bZIP28 is an essential component of a membrane-thethered transcription factor-based signaling pathway that contributes to heat tolerance. BiP2 | bZIP28 | endoplasmic reticulum | signal transduction | thermotolerance

The objective of this study was to quantify the effect of heat stress during the life of a pig on its final weight, as a first step toward a genetic evaluation for heat tolerance. Data included carcass weights of 23,556 crossbred pigs [Duroc x (Landrace x Large White)] raised on 2 farms in North Carolina and slaughtered from May 2005 through December 2006. Weather data were available from a nearby weather station. Lifetime of a pig was assumed to be partitioned into 2 periods. During an initial period, the effect of heat stress was assumed to be negligible or compensated for later. During the second period ending in slaughtering, the ADG was assumed to be affected linearly by heat load. Weekly heat load was calculated as degrees of average temperature-humidity index in excess of a threshold (18[degrees]C). The total heat load (H) was the sum of weekly heat loads during the second period. During the months of January to May H was 0; H reached a peak in September. The final BW during the peak of heat stress decreased about 6 kg compared with BW during months of non-heat stress. Weekly and monthly averages of carcass weight generally moved similarly to H. However, there were large fluctuations unrelated to H; the fluctuations were different on the 2 farms. The model included the effects of farm-year of slaughter, sex, age at slaughter, and H, where age at slaughter and H were linear regressions. In analyses, the threshold was varied from 16 to 20[degrees]C, and the second period was varied from 8 to 16 wk. The greatest [R.sup.2] (10.4%) was at the threshold of temperature-humidity index = 18[degrees]C for a period of 10 wk. Varying the threshold and the length of time reduced [R.sup.2] less than 1%. Least squares means of year-month and year-week of carcass weight were calculated using a model with the fixed effects farm-year-month or farm-year-week of slaughter, sex, and age at slaughter (linear covariate), and the random effect of birth litter. Changes in BW of finisher pigs due to heat stress can be quantified by H during the last 10 wk of the life of the pig. Key words: carcass weight, heat stress, pig

The objective of this study was to describe genetic variability of pig carcass weight as a function of heat stress. Data included carcass weights of 23,556 crossbred pigs [Duroc x (Landrace x Large White)] raised on 2 farms in North Carolina and harvested from May 2005 through December 2006. Weather data were obtained from a weather station located about 20 km from the furthest farm. Weekly heat load was calculated as degrees of average temperature-humidity index (THI) in excess of 18[degrees]C. The total heat load (H) was the sum of heat loads for 10 wk before harvest. Variance components were estimated with 3 models: univariate (UNI)--not accounting for heat stress, 2-trait (MT2), and random regression (RR). In all of the models, effects included contemporary group, sex, age at harvest, sire, and litter. In MT2, observations in months in which heat stress was observed ('hot') and not observed ('cold') were treated as separate traits. Heat stress was observed in the months of August to November 2005, as well as July to October 2006. No heat stress was observed in the months of May to July 2005, January to June 2006, and November to December 2006. The RR model added a random regression on heat load for the sire effect. Heat load was adjusted to a scale ranging from 0 (no heat stress) to 5 (greatest heat stress). The heritability estimate [+ or -] SE of carcass weight in UNI was 0.17 [+ or -] 0.01. In MT2, the estimates were 0.14 [+ or -] 0.01 for 'cold' and 0.28 [+ or -] 0.01 for 'hot'; the genetic correlation between carcass weight in 'hot' and 'cold' months was 0.42 [+ or -] 0.13. The heritability estimates obtained with RR were 0.20 [+ or -] 0.11, 0.19 [+ or -] 0.15, and 0.51 [+ or -] 0.17 for H = 0, 2.5, and 5, respectively. The genetic correlation between the performance in 'cold' months (H = 0), and performance under maximum heat load (H = 5) was 0.02, between H = 0 and intermediate heat load (H = 2.5) was 0.52, and between H = 2.5 and H = 5 was 0.86. Rank correlations between EPD derived from the different models ranged from 0.82 to 0.94 between carcass weights under similar H, 0.18 to 0.54 between carcass weights under high and low H, and 0.66 to 0.91 between carcass weights of intermediate and high/low H. Heritability for growth was greater under heat stress. Selection for crossbred performance would be optimal when data for periods both in the absence and presence of heat stress were considered. Key words: carcass weight, genetic parameter, heat stress, pig, random regression

U-shaped dose-response relationships (hormesis) have been documented in numerous biological, toxicological, and pharmacological investigations. For example, in response to a mild 35[degrees]C heat shock, the longevity of Caenorhabditis elegans exhibits an inverted U-shaped dose-response. By applying the demographic concept of heterogeneity, we find that this U-shaped curve for longevity response is driven by a U-shaped dose-response of initial mortality. When worms are subjected to mild heat shock, the initial mortality decreases compared to the control. This initial mortality benefit increases with moderate increases in the length of heat shock, peaking at a point that coincides with the induction of damage to the worms. The dose of heat shock that coincided with this benefit in initial mortality did not affect the rate of increase in mortality. Key Words: Hidden heterogeneity--Initial mortality--U-shaped response--Heat shock--Caenorhabditis elegans.

Introduction Environmental heat is a natural and anthropogenically enhanced hazard with well-documented adverse impacts on human health and well-being (Gasparrini et al. 2015; Parsons 2014). Despite decades of physiological, epidemiological, [...], Background: Environmental heat exposure is a public health concern. The impacts of environmental heat on mortality and morbidity at the population scale are well documented, but little is known about specific exposures that individuals experience. Objectives: The first objective of this work was to catalyze discussion of the role of personal heat exposure information in research and risk assessment. The second objective was to provide guidance regarding the operationalization of personal heat exposure research methods. DISCUSSION: We define personal heat exposure as realized contact between a person and an indoor or outdoor environment that poses a risk of increases in body core temperature and/or perceived discomfort. Personal heat exposure can be measured directly with wearable monitors or estimated indirectly through the combination of time-activity and meteorological data sets. Complementary information to understand individual-scale drivers of behavior, susceptibility, and health and comfort outcomes can be collected from additional monitors, surveys, interviews, ethnographic approaches, and additional social and health data sets. Personal exposure research can help reveal the extent of exposure misclassification that occurs when individual exposure to heat is estimated using ambient temperature measured at fixed sites and can provide insights for epidemiological risk assessment concerning extreme heat. CONCLUSIONS: Personal heat exposure research provides more valid and precise insights into how often people encounter heat conditions and when, where, to whom, and why these encounters occur. Published literature on personal heat exposure is limited to date, but existing studies point to opportunities to inform public health practice regarding extreme heat, particularly where fine-scale precision is needed to reduce health consequences of heat exposure. https://doi.org/10.1289/EHP556

High temperature stress imposed during the cell division stage of maize (Zea mays L.) kernel development adversely affects growth and mature mass. However, the processes affected by heat stress are not known. The goal of this study was to determine the mechanisms by which heat stress affects early zein accumulation in maize kernels. Intact ears of growth chamber-grown plants were subjected to heat stress (continuous 35[degrees]C) for 2 or 4 d, starting at 5 d after pollination (DAP). Both the 27 kDa and cluster 1 zeins of subfamily 4 (ZSF4C1) zein mRNA steady-state levels were significantly delayed by 4 d of heal stress (DHS), but were not affected by 2 DHS. Similarly, transcription rates of both zeins were reduced in the endosperm of kernels exposed to 4 DHS treatment up to 17 DAP. The 2 DHS treatment significantly delayed endosperm endoreduplication, up to 17 DAP, whereas 4 DHS significantly repressed it. The lack of coordinate changes among mRNA steady-state levels, transcription rates, and endoreduplication during heat stress indicates that the effects of heat stress on zein transcription rates may not be directly related to alterations in endoreduplication. Instead, zein transcription is most likely affected by a delay in endosperm development.

In humans, the nocturnal fall in internal temperature is associated with increased endogenous melatonin and with a shift in the thermoregulatory control of skin blood flow (SkBF), suggesting a role for melatonin in the control of SkBF. The purpose of this study was to test whether daytime exogenous melatonin would shift control of SkBF to lower internal temperatures during heat stress, as is seen at night. Healthy male subjects (n = 8) underwent body heating with melatonin administration (Mel) or without (control), in random order at least 1 wk apart. SkBF was monitored at sites pretreated with bretylium to block vasoconstrictor nerve function and at untreated sites. Cutaneous vascular conductance, calculated from SkBF and arterial pressure, sweating rate (SR), and heart rate (HR) were monitored. Skin temperature was elevated to 38[degrees]C for 35-50 min. Baseline esophageal temperature ([T.sub.es]) was lower in Mel than in control (P < 0.01). The [T.sub.es] threshold for cutaneous vasodilation and the slope of cutaneous vascular conductance with respect to [T.sub.es] were also lower in Mel at both untreated and bretylium-treated sites (P < 0.05). The [T.sub.es] threshold for the onset of sweating and the [T.sub.es] for a standard HR were reduced in Mel. The slope of the relationship of HR, but not SR, to [T.sub.es] was lower in Mel (P < 0.05). These findings suggest that melatonin affects the thermoregulatory control of SkBF during hyperthermia via the cutaneous active vasodilator system. Because control of SR and HR are also modified, a central action of melatonin is suggested. circadian rhythm; skin blood flow; sweating; thermoregulation doi: 10.1152/ajpregu.00117.2006.

Glutamine (GLN) has been shown to protect cells, tissues, and whole organisms from stress and injury. Enhanced expression of heat shock protein (HSP) has been hypothesized to be responsible for this protection. To date, there are no clear mechanistic data confirming this relationship. This study tested the hypothesis that GLN-mediated activation of the HSP pathway via heat shock factor-1 (HSF-1) is responsible for cellular protection. Wild-type HSF-1 (HSF-[1.sup.+/+]) and knockout (HSF-[1.sup-/-]) mouse fibroblasts were used in all experiments. Cells were treated with GLN concentrations ranging from 0 to 16 mM and exposed to heat stress injury in a concurrent treatment model. Cell viability was assayed with phenazine methosulfate plus tetrazolium salt, HSP-70, HSP-25, and nuclear HSF-1 expression via Western blot analysis, and HSF-1/heat shock element (HSE) binding via EMSA. GLN significantly attenuated heat-stress induced cell death in HSF-[1.sup.+/+] cells in a dose-dependent manner: however, the survival benefit of GLN was lost in HSF-[1.sup-/-] cells. GLN led to a dose-dependent increase in HSP-70 and HSP-25 expression after heat stress. No inducible HSP expression was observed in HSF-[1.sup.-/-] cells. GLN increased unphosphorylated HSF-1 in the nucleus before heat stress. This was accompanied by a GLN-mediated increase in HSF-1/HSE binding and nuclear content of phosphorylated HSF-1 after heat stress. This is the first demonstration that GLN-mediated cellular protection after heat-stress injury is related to HSF-1 expression and cellular capacity to activate an HSP response. Furthermore, the mechanism of GLN-mediated protection against injury appears to involve an increase in nuclear HSF-1 content before stress and increased HSF-1 promoter binding and phosphorylation. knockout cells; amino acid; heat stress mechanism

Two experiments were conducted to investigate the physiological responses of Bos taurus (Angus cross, n = 6) and Bos indicus (Brahman, n = 6) cattle to prolonged heat and humidity, as can occur during live export by sea. Each experiment was carried out in climate-controlled rooms, where heifers were exposed to 15 d of sustained heat and humidity. The treatment was designed to be representative of a long-haul, live-export voyage leaving a southern Australian winter and traveling to a Middle Eastern summer. Wet bulb temperature (WBT) was used to give a combined measure of dry bulb temperature and relative humidity and was increased over several days, culminating in 5 d at 32[degrees]C WBT between d 7 and 11. By d 11, the respiratory rate and core body temperature increased (P < 0.001) compared with values at lower ambient temperature on d 1 and 2 when climate-controlled rooms were not operating. Feed intake of Bos taurus was reduced (P < 0.001) by d 11, whereas that of Bos indicus did not change (P = 0.14). Despite no diurnal variation in climatic conditions, core body temperature of both Bos taurus and Bos indicus continued to show a circadian amplitude of approximately 1[degrees]C throughout the hottest period. This amplitude increased during the recovery period after heat was removed (up to 1.8[degrees]C for Bos indicus and 1.6[degrees]C for Bos taurus). Water intake for both Bos taurus and Bos indicus increased when WBT increased (P < 0.01 on d 11). Significant acid-base and blood electrolyte imbalances occurred in both Bos taurus and Bos indicus, with changes in Bos taurus being more substantial and prolonged. The increase in respiratory rate coincided with a decrease in the partial pressures of carbon dioxide and bicarbonate in venous blood. However, during the hottest period, average daily venous blood pH remained unchanged. When the heat load was reduced after d 11, the blood pH decreased, indicating metabolic acidosis. Blood pH declined from 7.44 to 7.36 for Bos taurus (P < 0.001) and from 7.44 to 7.38 for Bos indicus (P < 0.001). Other parameters measured include heart rate; packed cell volume; plasma and urine Na, K, and Cl; urine pH; and specific gravity. Our results suggest that Bos taurus cattle experience significant physiological changes during exposure to prolonged and continuous high heat and humidity, with alterations persisting for some days after the heat-stress conditions subside. Bos indicus experience similar but less pronounced physiological changes. Key words: acid-base, Bos indicus, Bos taurus, electrolyte, heat stress, temperature

Data from 3 summer feedlot studies were utilized to determine the environmental factors that influence heat stress in cattle and also to determine wind speed (WSPD; m x [s.sup.-1]) and solar radiation (RAD; W x [m.sup.-2]) adjustments to the temperature-humidity index (THI). Visual assessments of heat stress, based on panting scores (0 = no panting to 4 = severe panting), were collected from 1400 to 1700. Mean daily WSPD, black globe temperature at 1500, and minimums for nighttime WSPD, nighttime black globe THI, and daily relative humidity were found to have the greatest influence on panting score from 1400 to 1700 ([R.sup.2] = 0.61). From hourly values for THI, WSPD, and RAD, panting score was determined to equal -7.563 + (0.121 x THI) - (0.241 x WSPD) + (0.00082 x RAD) ([R.sup.2] = 0.49). Using the ratio of WSPD to THI and RAD to THI (-1.992 and 0.0068 for WSPD and RAD, respectively), adjustments to the THI were derived for WSPD and RAD. On the basis of these ratios and the average hourly data for 1400 to 1700, the THI, adjusted for WSPD and RAD, equals [4.51 + THI - (1.992 x WSPD) + (0.0068 x RAD)]. Four separate cattle studies, comparable in size, type of cattle, and number of observations to the 3 original studies, were utilized to evaluate the accuracy of the THI equation adjusted for WSPD and RAD, and the relationship between the adjusted THI and panting score. Mean panting score derived from individual observations of black-hided cattle in these 4 studies were 1.22, 0.94, 1.32, and 2.00 vs. the predicted panting scores of 1.15, 1.17, 1.30, and 1.96, respectively. Correlations between THI and panting score in these studies ranged from r = 0.47 to 0.87. Correlations between the adjusted THI and mean panting score ranged from r = 0.64 to 0.80. These adjustments would be most appropriate to use, within a day, to predict THI during the afternoon hours using hourly data or current conditions. In addition to afternoon conditions, nighttime conditions, including minimum WSPD, minimum black globe THI, and minimum THI, were also found to influence heat stress experienced by cattle. Although knowledge of THI alone is beneficial in determining the potential for heat stress, WSPD and RAD adjustments to the THI more accurately assess animal discomfort. Key words: bioclimatic index, cattle, environmental factor, feedlot, heat stress

In chickens, elevated environmental temperature reduces food intake. We have previously reported that, during heat stress, the intestinal mucosa has an increased capacity to take up sugars. To investigate whether the effects of warm environment on sugar uptake are an intestinal adaptation to lower energy intake or a response attributable to heat stress, we examined the glucose transport kinetics of apical and basolateral membranes of the jejunum and the mucosal morphology of broiler chickens maintained in climatic chambers for 2 wk. Experimental groups were 1) control ad libitum (CAL), fed ad libitum and in thermoneutral conditions (20[degrees]C); 2) heat stress ad libitum (HSAL), fed ad libitum and kept in a heated environment (30[degrees]C); and 3) control pair-fed (CPF), maintained in thermoneutral conditions and fed the same amount of food as that consumed by the HSAL group. Both the CPF and the HSAL groups showed reduced body weight gain, but only the HSAL chickens had lower plasma thyroid hormones and higher corticosterone than CAL and CPF groups. The fresh weight and length of the jejunum were only reduced in the HSAL group. The activity and expression of apical sodium-dependent glucose transporter l (SGLT-1) were increased by ~50% in the HSAL chickens, without effects in the CPF group. No changes in [K.sub.d] or in SGLT-1 and glucose transporter-2 [K.sub.m] were observed in the pair-fed and heated birds. These results support the view that increased intestinal hexose transport capacity is entirely dependent on adaptations of apical SGLT-1 expression to heat stress and is not due to reduced food intake. chronic heat exposure; glucose transporter 2; hexose transport; intestinal absorption; sodium-dependent glucose transporter 1

Battle may not worry about job security or credit history, but that doesn't mean their lives are stress free. For some cattle, rising stress levels correspond with rising temperatures. This [...]

Drosophila melanogaster is a widely used model for heat stress. Most studies, however, have subjected flies to a single bout of high temperature. In nature, developing larvae and pupae of D. melanogaster are likely to encounter high temperatures on a daily basis. We examined the effects of daily heat stress (35 minutes at 39[degrees]C) on larval development and adult body size and water balance. Heat-stressed larvae suffered >90% mortality and took 4 days longer to reach adulthood than unstressed controls. Surviving adults were 30% less resistant to desiccation stress than controls, due to significantly higher water-loss rates. The effects of heat stress were reversed by a daily one-hour pre-treatment at 36[degrees]C, followed by 35 minutes at 39[degrees]C. Pre-treated larvae developed nearly as rapidly as unstressed controls, achieved the same body size, and were equally resistant to desiccation. We propose that daily heat stress disrupts cuticular development, and that this damage is prevented by synthesis of heat-shock proteins at 36[degrees]C. Supported by NSF award 0110626 to AGG.