Convective heat transfer measured directly with a heat flux sensor

A heat flux disk has been developed that directly measures the convective heat transfer in W/m2. When the sensor is calibrated on an aluminum cylinder, the calibration constant obtained is greatest in still air. As air movement increases, the calibration constant is reduced with increasing convective heat transfer coefficient, 0.5%.W-1.m2.K. The influence of wind on the calibration value is greatly reduced when the sensor is attached to a surface with lower thermal conductivity. The local convective heat transfer coefficient (hc) of the human body was measured. The leg acts in a manner similar to that of a cylinder, with the highest hc value at the front facing the wind and the lowest approximately 90 degrees from the wind, and in the wake a value is obtained that is close to the average hc value of the leg. When hc is measured at several angles and positions all over the body, the results indicate that the body acts approximately as a cylinder with a hc value related to the wind speed as hc = 8.6.v0.6 W.m-2.K-1, where v is velocity.     

CHIP interacts with heat shock factor 1 during heat stress

Heat shock factor 1 (HSF1) is a major transactivator of heat shock genes in response to stress and mediates cell protection against various harmful conditions. In this study, we identified the interaction of CHIP (carboxyl terminus of the heat shock cognate protein 70-interacting protein) with the N-terminus of HSF1. Using GST full-down assay, we found that CHIP directly interacts with C-terminal deleted HSF1 (a.a. 1-290) but not with full-length HSF1 under non-stressed conditions. Interestingly, interaction of CHIP with full-length HSF1 was induced by heat shock treatment. The structural change of HSF1 was observed under heat stressed conditions by CD spectra. These observations demonstrate the direct interaction between HSF1 and CHIP and this interaction requires conformational change of HSF1 by heat stress.     

Isoproterenol sensitivity in heat tolerant and relatively heat intolerant men

Recent research has demonstrated that pharmacologic blockade of beta-adrenoceptors predisposes to hyperthermia during prolonged exercise. To investigate the hypothesis that beta-adrenoceptor sensitivity to catecholamines may be an important determinant of exertional heat tolerance, we performed a cross-sectional study comparing the heart rate responses to graded doses of isoproterenol in 6 heat tolerant and 6 relatively heat intolerant men. We observed no significant difference (p greater than 0.1) between the heat tolerant (0.9 +/- 0.68 microgram) and heat intolerant (1.19 +/- 0.61 microgram) subjects in the dose of isoproterenol that produced a 25 beat.min-1 increment in heart rate. Although the possibility of a relationship between beta-adrenoceptor sensitivity and the ability to tolerate exercise in heat cannot be entirely excluded on the basis of these data, our study clearly demonstrates the lack of a correlation between cardiac pacemaker sensitivity to isoproterenol and exertional heat tolerance.     

Extreme heat changes post‐heat wave community reassembly

Climate forecasts project further increases in extremely high‐temperature events. These present threats to biodiversity, as they promote population declines and local species extinctions. This implies that ecological communities will need to rely more strongly on recovery processes, such as recolonization from a meta‐community context. It is poorly understood how differences in extreme event intensity change the outcome of subsequent community reassembly and if such extremes modify the biotic environment in ways that would prevent the successful re‐establishment of lost species. We studied replicated aquatic communities consisting of algae and herbivorous rotifers in a design that involved a control and two different heat wave intensity treatments (29°C and 39°C). Animal species that suffered heat‐induced extinction were subsequently re‐introduced at the same time and density, in each of the two treatments. The 39°C treatment led to community closure in all replicates, meaning that a previously successful herbivore species could not re‐establish itself in the postheat wave community. In contrast, such closure never occurred after a 29°C event. Heat wave intensity determined the number of herbivore extinctions and strongly affected algal relative abundances. Re‐introduced herbivore species were thus confronted with significantly different food environments. This ecological legacy generated by heat wave intensity led to differences in the failure or success of herbivore species re‐introductions. Reassembly was significantly more variable, and hence less predictable, after an extreme heat wave, and was more canalized after a moderate one. Our results pertain to relatively simple communities, but they suggest that ecological legacies introduced by extremely high‐temperature events may change subsequent ecological recovery and even prevent the successful re‐establishment of lost species. Knowing the processes promoting and preventing ecological recovery is crucial to the success of species re‐introduction programs and to our ability to restore ecosystems damaged by environmental extremes.     

Evolving heat waves characteristics challenge heat warning systems and prevention plans

International Journal of Biometeorology - This paper analyses how recent trends in heat waves impact heat warning systems. We performed a retrospective analysis of the challenges faced by the...     

Solar heat load: heat balance during exercise in clothed subjects

Six subjects exercised for 60 min on a cycle ergometer. Their backs were exposed to an artificial 'sun' with a spectral distribution similar to sunlight and an intensity of 724 W m-2. Each subject took part in four experiments in random order: wearing suits of polyester (insulation value = 0.5 clo), white (WP) or black (BP), or cotton (0.6 clo), white (WC) or black (BC). Measured by partitional calorimetry, the calculated heat losses and gains for the four conditions balanced within less than 10%. The differences between the short-wave radiation gains of subjects in white or black garments were small. This is due to the transparency of the white materials, which allows a larger percentage of the radiation to penetrate the clothing. The surface temperatures of the sun-exposed areas were very high, especially in the black suits. This promotes dry heat loss. Therefore the sweat loss in the black suits and the differences between the black and white clothes became relatively small. The physiological strain in steady-state exercise, as expressed by average heart rates, was 142 (WP), 154 (BP), 151 (WC), and 160 (BC) beats min-1; the sweat losses were 649 (WP), 666 (BP), 704 (WC), and 808 (BC) g. For both of these measures values for white polyester were significantly less than those for black cotton.     

Molecular genetics of heat tolerance and heat shock proteins in cereals

Heat stress is common in most cereal-growing areas of the world. In this paper, we summarize the current knowledge on the molecular and genetic basis of thermotolerance in vegetative and reproductive tissues of cereals. Significance of heat stress response and expression of heat shock proteins (HSPs) in thermotolerance of cereal yield and quality is discussed. Major avenues for increasing thermotolerance in cereals via conventional breeding or genetic modification are outlined.     

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T+HE), dexamethasone (D+HE), and turpentine and dexamethasone combined (TD+HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T(c)) was 42 degrees C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T(c) 40 degrees C (T40), and 15 min after achieving T(c) 42 degrees C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD+HE rats (37.5%), followed by the HE (62.5%), T+HE (75%), and D+HE (100%) rats (P < 0.05). The duration of survival at T42 degrees C was shortest in the TD+HE rats (9.9 +/- 6.2 min) (P < 0.01), followed by the T+HE (11.3 +/- 6.1 min) and the HE (12.2 +/- 4 min) (P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T+HE (352%) and HE (178%) rats (P < 0.05). D+HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.     

Interaction of the Neurospora crassa heat shock factor with the heat shock element during heat shock and different developmental stages

The interaction of the heat shock factor (HSF) with the heat shock element (HSE) was determined by a non-radioactive electrophoretic mobility shift assay, in order to analyze HSF regulation in Neurospora crassa. HSF binds to HSE under normal, non-stress conditions and is thus constitutively trimerized. Upon heat shock, the HSF-HSE complex shows a retarded mobility. This was also observed in Saccharomyces cerevisiae, where this mobility shift was shown to be due to HSF phosphorylation [Sorger and Pelham (1988) Cell 54, 855-864]. In N. crassa, HSE-dependent electrophoretic mobility shift is temperature- and time-dependent. Under normal growth conditions, the HSF is located in the cytoplasm as well as in the nucleus. In germinating conidia the HSF shows a retarded mobility typical for heat shock even at normal growth temperatures. No HSF-dependent mobility shift was detectable in aerial hyphae.     

Birgean heat budgets and rates of heat uptake in two monomictic lakes

Thermal profile development, rates of heat uptake and annual heat budgets are presented for two monomictic lakes, Whatcom and Washington, in the Puget Sound lowlands of Washington State. The rates of heat gain in the lakes were found to be significantly affected by lake morphometry. In turn, the differing rates of heat gain affected the annual heat budgets.     

Elevation of the heat resistance of Salmonella typhimurium by sublethal heat shock

The survival of Salmonella typhimurium after a standard heat challenge at 55°C for 25 min increased by several orders of magnitude when cells grown at 37°C were pre-incubated at 42°, 45° or 48°C before heating at the higher temperature. Heat resistance increased rapidly after the temperature shift, reaching near maximum levels within 30 min. Elevated heat resistance persisted for at least 10 h. Preincubation of cells at 48°C for 30 min increased their resistance to subsequent heating at 50°, 52°, 55°, 57° or 59°C. Survival curves of resistant cells were curvilinear. Estimated times for a '7D' inactivation increased by 2.6- to 20-fold compared with cells not pre-incubated before heat challenge.     

Body heat balance in man subjected to endogenous and exogenous heat load

The body heat balance, measured by a thermometric method, was investigated in humans subjected to endogenous and exogenous heat load. The purpose of the present study was to test the concept of heat exchange by a servomechanism in human thermoregulation. Two series of experiments were performed on male volunteers. In series I 15 subjects performed physical exercise (50% VO2 max) for 60 min at a constant ambient temperature of 25 degrees C. In series II 16 subjects rested in a climatic chamber where the ambient temperature was elevated over 30 min from 22 to 42 degrees C and kept stable at this level during the subsequent 60 min. It was found that in both series of experiments the sweating rate followed an exponential curve exhibiting an inertial course. Heat was stored in the body mainly at the beginning of experiment. In series I the net body heat load of 125 W/m2 was equalized by sweat evaporation, beginning after 40 min of the exercise. In series II the net body heat load of 80 W/m2 was equalized in the same way, starting after 35 min of the constant high ambient temperature. In both series of experiments the amount of heat stored in the body calculated from the body heat balance was quite close to the amount of heat calculated from the calorimetric equation. It is concluded, that under the present experimental conditions, heat loss from the body by sweat evaporation seems to be a regulated variable in the human thermoregulatory system. The observed increase in rectal temperature may result from an inertial course of the sweating reaction.     

Elevation of the heat resistance of Salmonella typhimurium by sublethal heat shock

The survival of Salmonella typhimurium after a standard heat challenge at 55 degrees C for 25 min increased by several orders of magnitude when cells grown at 37 degrees C were pre-incubated at 42 degrees, 45 degrees or 48 degrees C before heating at the higher temperature. Heat resistance increased rapidly after the temperature shift, reaching near maximum levels within 30 min. Elevated heat resistance persisted for at least 10 h. Pre-incubation of cells at 48 degrees C for 30 min increased their resistance to subsequent heating at 50 degrees, 52 degrees, 55 degrees, 57 degrees or 59 degrees C. Survival curves of resistant cells were curvilinear. Estimated times for a '7D' inactivation increased by 2.6- to 20-fold compared with cells not pre-incubated before heat challenge.     

Brown adipose tissue heat production in heat acclimated and perchlorate treated rats

The noradrenaline-induced energy dissipation rate was measured with a direct microcalorimeter in brown adipose tissue taken from rats acclimated to 34 degrees C (HA), perchlorate treated (PC) and heat acclimated-perchlorate treated (HAPC). The response to 10(-7) M NA was reduced by 45%, 47% and 86% in HA, PC and HAPC groups, respectively, as compared to a control group kept at 24 degrees C. In the same groups, the response to 10(-6) M NA was reduced by 34%, 7% and 64%, respectively. The specific activity of the soluble alpha-glycerophosphate dehydrogenase in brown fat from HA rats was reduced by 50%, whereas it was not altered in the PC animals. It is concluded that the sensitivity to noradrenaline of the brown adipose tissue thermogenic mechanisms is decreased in hypothyroidism, and that the acclimation temperature and the thyroid status per se each have a different influence on brown adipose tissue function.