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PubMed1976

Cutaneous heat flow during heating and cooling in Alligator mississipiensis.

Direct in vivo measurement of heat flow across the skin of the American alligator (Alligator mississipiensis) showed increased heat flow during warming. Mean values at 25 degrees C during warming (15-35 degrees C) in air (airspeed 300 cm/s) were 17.9 +/- 92 SE cal/cm2 per h (mean alligator wt 3.27 kg). Cooling heat flow at the same temperature was 13.6 +/- 0.57 cal/cm2 per h. Subdermal heat flow was reduced during warming and was not significantly different from cutaneous heat flow during cooling. This indicated that the alligator was able to control its rate of heat exchange with the environment by altering cutaneous perfusion. Atropine, phenoxybenzamine, nitroglycerin, and Xylocaine did not affect cutaneous heat flow or heating and cooling rates. Atropine blocked bradycardia during cooling.

Alligators and Crocodiles↗
PubMed1998

Capsaicin activates heat loss and heat production simultaneously and independently in rats.

Subcutaneous administration of capsaicin (5 mg/kg) immediately increased the temperature of the tail skin (Tsk) for 2 h in urethan-anesthetized rats, suggesting an increase in heat loss. O2 consumption, an index of heat production, also immediately increased after the capsaicin injection, and this increase lasted for >10 h. Colonic temperature (Tco) decreased within 1 h after the injection, and this decrease was followed by a long-lasting hyperthermic period. Adrenal demedullation largely attenuated the capsaicin-induced increase in O2 consumption, and sympathetic denervation of the interscapular brown adipose tissue partly attenuated the increase in O2 consumption. However, capsaicin-induced heat loss was normal in these rats. In rats with cutaneous vasodilation maximized by warming and administration of hexamethonium, capsaicin did not further increase Tsk but normally induced heat production, and Tco gradually rose without a hypothermic period. Thus capsaicin simultaneously increased heat loss and heat production, and inhibition of one response did not affect the other. These findings suggest that capsaicin simultaneously activates independent networks for heat loss and heat production.

Adipose Tissue, Brown↗
PubMed1984

Heat exchange following atropine injection before and after heat acclimation.

The effect of saline and atropine injection (2 mg, im) on eight healthy male subjects before and after heat acclimation was studied while each subject walked on a treadmill (1.34 m X s-1) in a hot-dry environment (ambient temperature = 48.4 degrees C, dew-point temperature = 20.5 degrees C). Partitional calorimetric analysis was done for the periods in which maximum sweat inhibition occurred (30 min). Mean skin temperature, rectal temperature, and heart rate were continuously observed. Evaporative loss from the skin was calculated by changes in body weight (Sauter balance); heat transfer coefficients were defined by Nishi equations. A prediction of sweat inhibition based on an analysis of heat storage and its effect on a theoretical temperature, which can be graphed on a psychrometric chart, was developed. A rational effective temperature (ET) defined as the operative temperature at the intersection of the 50% rh, which encompasses total heat exchange, was used to compare the effects of atropine before and after heat acclimation. The results show that heat acclimation reduced ET by approximately 2.5 degrees C when compared with the unacclimated state after atropine injection. Thus heat acclimation reduces the hazards of heatstroke caused by exercise in the heat with atropine injection.

Acclimatization↗
PubMed2005

Heat shock protein and heat shock factor 1 expression and localization in vaccinia virus infected human monocyte derived macrophages.

BACKGROUND: Viruses remain one of the inducers of the stress response in the infected cells. Heat shock response induced by vaccinia virus (VV) infection was studied in vitro in human blood monocyte derived macrophages (MDMs) as blood cells usually constitute the primary site of the infection. METHODS: Human blood monocytes were cultured for 12-14 days. The transcripts of heat shock factor 1 (HSF1), heat shock protein 70 (HSP70), heat shock protein 90 (HSP90) and two viral genes (E3L and F17R) were assayed by reverse transcriptase-polymerase chain reaction (RT-PCR), and the corresponding proteins measured by Western blot. Heat shock factor 1 DNA binding activities were estimated by electrophoretic mobility shift assay (EMSA) and its subcellular localization analyzed by immunocytofluorescence. RESULTS: It appeared that infection with vaccinia virus leads to activation of the heat shock factor 1. Activation of HSF1 causes increased synthesis of an inducible form of the HSP70 both at the mRNA and the protein level. Although HSP90 mRNA was enhanced in vaccinia virus infected cells, the HSP90 protein content remained unchanged. At the time of maximum vaccinia virus gene expression, an inhibitory effect of the infection on the heat shock protein and the heat shock factor 1 was most pronounced. Moreover, at the early phase of the infection translocation of HSP70 and HSP90 from the cytoplasm to the nucleus of the infected cells was observed. CONCLUSION: Preferential nuclear accumulation of HSP70, the major stress-inducible chaperone protein, suggests that VV employs this particular mechanism of cytoprotection to protect the infected cell rather than to help viral replication. The results taken together with our previous data on monocytes or MDMs infected with VV or S. aureus strongly argue that VV employs multiple cellular antiapoptotic/cytoprotective mechanisms to prolong viability and proinflammatory activity of the cells of monocytic-macrophage lineage.

Journal Article↗
PubMed1985

Thyroid and adrenal response to heat stress in chickens and quail differing in heat tolerance.

Three experiments were conducted to evaluate the thyroid and adrenal response in groups of birds with altered heat tolerance. Groups of chickens that had been handled on each of 4 days and a nonhandled control group were bled on the 5th day with or without heating for 1 hr at 50 C. Handling did not affect the thyroid response as indicated by thyroxine (T4) or triiodothyronine (T3) levels. Corticosterone levels were lower in handled birds than nonhandled birds after heating. In a second experiment, groups of broilers were fed a diet containing .2% thiouracil or a control diet. After 2 weeks they were bled either with or without 1 hr of heating at 50 C. The T3 and T4 levels were reduced by thiouracil feeding both with and without heating, but adrenal function was not affected. In Experiment 3, T3 and T4 levels were compared for four lines of Japanese quail. The nongrowth-selected line had higher T3 and T4 levels than growth-selected lines but did not have elevated levels of T3 or T4 in response to heat stress. The growth-selected lines (T, S, and P) responded to heating with increased T3 and T4 levels. Levels of T4 in Line T (selected on a thiouracil diet) after heating were significantly higher than all other lines.

Adrenal Cortex↗
PubMedDate not supplied

Measuring the thermal resistance of microorganisms: selecting an appropriate test system, correcting for heat-transfer lags, and determining minimum heating times.

Errors that occur in physical systems used to evaluate the heat resistance of microorganisms are discussed: namely, (a) not knowing the test heating-medium temperature accurately, (b) using heating times that are so short that the maximum temperature reached in the test unit is significantly below the test heating-medium temperature, and (c) ignoring significant heat-transfer lags, first in the heating and later in the cooling of the test units. Procedures and methods that can be used to minimize the effect of potential test-system errors on microbial resistance data are reported. Examples are included regarding the treatment of the different types of errors. Heating and cooling lag-correction values for several commonly-used testing systems, gleaned from the published literature and from the author's experience, are listed. A method is described and illustrated regarding how we may determine (in advance of carrying out an experiment to gather enumeration or survivor-curve data), the shortest heating time--highest temperature that should be used with a specific test-unit system and microbial DT -value.

Hot Temperature↗
PubMed1978

The effect of cholera toxin and heat labile and heat stable Escherichia coli enterotoxin on cyclic AMP concentrations in small intestinal mucosa of pig and rabbit.

The effect of cholera toxin, heat labile and heat stable Escherichia coli enterotoxin on mucosal cyclic AMP concentrations was determined on the proximal jejunum of weanling pigs and young rabbits. Ligated loops were injected with solutions containing no enterotoxin for control and either cholera toxin, heat labile or heat stable E. coli enterotoxin. The loops were drained after either two, four or six hours incubation at which time accumulated fluid was recorded and mucosal samples removed for determination of cyclic AMP concentration. In the rabbit, cholera toxin and heat labile, but not heat stable E. coli enterotoxin stimulated intestinal secretion while in the pig all three enterotoxins induced net fluid accumulation. Cholera toxin and heat labile, but not heat stable E. coli enterotoxin elevated rabbit mucosal cyclic AMP concentrations. In the pig these enterotoxins had no significant effect on mucosal cyclic AMP concentrations. The results are inconsistent with the hypothesis that the adenyl cyclase system is an essential step for enterotoxin induced intestinal secretion. The activation of intestinal adenyl cyclase by bacterial enterotoxins may only be an associated and not a necessary event for the stimulation of intestinal secretion.

Animals↗
PubMed1978

Effects of intraluminal glucose on intestinal secretion induced by heat stable and heat labile Escherichia coli enterotoxin, cholera toxin and theophylline.

Glucose, l-alanine, l-aspartate, l-methionine and glycine enhanced net fluid and electrolyte absorption in acute isolated loops of the proximal jejunum of weanling swine. The effect of glucose on intestinal secretion induced by heat stable and heat labile Escherichia coli entero-toxin, cholera toxin and theophylline was examined in both the proximal and distal jejunum of weanling swine. In the proximal jejunum glucose enhanced the rate of net fluid and electrolyte absorption. This increase was accompanied by an increase in unidirectional dosium absorption. In loops exposed to either heat stable or heat labile enterotoxins, glucose significantly decreased the rate of net fluid and electrolyte secretion. The magnitude of glucose enhancement in loops exposed to heat stable and heat labile enterotoxins was similar to adjacent control loops. However, glucose enhancement did not occur in loops exposed previously to cholera toxin or concurrently to theophylline. Therefore, cholera toxin and theophylline may inhibit substrate dependent sodium absorption in the proximal jejunum. In the distal jejunum glucose enhancement did occur but the rate of enhancement was less than in the proximal jejunum. In this region glucose enhancement was not evident in loops exposed to either theophylline, heat stable, heat labile or cholera toxin.

Amino Acids↗
PubMedDate not supplied

Effects of drill speed on heat production and the rate and quality of bone formation in dental implant osteotomies. Part I: Relationship between drill speed and heat production.

The amount of heat produced by dental implant osteotomy (receptor site) preparation at different speeds and the effects of heat production on the prognosis of implant treatment are controversial. In Part I of this two-part study, heat production was measured in vivo during osteotomy preparation at low (maximum 2,000 rpm), intermediate (maximum 30,000 rpm), and high (maximum 400,000 rpm) speeds in the rabbit tibia, and an inverse relationship was observed between drill speed and heat production. For the measurement of heat production (Part I), a thermocouple probe was inserted into a prepared receptor site in the anteromedial aspect of the tibial metaphysis. Temperature was recorded while an osteotomy was drilled 1 mm from the thermocouple receptor site. Distilled water was used as coolant in conjunction with all drilling, and all osteotomies were prepared by a single researcher to eliminate the variable of interoperator difference in technique. An inverse relationship was observed between drill speed and heat production. An analysis of variance indicated significant differences in heat production among the three drilling speeds (P < 0.05). The results of Part 1 of this study indicate that for the configuration and material of bur used, the high-speed range minimizes heat production.

Analysis of Variance↗
PubMed1998

Regional brain heating during microwave exposure (2.06 GHz), warm-water immersion, environmental heating and exercise.

Nonuniform heating may result from microwave (MW) irradiation of tissues and is therefore important to investigate in terms of health and safety issues. Hypothalamic (Thyp), cortical (Tctx), tympanic (Tty), and rectal (Tre) temperatures were measured in rats exposed in the far field, k-polarization (i.e., head pointed toward the transmitter horn and E-field in vertical direction) to two power densities of 2.06 GHz irradiation. The high-power density (HPM) was 1700 mW/cm2 [specific absorption rate (SAR): hypothalamus 1224 W/kg; cortex 493 W/kg]; the low-power density (LPM) was 170 mW/cm2 (SAR: hypothalamus 122.4 W/kg; cortex 49.3 W/kg). The increase (rate-of-rise, in degrees C/s) in Thyp was significantly greater than those in Tctx or Tre when rats were exposed to HPM. LPM produced more homogeneous heating. Quantitatively similar results were observed whether rats were implanted with probes in two brain sites or a single probe in one or the other of the two sites. The qualitative difference between regional brain heating was maintained during unrestrained exposure to HPM in the h-polarization (i.e., body parallel to magnetic field). To compare the temperature changes during MW irradiation with those produced by other modalities of heating, rats were immersed in warm water (44 degrees C, WWI); exposed to a warm ambient environment (50 degrees C, WSED); or exercised on a treadmill (17 m/min 8% grade) in a warm ambient environment (35 degrees C, WEX). WWI produced uniform heating in the regions measured. Similar rates-of-rise occurred among regions following WSED or WEX, thus maintaining the pre-existing gradient between Thyp and Tctx These data indicate that HPM produced a 2-2.5-fold difference in the rate-of-heating within brain regions that were separated by only a few millimeters. In contrast, more homogeneous heating was recorded during LPM or nonmicrowave modalities of heating.

Animals↗
PubMed2001

Activation of heat shock transcription factor in yeast is not influenced by the levels of expression of heat shock proteins.

Heat shock transcription factor (HSF) transiently induces the expression of a universally conserved set of proteins, the heat shock proteins (Hsps), when cells are exposed to elevated temperatures as well as to a wide range of other environmental stresses. The tight control of heat shock gene expression has prompted a model, according to which HSF activity and 'free' heat shock protein levels are tied up in a regulatory loop. Other data have indicated that HSF senses stress directly. Here, we report that yeast cells in which the basal expression levels of Hsps have been significantly increased exhibit improved thermotolerance but display no detectable difference in the temperature required for transient activation of HSF. In a separate experiment, overexpression of SSA2, a member of the Hsp70 family and a prominent candidate for the feedback regulation of HSF, did not inhibit the heat shock response. Our findings challenge the dogma that relief of the suppression of HSF activity by Hsps can account for the acute heat shock response.

DNA-Binding Proteins↗
PubMed2005

The maize heat shock factor-binding protein paralogs EMP2 and HSBP2 interact non-redundantly with specific heat shock factors.

The heat shock response (HSR) is a conserved mechanism by which transcripts of heat shock protein (hsp) genes accumulate following mobilization of heat shock transcription factors (HSFs) in response to thermal stress. Studies in animals identified the heat shock factor-binding protein1 (HSBP1) that interacts with heat shock transcription factor1 (HSF1) during heat shock attenuation; overexpression analyses revealed that the coiled-coil protein HSBP1 functions as a negative regulator of the HSR. Zea mays contains two HSBP paralogs, EMP2 and HSBP2, which exhibit differential accumulation during the HSR and plant development. Embryo-lethal recessive emp2 mutations revealed that EMP2 is required for the down-regulation of hsp transcription during embryogenesis, whereas accumulation of HSBP2 is induced in seedlings following heat shock. Notwithstanding, no interaction has yet been demonstrated between a plant HSBP and a plant HSF. In this report 22 maize HSF isoforms are identified comprising three structural classes: HSF-A, HSF-B and HSF-C. Phylogenetic analysis of Arabidopsis, maize and rice HSFs reveals that at least nine ancestral HSF isoforms were present prior to the separation of monocot and eudicots, followed by differential amplification of HSF members in these lineages. Yeast two-hybrid analyses show that EMP2 and HSBP2 interact non-redundantly with specific HSF-A isoforms. Site-specific mutagenesis of HSBP2 reveals that interactions between hydrophobic residues within the coiled coil are required for HSF::HSBP2 binding; domain swapping demonstrate that the isoform specificity of HSF::HSBP interaction is conferred by residues outside of the coiled coil. These data suggest that the non-redundant functions of the maize HSBPs may be explained, at least in part, by the specificity of HSBP::HSF interactions during plant development.

Amino Acid Motifs↗
PubMed2006

Global transcriptome response of recombinant Escherichia coli to heat-shock and dual heat-shock recombinant protein induction.

Recombinant Escherichia coli cultures are used to manufacture numerous therapeutic proteins and industrial enzymes, where many of these processes use elevated temperatures to induce recombinant protein production. The heat-shock response in wild-type E. coli has been well studied. In this study, the transcriptome profiles of recombinant E. coli subjected to a heat-shock and to a dual heat-shock recombinant protein induction were examined. Most classical heat-shock protein genes were identified as regulated in both conditions. The major transcriptome differences between the recombinant and reported wild-type cultures were heavily populated by hypothetical and putative genes, which indicates recombinant cultures utilize many unique genes to respond to a heat-shock. Comparison of the dual stressed culture data with literature recombinant protein induced culture data revealed numerous differences. The dual stressed response encompassed three major response patterns: induced-like, in-between, and greater than either individual stress response. Also, there were no genes that only responded to the dual stress. The most interesting difference between the dual stressed and induced cultures was the amino acid-tRNA gene levels. The amino acid-tRNA genes were elevated for the dual cultures compared to the induced cultures. Since, tRNAs facilitate protein synthesis via translation, this observed increase in amino acid-tRNA transcriptome levels, in concert with elevated heat-shock chaperones, might account for improved productivities often observed for thermo-inducible systems. Most importantly, the response of the recombinant cultures to a heat-shock was more profound than wild-type cultures, and further, the response to recombinant protein induction was not a simple additive response of the individual stresses.

Cell Culture Techniques↗
PubMed2006

The heat stress transcription factor HsfA2 serves as a regulatory amplifier of a subset of genes in the heat stress response in Arabidopsis.

Within the Arabidopsis family of 21 heat stress transcription factors (Hsfs) HsfA2 is the strongest expressed member under heat stress (hs) conditions. Irrespective of the tissue, HsfA2 accumulates under heat stress similarly to other heat stress proteins (Hsps). A SALK T-DNA insertion line with a complete HsfA2-knockout was analyzed with respect to the changes in the transcriptome under heat stress conditions. Ascorbate peroxidase 2 (APX2) was identified as the most affected transcript in addition to several sHsps, individual members of the Hsp70 and Hsp100 family, as well as many transcripts of genes with yet unknown functions. For functional validation, the transcription activation potential of HsfA2 on GUS reporter constructs containing 1 kb upstream promoter sequences of selected target genes were analyzed using transient reporter assays in mesophyll protoplasts. By deletion analysis the promoter region of the strongest affected target gene APX2 was functionally mapped in detail to verify potential HsfA2 binding sites. By electrophoretic mobility shift assays we identified TATA-Box proximal clusters of heat stress elements (HSE) in the promoters of selected target genes as potential HsfA2 binding sites. The results presented here demonstrate that the expression of HsfA2 in Arabidopsis is strictly heat stress-dependent and this transcription factor represents a regulator of a subset of stress response genes in Arabidopsis.

Arabidopsis↗
PubMed2004

Ascorbic acid decreases heat shock protein 70 and plasma corticosterone response in broilers (Gallus gallus domesticus) subjected to cyclic heat stress.

It is known that ascorbic acid (AA) supplementation can ameliorate the chicken's responses to heat stress. The influence of AA on heart heat shock protein 70 (hsp70) and plasma corticosterone (CS) was evaluated in young male broiler chickens fed either no AA (N-AA) or 500 mg AA /kg (AA) and exposed to cyclic high temperatures (21 to 30 to 21 degrees C) over a 3.5 h period on three consecutive days. Dietary AA supplementation elevated plasma AA and maintained it at high levels after heating, but in N-AA birds, only heat elevated plasma AA. In N-AA fed chickens, plasma CS was elevated and was further increased by heat stress as compared with AA-fed birds. Heart hsp70 expression was greater in N-AA-fed chickens compared to AA-fed chickens, and heat stress further elevated hsp70 in both N-AA- and AA-fed birds. The hsp70 increase after heat was two-fold greater in N-AA- vs. AA-fed birds. Plasma CS and heart hsp70 were positively correlated, plasma AA and heart hsp70 were negatively correlated, and plasma CS and AA were negatively correlated. It was concluded that chickens experience a less severe stress response after exposure to high temperatures when they are provided dietary AA.

Animals↗
PubMed1999

Heat shock protein 70 and heat shock cognate protein 70 messenger ribonucleic acid induction in the brains, hearts, and livers of neonatal rats after hypoxic stress.

OBJECTIVE: The aim of this study was to examine the production of 2 types of heat shock protein 70 in the organs of neonatal rats during an episode of mild hypoxic stress that was insufficient to produce histologic changes. STUDY DESIGN: Seven-day-old rats were subjected to hypoxia (inspired gas of 8% oxygen and 92% nitrogen) at 33 C for 2 hours (n = 5), 3 hours (n = 5), and 4 hours (n = 5). Control rats (n = 5) inspired room air for 4 hours. The brains, hearts, and livers were removed after 4 hours of recovery. The levels of heat shock protein 70 and heat shock cognate protein 70 messenger ribonucleic acid were measured by Northern blot analysis. Arterial pH, Pao 2, PACO 2, and brain temperature were measured before, during, and at 4 hours of hypoxia in another 16 animals. Histologic examinations were carried out in these 16 animals 7 days after hypoxic stress. RESULTS: PaO 2, PACO 2, and brain temperature decreased during the hypoxic stress and returned to prehypoxic values at recovery time. Arterial pH did not change. No histologic changes were observed in any areas of the brain. Heat shock cognate protein 70 messenger ribonucleic acid was normally expressed in the brain, heart, and liver and was further induced after hypoxia in the brain and the heart. There was, however, no additional increase of heat shock cognate protein 70 messenger ribonucleic acid in the liver. there were no increments of the stress-induced form of heat shock protein 70 messenger ribonucleic acid in these organs. CONCLUSION: Mild hypoxia selectively induced messenger ribonucleic acid of heat shock cognate protein 70, which may play an important role in protecting the brain and the heart against stress.

Animals↗
PubMed1999

The protein kinase inhibitor, H-7, suppresses heat induced activation of heat shock transcription factor 1.

We investigated the effects of a protein kinase (PK) inhibitor, H-7 (1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride), on the regulation of heat shock protein (hsp)72 gene expression in a human glioblastoma cell line (A-172) using a gel mobility-shift assay and Western blot analysis. Heat shock transcription factor 1 (HSF1) was phosphorylated immediately after heat treatment (44 degrees C, 30 min) and the phosphorylation of HSF1 was suppressed by H-7. The increase in DNA binding ability of HSFI to heat shock element (HSE) by heat shock was significantly suppressed by the addition of H-7 in a dose-dependent manner. Similarly, the accumulation of hsp72 by heat shock was suppressed by the addition of H-7 in a dose-dependent manner. Since H-7 is known to be a potent inhibitor of some PKs, especially calcium-dependent PK (PKC), cyclicAMP-dependent PK (PKA) and cyclicGMP-dependent PK (PKG), it is possible that the activation of HSF1 by phosphorylation and subsequent hsp72 gene expression are dependent on some of those PKs. The nature of H-7 as a non-specific inhibitor for PKs is discussed in relation to its availability for regulation of heat sensitivity of cells depending on cellular level of hsp72.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2004

Galactinol synthase1. A novel heat shock factor target gene responsible for heat-induced synthesis of raffinose family oligosaccharides in Arabidopsis.

Heat shock factors (HSFs) are transcriptional regulators of the heat shock response. The major target of HSFs are the genes encoding heat shock proteins (HSPs), which are known to have a protective function that counteracts cytotoxic effects. To identify other HSF target genes, which may be important determinants for the generation of stress tolerance in Arabidopsis, we screened a library enriched for genes that are up-regulated in HSF3 (AtHsfA1b)-overexpressing transgenic plants (TPs). Galactinol synthase1 (GolS1) is one of the genes that is heat-inducible in wild type, but shows constitutive mRNA levels in HSF3 TPs. The generation and analysis of TPs containing GolS1-promoter::beta-glucuronidase-reporter gene constructs showed that, upon heat stress, the expression is transcriptionally controlled and occurs in all vegetative tissues. Functional consequences of GolS1 expression were investigated by the quantification of raffinose, stachyose, and galactinol contents in wild type, HSF3 TPs, and two different GolS1 knockout mutants (gols1-1 and gols1-2). This analysis demonstrates that (1) raffinose content in leaves increases upon heat stress in wild-type but not in the GolS1 mutant plants; and (2) the level of raffinose is enhanced and stachyose is present at normal temperature in HSF3 TPs. These data provide evidence that GolS1 is a novel HSF target gene, which is responsible for heat stress-dependent synthesis of raffinose, a member of the raffinose family oligosaccharides. The biological function of this osmoprotective substance and the role of HSF-dependent genes in this biochemical pathway are discussed.

Arabidopsis↗