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PubMed2000

Regulation of heat shock protein 72 kDa and 90 kDa in human breast cancer MDA-MB-231 cells.

It has been shown that expression of HSPs can negatively regulate the effectiveness of cytotoxic drugs. In this study, we conducted experiments to study the regulation of expression of heat shock proteins (HSPs) in human breast cancer MDA-MB-231 cells. Using [35S]methionine incorporation and Western immunoblots, we established that heat shock increased production of HSP-72 and -90. Cells exposed to 44 degrees C for 20 min displayed increased expression of HSP-72 and -90, that reached a maximum 3-7 h later and returned to baseline levels within 24 h. The synthesis of both HSP-72 and -90 was attenuated when cells were exposed to heat shock in medium devoid of Ca2+ or pretreated with the calcium chelator BAPTA for 30 min prior to heat shock. Similarly, synthesis of HSP-72 and -90 was inhibited when cells were treated with the protein kinase A inhibitor, H89. These data indicate that Ca2+ and PKA are involved in the regulation of HSP-72 and -90 protein synthesis. Levels of HSP-72 mRNA in cells exposed to heat shock increased, suggesting that the heat-induced increase in HSP-72 occurs at the transcriptional level. Also, heat shock caused phosphorylation and translocation from the cytosol to the nucleus of heat shock factor 1 (HSF 1), a transcription factor for heat shock protein synthesis. Removal of external Ca2+ or treatment with a PKA inhibitor prevented the phosphorylation and the translocation of HSF 1. Cells overexpressing HSP-72 and -90 induced by exposure to a sublethal temperature displayed cytoprotection from thermal injury. Removal of external Ca2+ and treatment with BAPTA or H89 prior to exposure to sublethal heat shock that reduced the amount of HSP-72 and -90 production still protected cells from subsequent thermal injury. The intracellular free calcium concentration ([Ca2+]i) in resting fura-2-loaded MDA-MB-231 cells was 175+/- nM. Heat shock increased [Ca2+]i in a time-and temperature-dependent manner. Exposure of cells to 44 degrees C for 20 min increased [Ca2+]i by 234+/-13%, which subsequently returned to baseline levels within 30 min. Removal of external Ca2+ eliminated the increase, indicating that the increase in [Ca2+]i was due to Ca2+ influx. Pretreatment of the cells with H89 but not GF-109203X for 30 min led to an attenuation of the increase in [Ca2+]i by a subsequent heat shock. The results suggest that HSP-72 and -90 are regulated by [Ca2+]i and PKA activity in MDA-MB-231 cells. Kiang JG, Gist ID, Tsokos GC: Regulation of Heat Shock Protein 72 kDa and 90 kDa in Human Breast Cancer MDA-MB-231 Cells.

Biological Transport↗
PubMed1984

Simultaneous heat and tension measurements from single muscle cells.

Simultaneous force and heat measurements were made in single cells from skeletal muscle of the frog during isometric twitches and tetani at 10 and 0 degree C. A Hill- Downing type thermopile of low heat capacity was used. In twitches, peak force development was found to be well correlated with heat production at both temperatures, during posttetanic twitch potentiation (at 10 degrees C) and during posttetanic twitch depression (at 0 degree C). In a twitch at 0 degree C, heat production started less than 14 msec after the stimulus had begun, before force development. As in whole muscle, the heat during a tetanus could be separated into two components: an early component produced at an exponentially decreasing rate, labile heat, and a steady rate, stable maintenance heat rate. Increasing temperature from 0 to 10 degrees C doubled the stable maintenance heat rate. At the higher temperature the time constant of labile heat production was halved and the quantity of labile heat decreased. When two tetani were given at 10 degrees C, a 5 min rest interval was required before the second tetanus produced the same force and heat as the first. At 0 degree C this interval was at least 10 min. With shorter intervals, both heat and force were depressed. At 10 degrees C both were depressed equally but at 0 degree C the effect on heat was greater than on force. At both temperatures labile heat was depressed to a greater extent than the stable maintenance heat rate. Results are interpreted in terms of possible calcium-parvalbumin interaction during a tetanus.

Animals↗
PubMedDate not supplied

Quantitative measurement of local blood flow with heat clearance.

Measurements of the local blood flow through organs by means of heated thermistor-probes enable one to perform continuous recordings of flow. The principle is based on the measurement between a heated and an unheated probe, both implanted in the tissue or placed on the superficial layer of the organ. The flow-measure for this type of blood flow recording is the heat transported from the heated site of the tissue. It is measured in cal-cm(-1)-sec(-1)-degree C(-1). This is the dimension of the heat conductance. Quantification of continuous blood flow measurements in ml flow/g tissue-min has been carried out with combinations of gas clearance and heat transport. It has now become possible to measure blood flow in ml blood-ml(-1) tissue-min(-1) solely with the aid implanted thermistors. Two types of local blood flow measurements are described. 1. Measurements with "slug heating" by which a thermistor is heated for a very short time and the temperature change is subsequently recorded. 2. The measurement of flow by sudden introduction of heat, if a heating coil around a micro-thermistor is switched on or off and the course of the tissue temperature is subsequently followed. It is proven, that the temperature of a point-shaped micro-thermistor in nonperfused tissue and in homogeneous perfused tissue differs only by an exponential factor (see article) where uslug is the temperature field after a slug injection of heat dependent on location, time, blood flow (phi) and partition coefficient for heat (lambda) and where index 0 = unperfused tissue. If the heater is not heated in the form of a delta function but is switched on and the temperature is subsequently recorded or if the heater, after a period of constant temperature, is switched off, the derivatives in respect to time differ only by an exponential factor and can be used as a measure of flow. The evaluation of blood flow is described in detail. The measurements show the following advantages, compared with former techniques: 1. Heat clearance and continuous blood flow measurements by means of heat transport measurements are both possible at the same site. 2. No other operation and procedures are necessary except implantation of the thermistor. 3. Turning on the heater does not affect the tissue and does not cause emotional reactions. As examples the measurements of local blood flow in brain tissue and in the myocardium of conscious animals are described.

Animals↗
PubMed1996

Residual analysis in the determination of factors affecting the estimates of body heat storage in clothed subjects.

Body heat storage can be estimated by calorimetry (from heat gains and losses) or by thermometry [from changes (delta) in mean body temperature (T b) calculated as a weighted combination of rectal (Tre) and mean skin temperatures (T sk)]. If an invariant weighting factor of Tre and T sk were to be used (for instance, delta T b = 0.8.delta Tre + 0.2 delta T sk under hot conditions), body heat storage could be over- or underestimated substantially relative to calorimetry, depending on whether the subject was wearing light or protective clothing. This study investigated whether discrepancies between calorimetry and thermometry arise from methodological errors in the calorimetric estimate of heat storage, from inappropriate weightings in the thermometric estimate, or from both. Residuals of calorimetry versus thermometric estimates were plotted against individual variables in the standard heat balance equation, applying various weighting factors to Tre and T sk. Whether light or protective clothing was worn, the calorimetric approach generally gave appropriate estimates of heat exchange components and thus heat storage. One exception was in estimating latent heat loss from sweat evaporation. If sweat evaporation exceeded 650 g.h-1 when wearing normal clothing, evaporative heat loss was overestimated and thus body heat storage was underestimated. Nevertheless, if data beyond this ceiling were excluded from the analyses, the standard 4:1 weighting matched calorimetric heat storage estimates quite well. When wearing protective clothing, the same 4:1 weighting approximated calorimetric heat storage with errors of less than approximately 10%, but only if environmental conditions allowed a subject to exercise for more than 90 min. The best thermometric estimates of heat storage were provided by using two sets of relative weightings, based upon the individual's metabolic heat production (M in kilojoules per meter squared per hour): (4 - [(M - x).x-1].2): 1 for an initial, thermoneutral environment and (4 + [(M - x).x-1].5):1 for a final, hot environment, the optimal value of x lay between 450 and 500 kJ.m-2.h-1. We concluded that the accuracy of thermometric estimates of heat storage can be improved by modifying weighting factors of Tre and T sk according to the environment, type of clothing, and metabolic rate.

Adult↗
PubMed2003

Development of a new membrane-type heated humidifier for laparoscopic surgery.

BACKGROUND: Recently, several animal studies showed that the core body temperature falls during pneumoperitoneum, and this hypothermia could be prevented by using heated and humidified gas insufflation. However, there are no satisfactory heated humidifiers to meet this purpose. Therefore, we developed a new membrane-type heated humidifier. MATERIALS AND METHODS: The newly developed heated humidifier employs an ion-exchange membrane (Nafion: Du Pont Co. Ltd) tube that passes water selectively in molecular form and a gas compartment is completely separated from distilled water to prevent infection. This humidifier consists of a Nafion tube assembly and a case that includes the heater. A perforated protecting tube is located outside the Nafion tube to prevent direct contact with the Nafion tube when it is assembled. The Nafion tube assembly is inserted in the case, and dry gas flows inside of the Nafion tube. The space between the case and the Nafion tube assembly is filled with distilled water. A heater raises the temperature of the distilled water, and heat and water vapor are transferred to cold and dry gas through the Nafion membrane. Four different types of insufflators were involved in this performance comparison study: a Nafion-based heated and humidified insufflator, a conventional heated insufflator, a conventional heated and humidified insufflator, and a conventional cold and dry insufflator. Temperature and relative humidity were measured once each minute for 15 min, which was repeated four times. Each insufflator was operated at two rates of flow: 5 L/min and 10 L/min. RESULTS: Temperature and humidity of the conventional cold and dry insufflator, the Nafion membrane-type heated and humidified insufflator, the conventional heated insufflator, and the conventional heated and humidified insufflator measured at the distal end of circuit reached 22.0 +/- 0.2 degrees C and 0%, 36.7 +/- 1.1 degrees C and 100%, 29.0 +/- 0.4 degrees C and 0%, and 31.3 +/- 0.4 degrees C and 70.5 +/- 5.3% in 15 min at 5 L/min flow rates. At 10 L/min flow rates, temperature and humidity were almost the same as those at 5 L/min. The membrane-type heated humidifier demonstrated statistically significant improvement in both the temperature ( p < 0.0001) and relative humidity ( p < 0.0001) parameters in comparison to the conventional normal, heated, or heated and humidified insufflators at 5 L/min and 10 L/min continuous flow rate in statistics using repeated-measure ANOVA. CONCLUSION: This newly developed heated humidifier offers the great advantages of maintaining intraabdominal temperature and humidity in comparison to conventional insufflators for laparoscopic surgery.

Equipment Design↗
PubMed2002

Effect of whole-body and local heating on cutaneous vasoconstrictor responses in humans.

Animal studies suggest that alpha-adrenergic-mediated vasoconstriction is compromised during whole-body heating. The purpose of this study was to identify whether whole-body heating and/or local surface heating reduce cutaneous alpha-adrenergic vasoconstrictor responsiveness in human skin. Protocol I: Six subjects were exposed to neutral skin temperature (i.e., 34 degrees C), whole-body heating, and local heating of forearm skin to increase skin blood flow to the same relative magnitude as that observed during whole-body heating. Protocol II: In eight subjects forearm skin was locally heated to 34, 37, 40, and 42 degrees C. During both protocols, alpha-adrenergic vasoconstrictor responsiveness was assessed by local delivery of norepinephrine (NE) via intradermal microdialysis. Skin blood flow was continuously monitored over each microdialysis membrane via laser-Doppler flowmetry. In protocol I, whole-body and local heating caused similar increases in cutaneous vascular conductance (CVC). The EC50 (log NE dose) of the dose-response curves for both whole body (-4.2 +/- 0.1 M) and local heating (-4.7 +/- 0.4 M) were significantly greater (i.e., high dose required to cause 50% reduction in CVC) relative to neutral skin temperature (- 5.6 +/- 0.0 M; P<0.05 for both). In both local and whole-body heated conditions CVC did not return to pre-heating values even at the highest dose of NE. In protocol II, calculated EC50 for 34, 37, 40, and 42 degrees C local heating was - 5.5 +/- 0.4, -4.6 +/- 0.3, -4.5 +/- 0.3, - 4.2 +/- 0.4 M, respectively. Statistical analyses revealed that the EC50 for 37,40 and 42 degrees C were significantly greater than the EC50 for 34 degrees C. These results indicate that even during administration of high concentrations of NE, alpha-adrenergic vasoconstriction does not fully compensate for local heating and whole-body heating induced vasodilatation in young, healthy subjects. Moreover, these data suggest that elevated local temperatures, above 37 degrees C, and whole-body heating similarly attenuate cutaneous alpha-adrenergic vasoconstriction responsiveness.

Adult↗
PubMed1976

Heat treatment of cobalt-chromium alloy wire.

This study shows that the ability of cobalt-chromium wire to resist permanent deformation is definitely affected by the temperature of heat treatment. For each temperature of heat treatment up to 1200 degrees F there is progressively greater resistance to permanent deformation; at temperatures of heat treatment above 1200 degrees F, however, there is a rapid decline in resistance to permanent deformation due to partial annealing. The maximum resistance to permanent deformation occurs from heat treatment in the temperature range of 1100 degrees to 1200 degrees F. A clinician desiring maximum resistance to permanent deformation from a .016 inches x .022 inches cobalt-chromium archwire should heat-treat the wire at 1100 degrees to 1200 degrees F for 5 minutes in a dental furnace. If the wire was in a highly work-hardened condition as were the wire specimens of this study, he could expect an increase in resistance to permanent deformation of approximately 174 percent. Heat treatment at lower temperatures could be used in situations requiring less than maximum resistance to permanent deformation. Heat treatment at 900 degrees F would give approximately a 95 percent increase in resistance to permanent deformation. Of course, heat treatment would not be indicated when the desired level of resistance to permanent deformation was not greater than the amount exhibited in the untreated wires of this study. When an electrical resistance heat-treatment unit and 950 degrees F temper-indicating paste were used, the clinician would expect increased resistance to permanent deformation similar to that seen in the wires heat-treated with a dental furnace at 800 degrees and 900 degrees F, i.e., about half of that obtained by the 1200 degrees F treatment. This study has determined the effects that various temperatures of heat treatment have on the resistance to permanent deformation of cobalt-chromium wire specimens which were formed into a specific pattern of loops. The following conclusions can be drawn from the results of this investigation: 1. Heat treatment at 1200 degrees F gives the maximum resistance to permanent deformation to .016 inches x .022 inches cobalt-chromium wire. 2. Increases in resistance to permanent deformation of approximately 95 percent and 174 percent may be expected from heat treatment of .016 inches x .022 inches cobalt-chrome wire at 900 degrees and 1200 degrees, respectively. 3. Wires, heat-treated with an electrical resistance unit using 950 degrees F temper-indicating paste, exhibit increases in resistance to permanent deformation similar to wires heat-treated in a dental furnace at 800 degrees and 900 degrees F.

Chromium Alloys↗
PubMed1995

Analysis by pulsed-field gel electrophoresis of DNA double-strand breaks induced by heat and/or X-irradiation in bulk and replicating DNA of CHO cells.

For a given amount of cell killing, heat alone (10-80 min, 45.5 degrees C) induced very few double-strand breaks (dsbs) compared with X-rays. Furthermore, 10 min at 45.5 degrees C immediately prior to X-rays caused only a 1.3-fold increase in the slope of the X-ray-induced dsb dose-response curve, i.e. 0.67 +/- 0.006 (95% confidence) dsbs/100Mbp/Gy for heated cells compared with 0.53 +/- 0.005 for unheated control cells. However, this same heat treatment caused > 5-fold inhibition in the rate of repair of dsbs induced by 60-Gy X-rays, with the degree of inhibition being much less in thermotolerant (TT) cells than in non-tolerant (NT) cells. This reduced inhibition of repair in TT cells correlated with the more rapid removal of excess nuclear protein from nuclei isolated from TT cells than from NT cells. These results plus a TT ratio of 2-3 for both heat-induced radiosensitization and heat-inhibition of repairing dsbs are consistent with the hypothesis that heat radiosensitization results primarily from heat aggregation of nuclear protein interfering with access of repair enzymes to DNA dsbs. The selective heat-radiosensitization of S-phase cells, however, may result from an increase in radiation-induced dsbs in or near replicating regions. For example, a preferential increase in dsbs in replicating DNA compared with bulk DNA was found following either hyperthermia alone (10-30 min, 45.5 degrees C) or a combined treatment (10 min, 45.5 degrees C before 60 Gy). A 30-min treatment at 45.5 degrees C induced dsbs equivalent to approximately 10 Gy in replicating DNA compared with 3-5 Gy in bulk DNA. When cells were heated immediately before irradiation, the increase in dsbs induced in the replicating DNA by 60 Gy was equivalent to 200 Gy. We hypothesize that the observed 2-fold increase in single-stranded regions in replicating DNA after heat resulted in radiation selectively inducing dsbs at or near the replication fork where the heat-induced increase in single-stranded DNA should occur. Thus, this preferential increase in dsbs in the replicating DNA by heat alone and especially when heat was combined with radiation may explain at least in part, the high sensitivity of S-phase cells to heat killing and heat radiosensitization.

Animals↗
PubMed1981

Regulated transcription of the genes for actin and heat-shock proteins in cultured Drosophila cells.

The transcription of three specific genes has been examined in heat-shocked drosophila cells by hybridizing pulse-labeled nuclear RNA with cloned DNA sequences. Actin gene transcription is rapidly and profoundly suppressed upon heat shock but returns to near- normal levels after cells are placed back at their normal culture temperature (23 degrees C). Conversely, the transcription of genes coding from 70,000- and 26,000-dalton heat- shock proteins increases dramatically and with extraordinary rapidity (60 s) after heat shock. The temporal patterns of 70,000- and 26,000-dalton heat-shock gene transcription are nearly superimposable, indicating that, although they are closely linked cytologically, these genes are nevertheless tightly coregulated. The abundance of heat- shock gene transcripts reaches remarkable levels, e.g., 70,000-dalton heat-shock gene transcripts account for 2-3 percent of the nuclear RNA labeled during the first 30 min of heat shock. When heat-shocked cells are returned to 25 degrees C, the rates of transcription of the heat-shock genes fall back to the low levels characteristic of untreated cells. To confirm the low level of heat-shock gene transcription in normal cells, nuclear RNA was purified from unlabeled (and otherwise unhandled) 25 degrees C cells, end-labeled in vitro with (32)P, and hybridized to cloned heat-shock DNA sequences. These and other data establish that the genes for 70,000- and 26,000-dalton heat-shock proteins in culture drosophila cells are active at 25 degrees C, and that their rate of transcription is greatly accelerated upon heat shock rather than being activated from a true "off" state. The rapidity, magnitude, and reversibility of the shifts in actin and heat-shock gene transcription constitute compelling advantages for the use of cultured drosophila cells in studying the transcriptional regulation of eukaryotic genes, including one related to the cytoskeleton.

Actins↗
PubMed1992

Is there a shortening-heat component in mammalian cardiac muscle contraction?

It has been suggested that there is a shortening-heat component that is an extra liberation of heat on shortening above that due to the external work, which contributes to the total energy expenditure of the beating heart. The presence of a shortening heat component was studied in isolated papillary muscles from the right ventricle of rabbits killed by cervical dislocation. At the onset of a contraction, muscles were shortened from various initial lengths through fixed distances at near maximum velocity before being allowed to develop force at the new length; the heat production accompanying such contractions was measured. The measured heat was compared with heat values predicted from previously established heat-stress curves obtained by using either preshortening or latency release methods. There was no shortening-related increment in heat output per contraction when comparison was made to a control heat-stress curve, obtained using the latency release method. An increase in heat production of 10% was observed with long shortening distances when comparison was made to a control heat-stress curve obtained by preshortening the muscles; however, this difference is most likely due to an underestimate of the magnitude of the activation heat component in these control heat-stress curves. An increase in isometric heat production due to maintained stretch per se was observed. The present data indicate that it is unlikely that there is a significant shortening heat component when cardiac muscle shortens. The absence of such a metabolic component may account for the rapid fall off in total enthalpy output in isotonic contractions at low to medium afterloads when compared with the skeletal muscle data.

Analysis of Variance↗
PubMed1999

Inhibition of rapid heat responses in nociceptive primary sensory neurons of rats by vanilloid receptor antagonists.

Recent studies demonstrated that heat-sensitive nociceptive primary sensory neurons respond to the vanilloid receptor (VR) agonist capsaicin, and the first cloned VR is a heat-sensitive ion channel. Therefore we studied to what extent heat-evoked currents in nociceptive dorsal root ganglion (DRG) neurons can be attributed to the activation of native vanilloid receptors. Heat-evoked currents were investigated in 89 neurons acutely dissociated from adult rat DRGs as models for their own terminals using the whole cell patch-clamp technique. Locally applied heated extracellular solution (effective temperature approximately 53 degrees C) rapidly activated reversible and reproducible inward currents in 80% (62/80) of small neurons (< or = 32.5 microm), but in none of nine large neurons (P < 0.001, chi(2) test). Heat and capsaicin sensitivity were significantly coexpressed in this subpopulation of small DRG neurons (P < 0.001, chi(2) test). Heat-evoked currents were accompanied by an increase of membrane conductance (320 +/- 115%; mean +/- SE, n = 7), had a reversal potential of 5 +/- 2 mV (n = 5), which did not differ from that of capsaicin-induced currents in the same neurons (4 +/- 3 mV), and were carried at least by Na(+) and Ca(2+) (pCa(2+) > pNa(+)). These observations are consistent with the opening of temperature-operated nonselective cation channels. The duration of action potentials was significantly higher in heat-sensitive (10-90% decay time: 4.45 +/- 0.39 ms, n = 12) compared with heat-insensitive neurons (2.18 +/- 0.19 ms, n = 6; P < 0.005, Student's t-test), due to an inflection in the repolarizing phase. This property as well as capsaicin sensitivity and small cell size are characteristics of nociceptive DRG neurons. When coadministered with heat stimuli, the competitive VR antagonist capsazepine (1 microM to 1 mM) significantly reduced heat-evoked currents in a dose-dependent manner (IC(50) 13 microM, Hill slope -0.58, maximum effect 75%). Preincubation for 12-15 s shifted the IC(50) by approximately 0.5 log(10) units to an estimated IC(50) of approximately 4 microM. The noncompetitive VR antagonist ruthenium red (5 microM) significantly reduced heat-evoked currents by 33 +/- 6%. The effects of both VR antagonists were rapidly reversible. Our results provide evidence for a specific activation of native VRs in nociceptive primary sensory neurons by noxious heat. The major proportion of the rapid heat-evoked currents can be attributed to the activation of these temperature-operated channels, and noxious heat may be the signal detected by VRs under physiological conditions.

Animals↗
PubMed2003

Hot bees in empty broodnest cells: heating from within.

Honeybee colonies maintain brood nest temperatures of 33-36 degrees C. We investigated brood nest thermoregulation at the level of individual worker behaviour and the transfer of heat from workers to the brood. Worker bees contribute to the regulation of brood nest temperature by producing heat while sitting motionless on the caps of brood cells. We report here an additional, newly observed heating strategy where heating bees enter empty cells between sealed brood cells and remain there motionless for periods of up to 45 min. Individually marked worker bees on the surface of sealed brood cells maintained thorax temperatures (T(th)) between 32.2+/-1.0 degrees C and 38.1+/-2.5 degrees C (mean +/- S.D.; N=20 bees) with alternating warming and cooling periods. Most of the observed bees made one or several long-duration visits (>2 min) to empty cells within the sealed brood area. T(th) at the time bees entered a cell [T(th(entry))] was 34.1-42.5 degrees C (N=40). In 83% of these cell visits, T(th(entry)) was higher (up to 5.9 degrees C; mean 2.5+/-1.5 degrees C; N=33) than the mean T(th) of the same bee. High values of T(th(entry)) resulted from preceding heating activity on the comb surface and from warm-ups just prior to cell visits during which T(th) increased by up to +9.6 degrees C. Bees inside empty cells had mean T(th) values of 32.7+/-0.1 degrees C (resting bees) to 40.6+/-0.7 degrees C (heat-producing bees) during long-duration cell visits without performing any visible work. Heating behaviour inside cells resembles heating behaviour on the brood cap surface in that the bees appear to be inactive, but repeated warmings and coolings occur and T(th) does not fall below the optimum brood temperature. Bees staying still inside empty cells for several minutes have previously been considered to be 'resting bees'. We find, however, that the heating bees can be distinguished from the resting bees not only by their higher body temperatures but also by the continuous, rapid respiratory movements of their abdomens. By contrast, abdominal pumping movements in resting bees are discontinuous and interrupted by long pauses. Heat transfer to the brood from individual bees on the comb surface and from bees inside empty cells was simulated under controlled conditions. Heating on the comb surface causes a strong superficial warming of the brood cap by up to 3 degrees C within 30 min. Heat transfer is 1.9-2.6 times more efficient when the thorax is in touch with the brood cap than when it is not. Heating inside empty cells raises the brood temperature of adjacent cells by up to 2.5 degrees C within 30 min. Heat flow through the comb was detectable up to three brood cells away from the heated thorax.

Animals↗
PubMed2003

Genetic divergence in cellular resistance to heat shock in cattle: differences between breeds developed in temperate versus hot climates in responses of preimplantation embryos, reproductive tract tissues and lymphocytes to increased culture temperatures.

The detrimental effects of heat stress on fertility in cattle are less pronounced in heat-tolerant breeds. Although these genetic differences reflect differences in thermoregulation, cells from heat-tolerant breeds are less adversely compromised by increased temperature (that is, heat shock) than cells from heat-sensitive breeds. Experiments were performed to test the hypothesis that cells and tissues from two thermotolerant breeds (Brahman and Senepol) are better able to survive and function after exposure to increased temperature than cells and tissues from two thermosensitive breeds (Holstein and Angus). Exposure of embryos at>eight-cell stage at day 5 after insemination to heat shock of 41.0 degrees C for 6 h decreased development to the blastocyst stage and the number of cells per embryo. However, the deleterious effect of heat shock on blastocyst formation and the number of cells per embryo was less pronounced for Brahman than for Holstein and Angus breeds. Embryos from Senepol cows had very low development and it was not possible to determine heat shock effects in this breed. In contrast to the sensitivity of embryos to heat shock, there was no effect of a 41.0 degrees C heat shock on [(3)H]leucine incorporation into proteins secreted by oviductal or endometrial explants. Lymphocytes from Brahman and Senepol cows were more resistant to heat-induced apoptosis than lymphocytes from other breeds. Heat shock reduced lymphocyte glutathione content but the magnitude of the decrease was not affected by breed. In conclusion, embryos from Brahman cows are more resistant to heat shock than embryos from Holstein or Angus cows. Genetic differences are also present in thermotolerance for apoptosis response in lymphocytes, with Brahman and Senepol cattle being more resistant to heat shock than Angus and Holstein breeds. It is likely that the evolutionary forces that led to the Brahman and Senepol breeds being adapted to hot climates resulted in the selection of genes controlling resistance to cellular heat shock.

Analysis of Variance↗
PubMed1979

The effect of heat inactivation of serum on aggregation of immunoglobulins.

Heating serum at 56 degrees is used to inactivate complement in several immunological assays. During heating, both heat-labile and heat-stable anticomplementary activity (ACA) develop. While heat-labile ACA can be completely inactivated, heat-stable ACA increases progressively with continued heating. Heat-stable ACA develops in deaggregated IgG and in normal, but not in hypogammaglobulinaemic, human and porcine serum heated at 56 degrees suggesting that this ACA is due to formation of immunoglobulin aggregates. These aggregates would produce false-positive tests for immune complexes and could inhibit a variety of cell-mediated reactions in assays which incorporate heat-inactivated serum. Other temperatures were tested to determine whether endogenous haemolytic activity could be destroyed without forming immunoglobulin aggregates. At 53 degrees both endogenous haemolytic activity and heat-labile ACA were inactivated and formation of heat-stable ACA in normal serum was minimal. ACA, however, could be induced in deaggregated IgG at 53 degrees. Moreover, the degree of heat-induced aggregation of IgG in vitro at either temperature was directly proportional to IgG concentrations and inversely related to albumin concentrations. Thus, pathological sera with these protein alterations might form more aggregates during heating than normal sera. These data suggest the following: (1) heat inactivation of complement at 53 degrees for 90 min is preferable to the traditional 56 degrees; (2) in any assay where immunoglobulin aggregates might interfere, normal serum may be an inadequate control and correlations will need to be made between serum IgG and albumin concentrations and the results obtained in these assays.

Adult↗
PubMed1997

[Assessment of allergenic activity of heated and ovomucoid-depleted egg white].

We investigated allergenic activity of heated and ovomucoid (OM)-depleted egg white by RAST inhibition tests, skin tests and and oral challenge tests. Freeze-dried egg white, OM and ovalbumin (OA) were coupled with CNBr-activated paper discs. Freeze-dried, heated, and heated and OM-depleted egg white antigens were used as inhibitors in RAST inhibition tests. Freeze-dried egg white significantly inhibited the IgE-binding to freeze-dried egg-white-, OM- and OA-discs. Heated egg white showed a significant inhibition against only OM-disc, but heated and OM-depleted egg white didn't effectively suppress IgE-binding to all discs. Fifty-six patients were subjected for skin tests and 27 patients for oral challenge tests with freeze-dried egg white, heated egg white and heated and OM-depleted egg white. Eighteen of 25 subjects with positive prick tests results to freeze-dried egg white showed negative results to heated egg white. Four of 7 cases with positive prick test results to heated egg white gave negative results to heated and OM-depleted egg white. 20-minutes patch tests showed almost similar results to prick tests. Four of 8 subjects showing positive oral challenge tests with freeze-dried egg white were negative to heated egg white. All of 4 with positive oral challenge tests by heated egg white were negative results to heated and OM-depleted egg white. These evidence indicated that heated and OM-depleted egg white was more hypoallergenic than heated egg white.

Allergens↗
PubMed1998

Characterization of tissue morphology, angiogenesis, and temperature in the adaptive response of muscle tissue to chronic heating.

Previous investigations on the in vivo effects of chronic heat on tissue suggest a response whereby heated tissue temperatures decrease over time. This response occurred in conjunction with localized angiogenesis, which possibly contributed to the temperature decreases by increasing local perfusion and enhancing tissue heat transfer. Our own studies were the first to use a chronic heat source to heat tissue at initial interfacial temperatures between 40 degrees C and 46 degrees C. Initial temperatures above 45.3+/-2.2 degrees C caused necrosis of adjacent tissue. Through an adaptive response, the necrosis was removed by 7 weeks and replaced by a highly vascularized tissue capsule at 41.8+/-0.5 degrees C. The present study sought to characterize the spatial distribution, number of capillaries, and temperatures associated with this adaptive response. Heated and control muscle tissue sections were removed after 2, 4, and 7 weeks of heating at 0.08 W/cm2. Tissue layer thicknesses and capillary densities were measured and correlated with corresponding tissue temperatures. Necrosis was present adjacent to the heat source at 2 and 4 weeks; however by 7 weeks, a highly vascularized fibrous tissue capsule had replaced nearly all necrosis. Capillary densities, particularly near the heat source, were significantly greater at 7 weeks than at either 2 or 4 weeks. Capillary densities in heated tissue capillary fronts tripled from 2 to 7 weeks (106.4+/-14.3 caps/mm2 versus 39.1+/-18.5 caps/mm2). Furthermore, a mean temperature of 41.7+/-0.9 degrees C was measured in heated tissue capillary fronts at all durations, suggesting that this may be a threshold temperature for heat-induced angiogenesis or endothelial cell survival. These findings more completely characterize the perfusion component of the current mathematical model for heat transfer in tissue and will help to establish guidelines for the functional heat loss that an implantable, heat-producing device may allow.

Acclimatization↗
PubMed2002

Expression pattern of HSP25 in mouse preimplantation embryo: heat shock responses during oocyte maturation.

Heat shock proteins (HSPs) are known to play an important role not only in various stress conditions such as exposure to heat shock, but also in normal development and/or differentiation. The role of small heat shock proteins such as HSP25 in early embryo development remains largely unknown. In the present study, we examined temporal and spatial expression patterns of HSP25 during mouse preimplantation embryo development. Reverse transcription-polymerase chain reaction (RT-PCR) showed that hsp25 mRNA was detected in unfertilized eggs. Hsp25 mRNA was induced by zygotic gene activation at 2-cell stage, decreased slightly at 4-cell, and re-increased at morula, with the highest level at blastocyst stage. Interestingly, another form of hsp25 variant of which 156 bp (52 a.a.) was truncated within the exon1 region was observed in all stages of preimplantation embryos. We also investigated the sub-cellular localization of HSP25 by fluorescence immunocytochemistry. HSP25 was detected in the cytoplasm under normal developmental condition. While acute heat shock (at 43 degrees C for 30 min) caused no significant changes in the sub-cellular localization of HSP25 in the developing mouse embryos, chronic heat shock (at 43 degrees C for 3 hr) resulted in a denser immunostaining of HSP25 in the nucleus than in the cytoplasm, indicating a nuclear translocation of HSP25 by heat shock. As hsp25 mRNA was detected in the unfertilized egg as a maternal transcript, we examined the expression of hsp25 mRNA with RT-PCR during oocyte maturation under normal and heat shock conditions. Hsp25 mRNA was detected at GV (germinal vesicle)-, GVBD (germinal vesicle breakdown)-, and MII (metaphase II)-oocytes. The expression of hsp25 mRNA was increased markedly by both acute (for 30 min and 1 hr) and chronic (for 4 hr) heat shock, but returned to the basal level during recovery from heat shock in a time-dependent manner, suggesting a thermo-protective role of HSP25. In contrast to preimplantation embryos, HSP25 was detected both in the cytoplasm and the nucleus except for the nucleolus, and the cellular localization was not altered by heat shock. Finally, we investigated the effect of heat shock on oocyte maturation. When GV-oocytes were exposed to acute heat shock (at 43 degrees C for 15 min to 1 hr), they underwent the GVBD and the PB (polar body) emission successfully. However, under more stringent heat shock conditions (at 43 degrees C for 2-4 hr), most oocytes were arrested at the GV-stage, and the first PB was not developed, indicating that chronic heat shock might be inhibitory to the mouse oocyte maturation. Taken together, these findings suggest that HSP25 is important for mouse preimplantation embryo development and oocyte maturation.

Animals↗
PubMed2005

Heat shock inhibits NF-kB activation in a dose- and time-dependent manner.

BACKGROUND: The heat shock response (HSR) attenuates NF-kappaB mediated activation of the acute inflammatory response by inhibiting IkB degradation. The HSR also confers a protective phenotype upon cells through production of heat shock proteins (HSP). However, the exact conditions that induce the HSR and stimulate the production of protective HSP are poorly defined. Consequently, we hypothesized that the inhibition of NF-kappaB activation through the HSR is dependent both on the degree of cellular injury and the length of the recovery period from the heat shock. METHODS: RAW 264.7 murine macrophages were heated to 43 degrees C for 15 (mild heat shock), 45 (moderate heat shock), or 90 min (severe heat shock), allowed to recover at 37 degrees C for 0 to 24 h, and then exposed to 100 ng/ml of Escherichia coli (055:B5) lipopolysaccharide (LPS). Cellular viability, HSP expression, and the activation of NF-kappaB after LPS exposure were determined by alamarBlue assay, immunoblot, and electrophoretic mobility shift assay, respectively. RESULTS: Transient attenuation of NF-kappaB activation and IkappaB preservation was observed only with moderate heat shock and 1 h of recovery. Mild heat shock had no effect on LPS-induced NF-kappaB activation or IkappaB degradation. Severe heat shock completely inhibited NF-kappaB activation and preserved IkappaB protein levels. Heat shock proteins were detectable 30 min after moderate heat shock, with maximal and sustained levels 2 to 24 h after heat shock. CONCLUSION: The attenuation of NF-kappaB activation after heat shock is both dose- and time-dependent.

Animals↗