Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Heating”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,495 records · Page 83Linked to original sources
PubMed2000

Heat shock inhibits phosphorylation of I-kappaBalpha.

Previous studies demonstrated that induction of the heat shock response is associated with inhibition of the proinflammatory transcription factor NF-kappaB by a mechanism involving inhibition of I-kappaBalpha degradation. To provide further insight regarding the interactions of these fundamental cellular responses, the present experiments were designed to elucidate the mechanism(s) by which heat shock inhibits degradation of I-kappaBalpha. In an in vitro model of inflammatory cell signaling, treatment of RAW 264.7 murine macrophages with LPS (100 ng/mL) caused rapid degradation of I-kappaBalpha. Heat shock, 1 h before treatment with LPS, completely inhibited LPS-mediated degradation of I-kappaBalpha. Immunoprecipitation studies demonstrated that heat shock inhibited LPS-mediated ubiquitination of I-kappaBalpha. Western-blot analyses using a phosphorylated I-kappaBalpha-specific antibody demonstrated that heat shock inhibited LPS-mediated phosphorylation of I-kappaBalpha. In contrast, heat shock induced phosphorylation of c-jun. In murine fibroblasts having genetic ablation of the heat shock factor-1 gene, heat shock inhibited tumor necrosis factor-alpha mediated degradation of I-kappaBalpha. We conclude that the mechanism by which heat shock inhibits LPS-mediated degradation of I-kappaBalpha involves specific inhibition of I-kappaBalpha phosphorylation and subsequent I-kappaBalpha ubiquitination. In addition, this mechanism does not involve activation of heat shock factor-1 or the heat shock proteins regulated by heat shock factor-1.

Animals↗
PubMed1994

Regulation of 70-kDa heat-shock-protein ATPase activity and substrate binding by human DnaJ-like proteins, HSJ1a and HSJ1b.

The DnaJ family of molecular chaperones is characterized by the presence of a highly conserved 70-amino-acid J domain. Escherichia coli DnaJ interacts with the 70-kDa heat-shock protein (DnaK), in vitro, to stimulate the 70-kDa heat-shock protein ATPase activity and modify substrate binding. The conservation of the interaction of DnaJ-like proteins with the 70-kDa heat-shock proteins has been demonstrated for the yeast protein YDJ1, a protein that shows full domain conservation with E. coli DnaJ. Human neurone-specific DnaJ-like proteins, HSJ1a and HSJ1b, possess a J domain and a glycine/phenylalanine-rich region in common with E. coli DnaJ, although the overall amino acid identity is less than 23%. We have investigated, in vitro, the interaction of HSJ1a and HSJ1b with the mammalian brain constitutive 70-kDa heat-shock protein (hsc70). The weak intrinsic ATPase activity of the constitutive 70-kDa heat-shock protein is enhanced more than fivefold by stoichiometric amounts of both HSJ1a and HSJ1b. This enhancement is mediated by an increase in the rate of bound ATP hydrolysis, whereas the rate of ADP release is unaffected. HSJ1 proteins appear to regulate the affinity of the 70-kDa constitutive heat-shock protein for the permanently unfolded substrate, carboxymethylated alpha-lactalbumin. A recent report [Palleros, D. R., Reid, K. L., Shi, L., Welch, W. J. & Fink, A. L. (1993) Nature 365, 664-666] has suggested that substrate release by 70-kDa heat-shock proteins requires a conformational change in these proteins induced by K+ in concert with ATP binding. In the presence of ATP, HSJ1 proteins reduce 70-kDa constitutive heat-shock protein/carboxymethylated alpha-lactalbumin complex formation both in the presence and absence of K+. This suggests that HSJ1 proteins induce a conformational change in the 70-kDa constitutive heat-shock protein that can mimic the effect mediated by K+ and therefore modulate 70-kDa heat-shock protein substrate release by another mechanism rather than merely stimulating the 70-kDa heat-shock protein ATPase activity. As HSJ1 proteins have limited similarity to DnaJ, we suggest that this action is being mediated by the J domain alone, and that this modulation of 70-kDa heat-shock-protein substrate binding will be common to all proteins that contain a J domain.

Adenosine Triphosphatases↗
PubMed1989

Heat shock affects cell cycling in the neural plate of cultured rat embryos: a flow cytometric study.

The effects of heat shock on cell cycling in the mammalian neuroectoderm were determined by applying heat shocks to cultured rat embryos at the neural plate stage, as part of a study on the teratogenic effects of heat shock on neural development. The heat shocks had been characterized previously (Walsh et al.: Teratology 36:181-191, 1987) with respect to their effects on the gross morphological development of the rat embryos. The effects on cell cycling were observed in DNA histograms of neural plate cells recorded in a flow cytometer after staining with DAPI. The mild heat shock (42 degrees C for 10 min) arrested cells at entry to S phase. The teratogenic heat shock (43 degrees C for 7.5 min) arrested cells at entry to S phase also but for a longer time and inhibited cycling through S phase. After each arrest, a synchronized peak of cells later entered S phase and progressed through the cycle. The induced-thermotolerance heat shock, which was the mild heat shock followed after an interval by the teratogenic heat shock, showed that pre-treatment with the mild heat shock reduced the magnitude of the response to the teratogenic heat shock. The cell-cycle inhibitor ICRF 159 showed the effects on cycling rates of the heat-shock treatments. The arrest of cells at entry to S phase by heat shock may function to prevent cells entering DNA synthesis under non-optimal conditions. We report estimates of proportions of non-proliferative cells in the neural plate of the rat embryos.

Animals↗
PubMed1996

Influence of skin temperature on heat pain threshold in humans.

We compared the effect of skin temperature on the critical threshold temperature eliciting heat pain with the effect of skin temperature on the response latency to the first heat pain sensation in healthy human subjects. Also, we determined the effect of the duration of a heat stimulus ramp on pain threshold. Furthermore, we determined the effect of skin temperature on mechanically induced pain. We found that the latency to the first pain sensation induced by a radiant heat stimulus was significantly decreased with an increase in the skin temperature (25-35 degrees C). However, independent of the rate of the stimulus rise (3-10 degrees C/s) and independent of the stimulus location (hairy vs glabrous skin), the threshold temperature for eliciting the heat pain sensation, determined with a contact thermostimulator, was not changed by a change in the skin temperature in the same subjects. With a fast rate of stimulus rise, a higher pain threshold was obtained than with a slow rise of stimulus temperature. However, this difference was found only with subject-controlled ascending stimuli (method of limits) but not with experimenter-controlled, predetermined stimulus ramps (method of levels). The heat pain threshold was higher in the glabrous skin of the hand than in the hairy skin of the forearm. With increasing stimulus duration (2.5-10 s), the threshold temperature eliciting the heat pain sensation was significantly decreased. The mechanically induced pain threshold was not influenced by the skin temperature. The results indicate that the critical temperature for eliciting heat pain is independent of the skin temperature in humans. However, a change in skin temperature is an important source of an artefactual change in heat pain sensitivity when the radiant heat method (latency or energy) is used as an index of pain sensitivity. With a method dependent on reaction time (the method of limits), the heat pain threshold was artefactually increased, with fast rates of stimulus rise due to the long delay of slowly conducting heat pain signals in reaching the brain. With an increase in the duration of the heat stimulus, the critical temperature for eliciting pain sensation was significantly decreased, which may be explained by central neuronal mechanisms (temporal summation).

Adult↗
PubMed1995

Promotion of sleep by heat in young rats.

The aim of the experiments was to study the effects of a moderate heat load on sleep in young (26-day-old) rats and to determine whether the sleep-promoting effect of heat results from stimulation of the homeostatic sleep process. The changes in sleep-wake activity, electroencephalogram slow wave activity (SWA) during non-rapid eye movement sleep (NREMS) and cortical temperature (Tcrt) were determined during and after long (24-h) and short (2.5-h) heat loads (elevation of ambient temperature from 26 degrees C to 32 degrees C), and after total sleep deprivation (SD) combined with a short-term heat load. The heat exposures elicited increases in Tcrt and rectal temperature (2 and 1.7 degrees C respectively). The long-term heat load induced persistent, albeit slight enhancements in NREMS. Rapid eye movement sleep (REMS) increased with a 12-h delay during the 24-h heat load. Heat elicited an immediate large increase in SWA. After this initial increase, SWA declined and tended to fall below the baseline level during the last 12 h of the 24-h heat load. SWA and REMS were significantly suppressed after termination of 24-h heat loading. The increased SWA during the short-term heat load was not followed by subsequent alterations in sleep when the ambient temperature had returned to normal. However, after the combination of SD with the short-term heat load the durations of NREMS and SWA were significantly enhanced compared with those found after SD at 26 degrees C. The results are interpreted as suggesting that heat increases NREMS in the young rat by the same mechanism as is involved in the enhancement of NREMS after SD: a stimulation of sleep drive.

Animals↗
PubMed2004

Biomechanical properties of heat-treated bone grafts.

INTRODUCTION: A possible critical complication associated with banking bone is human immunodeficiency virus (HIV) infection. Recently, since the report of HIV infection in bone allografts from an HIV-seronegative donor, a more reliable method of sterilization for preserved bone graft has become necessary. Heat treatment of banking bone is one of the simple sterilization methods. This method is especially safe and practical for the prevention of HIV infection. MATERIALS AND METHODS: We previously reported a biological study on heat-treated bone graft. In that study, we showed that revascularization and new bone formation of bone graft after heat treatment at 60 degrees C was nearly the same as that of non-heat-treated bone graft, while at 100 degrees C, revascularization and new bone formation showed a significant delay. This time, we examined the change of mechanical strength of heat-treated bone grafts after transplantation in an experiment. To eliminate the problem of antigenicity of grafted bone, we used autografts, not allografts. Two types of heat-treated autografts were employed: heat-treated at 60 degrees C for 30 min and heat-treated at 100 degrees C for 5 min; as a control, fresh autografts were replaced in the left femur of rabbits. A strength test was performed for both the transplanted bone and the untreated intact right femur with time after transplantation. The strength test consisted of a compression test and torsional test, and the strength was compared between transplanted bone and the untreated intact right femur. RESULTS: In the compression test, the grafts heat-treated at 60 degrees C showed a strength ratio before transplantation of 97.3%. The strength ratio decreased to 63.5% at 18 weeks after transplantation. Then the strength ratio increased and recovered to 94.5% at 48 weeks after transplantation. However, the grafts heat-treated at 100 degrees C showed unsatisfactory mechanical strength, at 48 weeks the strength ratio was 60.1%, which was significantly lower compared with controls. In the torsional test, the grafts heat-treated at 60 degrees C showed almost the same strength observed in the compression test. However, the grafts heat-treated at 100 degrees C showed unsatisfactory mechanical strength: at 48 weeks, the strength ratio was 57.3%. CONCLUSION: Therefore, heat treatment at 60 degrees C is a useful sterilization method, not only in biological but also mechanical terms.

Animals↗
PubMed2000

Effect of heat stress on the inhibition and recovery of the ribulose-1,5-bisphosphate carboxylase/oxygenase activation state.

Experiments were conducted to determine the relative contributions of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco; EC 4.1.1.39) activation state vis-a-vis Rubisco activase and metabolite levels to the inhibition of cotton (Gossypium hirsutum L.) photosynthesis by heat stress. Exposure of leaf tissue in the light to temperatures of 40 or 45 degrees C decreased the activation state of Rubisco to levels that were 65 or 10%, respectively, of the 28 degrees C control. Ribulose-1,5-bisphosphate (RuBP) levels increased in heat-stressed leaves, whereas the 3-phosphoglyceric acid pool was depleted. Heat stress did not affect Rubisco per se, as full activity could be restored by incubation with CO2 and Mg2+. Inhibition and recovery of Rubisco activation state and carbon dioxide exchange rate (CER) were closely related under moderate heat stress (up to 42.5 degrees C). Moderate heat stress had negligible effect on Fv/Fm, the maximal quantum yield of photosystem II. In contrast, severe heat stress (45 degrees C) caused significant and irreversible damage to Rubisco activation, CER, and Fv/Fm. The rate of Rubisco activation after alleviating moderate heat stress was comparable to that of controls, indicating rapid reversibility of the process. However, moderate heat stress decreased both the rate and final extent of CER activation during dark-to-light transition. Treatment of cotton leaves with methyl viologen or an oxygen-enriched atmosphere reduced the effect of heat stress on Rubisco inactivation. Both treatments also reduced tissue RuBP levels, indicating that the amount of RuBP present during heat stress may influence the degree of Rubisco inactivation. Under both photorespiratory and non-photorespiratory conditions, the inhibition of the CER during heat stress could be completely reversed by increasing the internal partial pressure of CO2 (Ci). However, the inhibition of the CER by nigericin, a K+ ionophore, was not reversible when the Ci was increased at ambient or high temperature. Our results indicate that inhibition of photosynthesis by moderate heat stress is not caused by inhibition of the capacity for RuBP regeneration. We conclude that heat stress inhibits Rubisco activation via a rapid and direct effect on Rubisco activase, possibly by perturbing Rubisco activase subunit interactions with each other or with Rubisco.

Carbon Dioxide↗
PubMed1994

Effect of heat-moisture treatment on the structure and physicochemical properties of cereal, legume, and tuber starches.

Native wheat, oat, lentil, yam, and potato starches were heat treated at 100 degrees C for 16 h at moisture contents between 10 and 30%. The heat treatment did not change granule size and shape. In oat starch, granules were less compactly packed after heat treatment. The X-ray diffraction intensities increased in wheat, oat, and lentil starches, but decreased in potato and yam. The X-ray patterns of wheat and oat starches remained unchanged, while those of lentil, potato, and yam starches became more cereal-like. In all starches, the swelling factor and amylose leaching decreased, being more pronounced in potato. Heat treatment induced complex formation between amylose and native lipids. Differential scanning calorimetry of the heat-treated samples showed a broadening of the gelatinization-temperature range and a shifting of the endothermal transition towards higher temperatures. These changes were more pronounced in potato starch. The gelatinization enthalpy of wheat, oat, and lentil starches remained unchanged, but those of potato and yam starches decreased on heat treatment. Heat treatment increased the 95 degrees C viscosity of wheat starch, but decreased those of oat lentil, potato, and yam starches. In all starches, thermal and shear stability increased after heat treatment. Acid hydrolysis decreased on heat treatment of wheat and lentil starches, but increased in oat, potato, and yam starches. However, in potato and yam starches, the foregoing trend was evident only during the first seven days of hydrolysis. Thereafter, acid hydrolysis was more pronounced in native than in heat-treated starches. The susceptibility towards hydrolysis by porcine pancreatic alpha amylase decreased on heat treatment of wheat and lentil starches, whereas increases were observed for oat, potato, and yam starches. The results indicated that the extent of starch-chain associations within the amorphous regions and the degree of crystalline order are altered during heat-moisture treatment. The magnitude of these changes were found to be dependent upon the moisture content during heat treatment and on the starch source.

Amylose↗
PubMed1987

Characteristics of a heat treated antihaemophilic cryoprecipitate.

In order to evaluate the influence of heat treatment (68 degrees C for 24 or 72 hours) on the essential components of antihaemophilic cryoprecipitate, i.e. factor VIII coagulant activity (VIII:C), von Willebrand factor (VIIIR:Ag and VIIIR:RCF) and fibrinogen, ordinary lyophilized cryoprecipitate was compared to heat treated, aminoacid-enriched specimens. The median reduction in factors VIII:C, VIIIR:Ag, VIIIR:RCF and fibrinogen during lyophilization of ordinary cryoprecipitate was 26 per cent, 11 per cent, 1 per cent and 8.5 per cent, respectively. Heat treatment of such cryoprecipitate resulted in 85 to 98.5 per cent reduction in these parameters, while the reduction following lyophilization and heat treatment (24 hours) of aminoacid-containing preparations was not significantly different from non-heated, ordinary cryoprecipitate. Following heating of aminoacid-enriched cryoprecipitate for 72 hours, only factor VIIIR:RCF was significantly reduced (32.5 per cent) compared to non-heated samples. Ordinary cryoprecipitate was almost insoluble following heat treatment. Enrichment with aminoacids, however, made the heat treated cryoprecipitate fully soluble, but the content of these vials were slightly slower in dissolving than non-heated preparations. Ultracentrifugation prior to lyophilization and heating did not improve the solubility. If heat treatment proves to be efficient in inactivating viral agents, we conclude that heated (68 degrees C for 24 hours), aminoacid-enriched cryoprecipitate may be a convenient product for treating haemophilia A, von Willebrand's disease and hypofibrinogenemia.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Pathophysiological changes after local heating of rat liver.

Changes in blood flow in rat liver by local heating of the left lateral lobe were studied. A small portion of the left lateral lobe was heated by capacitive application of 8 MHz RF with a 2 cm diameter electrode on the ventral surface and a 7 cm diameter electrode on the dorsal surface of upper body of rats. A circular area with diameter of about 1 cm in the left lateral lobe could be heated to relatively homogeneous temperatures. The temperature in the remaining part of the left lateral lobe as well as in the rest of liver tissue also increased to varying degrees during the local heating of the left lateral lobe. When heated at 39 degrees or 41 degrees C for 45 min, the arterial blood flow, as measured with the radioactive microsphere method, in the heated area, and that in the rest of the left lateral lobe as well as in the whole liver initially increased during the first 30 min and then started to decline. During a 45 min heating at 43 degrees C, the arterial blood flow in the heated area slightly increased for 15 min and then significantly decreased thereafter. The arterial blood flow in the rest of the liver tissue also increased during the first 15 min of a 43 degrees C heating and began to decline. Histological examination of liver heated at 43 degrees C for 30 min showed wedge-shaped infarctions early on, which appeared to be organized into scar tissue by 7 days after heating. The concentrations of glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and lactate dehydrogenase (LDH) in the serum significantly increased 2 hr after heating the small portion of the left lateral lobe at 43 degrees C for 30 min and began to decrease thereafter although the serum level of GOT and GPT was still greater than the control value 24 hr after heating.

Alanine Transaminase↗
PubMedDate not supplied

Treating acute low back pain with continuous low-level heat wrap therapy and/or exercise: a randomized controlled trial.

BACKGROUND CONTEXT: Restorative exercise and palliative modalities are frequently used together for the treatment of acute low back pain. However, little is known about the effects of combining these treatments. PURPOSE: To evaluate the efficacy of combining continuous low-level heat wrap therapy with directional preference-based exercise on the functional ability of patients with acute low back pain. STUDY DESIGN/SETTING: A randomized controlled trial was conducted at three outpatient medical facilities. PATIENT SAMPLE: One hundred individuals (age 31.2+/-10.6 years) with low back pain of less than 3 months duration. OUTCOME MEASURES: The primary outcome measure was functional ability assessed by the Multidimensional Task Ability Profile questionnaire. Secondary outcomes were disability assessed by the Roland-Morris Disability Questionnaire and pain relief assessed by a 6-point verbal rating scale. METHODS: Participants were randomized to one of four groups: Heat wrap therapy alone (heat wrap, n=25); directional preference-based exercise alone (exercise, n=25); combination of heat wrap therapy and exercise (heat+exercise, n=24); or control (booklet, n=26). Treatment was administered for five consecutive days and included four visits to the study center over 1 week. RESULTS: At 2 days after the conclusion of treatment (Day 7), functional improvement for heat+exercise was 84%, 95%, and 175% greater than heat wrap, exercise, and booklet, respectively (p<.05). Seventy-two percent of the subjects in the heat+exercise group demonstrated a return to pre-injury function compared with 20%, 20%, and 19% for heat wrap, exercise, and booklet, respectively (p<.05). Disability reduction for heat+exercise was 93%, 139%, and 400% greater than heat wrap, exercise, and booklet, respectively (p<.05). Pain relief for heat+exercise was 70% and 143% greater than exercise and booklet, respectively (p<.05). CONCLUSIONS: Combining continuous low-level heat wrap therapy with directional preference-based exercise during the treatment of acute low back pain significantly improves functional outcomes compared with either intervention alone or control. Either intervention alone tends to be more effective than control.

Activities of Daily Living↗
PubMed2001

Heat shock proteins in health and disease: therapeutic targets or therapeutic agents?

For many years, heat shock or stress proteins have been regarded as intracellular molecules that have a range of housekeeping and cytoprotective functions, only being released into the extracellular environment in pathological situations such as necrotic cell death. However, evidence is now accumulating to indicate that, under certain circumstances, these proteins can be released from cells in the absence of cellular necrosis, and that extracellular heat shock proteins have a range of immunoregulatory activities. The capacity of heat shock proteins to induce pro-inflammatory responses, together with the phylogenetic similarity between prokaryotic and eukaryotic heat shock proteins, has led to the proposition that these proteins provide a link between infection and autoimmune disease. Indeed, both elevated levels of antibodies to heat shock proteins and an enhanced immune reactivity to heat shock proteins have been noted in a variety of pathogenic disease states. However, further evaluation of heat shock protein reactivity in autoimmune disease and after transplantation has shown that, rather than promoting disease, reactivity to self-heat shock proteins can downregulate the disease process. It might be that self-reactivity to heat shock proteins is a physiological response that regulates the development and progression of pro-inflammatory immunity to these ubiquitously expressed molecules. The evolving evidence that heat shock proteins are present in the extracellular environment, that reactivity to heat shock proteins does not necessarily reflect adverse, pro-inflammatory responses and that the promotion of reactivity to self-heat shock proteins can downregulate pathogenic processes all suggest a potential role for heat shock proteins as therapeutic agents, rather than as therapeutic targets.

Journal Article↗
PubMed1992

Cutaneous heat loss shortly after burn injury in children.

1. Total heat loss and its components have been studied in cool (20 degrees C) and warm (30 degrees C) environments in 30 healthy children and 21 children who had been burned (10-17% body surface area) 0.5-29 h previously. 2. In healthy naked children at 20 degrees C, the partition of total heat loss was: radiation, 64%; convection, 32%; evaporation, 4%. On transfer to the warm, total heat loss was reduced by approximately 50%, with disproportionate reductions in the contributions from radiation and convection being offset, to some extent, by an increase in evaporative heat loss. 3. In patients during the first 5.5h after injury, the magnitude and pattern of heat loss at 20 degrees C and 30 degrees C were similar to those in control subjects and were unaffected by bandaging. 4. Ten to twenty-nine hours after injury, when the patients were bandaged and body temperature and heat content were significantly higher than in control subjects, radiant and convective heat losses were increased, but as evaporative heat loss tended to be reduced; total heat loss in the warm was unchanged. However, at this time at 20 degrees C, total heat loss was reduced compared with healthy children at the same ambient temperature. 5. The findings of unchanged or reduced total heat loss and reduced evaporative heat loss in injured patients are interpreted as inappropriate responses to an increased body temperature and heat content in children after burn injury.

Body Temperature Regulation↗
PubMed2000

Low-threshold heat response antagonized by capsazepine in chick sensory neurons, which are capsaicin-insensitive.

The heat-transducing receptor VR1 cloned from rat sensory neurons can be activated by both noxious heat and capsaicin. As the response of sensory neurons to capsaicin is species dependent, it is conceivable that the responses to noxious heat and to capsaicin are transduced by distinct receptors across different species. Therefore, we investigated responses to noxious heat from a capsaicin-insensitive (chick) and a capsaicin-sensitive (rat) species. In chick, whole-cell patch-clamp experiments in isolated dorsal root ganglion neurons revealed two populations of neurons with different thresholds to noxious heat, activated at approximately 43 degrees C and approximately 53 degrees C. In cobalt uptake experiments, the proportion of neurons showing a heat-induced response increased with increasing heat stimuli. Application of capsaicin (1-10 microM) did not result in inward currents or cobalt uptake. Rat neurons yielded comparable results in heat experiments, but were capsaicin-sensitive. Although chick neurons are insensitive to capsaicin, the competitive capsaicin antagonist capsazepine (1-10 microM) was effective in blocking heat-induced responses, verified by patch-clamp and cobalt uptake methods. The noncompetitive capsaicin antagonist ruthenium red (10 microM) reduced to almost nil the proportion of heat-responsive neurons identified with the cobalt uptake method. These findings suggest that chick DRG neurons express a low-threshold heat-transducing receptor with a pharmacological profile distinct from the low-threshold heat receptor VR1 cloned from rat DRG neurons. The data support the idea that there might be heat receptor subtypes with differences in the capsaicin binding site.

Animals↗
PubMed2004

[Heat transfer by conductive warming with circulating-water mattresses].

AIM OF THE STUDY: To determine the heat transfer by circulating-water mattresses placed under the back and over both legs of human volunteers. METHODS: With approval by the local ethics committee and informed consent eight minimally clothed volunteers were included in the study. Six calibrated heat flux transducers were placed on the back and additionally eight sensors were placed on both legs of each volunteer. The volunteers reclined on a circulating-water mattress (ComfortPad Plus(R), Cincinnati Sub-Zero Products Inc., Cincinnati, OH, USA) coated with gel (Granulab International, Armersfoort, Niederlande). Another circulating-water mattress (Plastipad trade mark, Cincinnati Sub-Zero Products Inc.) was placed over both legs. Both devices were heated to 41 degrees C by a hypo-hyperthermia system (Hico-Variotherm 530, Hirtz and Co. Hospitalwerk, Cologne, Germany). Heat flux data were sampled during steady-state conditions. After determination of the contact area between the mattresses and the skin, heat transfer was calculated by multiplication of the heat flux per area by the contact area. RESULTS: Heat flux per area to the back was 45.6 +/- 4.5 W m (- 2), the contact area was 0.39 +/- 0.03 m (2). This resulted in a heat transfer of 18.0 +/- 2.4 W. Heat flux per area to the legs was 24.7 +/- 4.3 W m (- 2), the contact area was 0.12 +/- 0.01 m (2). This resulted in a heat transfer of 2.9 +/- 0.6 W. CONCLUSION: The heat transfer of the circulating-water mattress to the back was much higher than the heat transfer to the legs. Nevertheless, model calculations show that conductive warming of the legs is more important for the prevention of perioperative hypothermia than conductive warming of the back, because it has a higher impact on the heat balance.

Adult↗
PubMed1997

Resistance to heat radiosensitization and protein damage in thermotolerant and thermoresistant cells.

Recently, randomized phase III trials have indicated that hyperthermia combined with radiation leads to significantly better tumour control of certain malignancies than does radio-therapy alone. Yet, the full capacity of such combined treatments might not have been optimally exploited as in vitro data indicate that repeated beating of cells can result in either the development of a transient heat resistance (thermotolerance) and/or the selection/induction of a stable heat resistant cell population. Although the mechanism of thermotolerance and its effect on thermo-radiotherapy has been studied extensively, little data are available on the mechanism of stable heat resistance and its impact on combined heat and radiation treatments. In the current study, a comprehensive analysis was made of the differences and similarities between thermotolerance (TT) and stable heat resistance (TR) in terms of the mechanism of resistance to the direct toxic action of heat and in terms of the impact on the extent of thermal radiosensitization. Using heat resistant mutants previously derived from a murine radiation-induced fibrosarcoma (RIF-1), it was observed that these cells were resistant to protein denaturation and aggregation in the cytoplasmic/membrane compartment (measured by ESR (electron spin resonance) analysis and by in situ thermal denaturation of the foreign firefly luciferase targeted to the cytoplasm) but not in the nuclear compartment (measured by TX-100 insoluble nuclear proteins and by in situ thermal denaturation of luciferase targeted to the nucleus). RIF-1-TT cells, in contrast, were resistant for a 1 end-points tested. The lack of protection of nuclear heat damage in the RIF-TR cells could not be explained by a failure of one or more of the HSP70 isoforms to enter the nuclei of these cells. In relation to the absence or presence of heat resistance in the nucleus, the extent of heat radiosensitization was reduced in RIF-1-TT but not RIF-TR cells. This implies that resistance for heat killing is not necessarily accompanied by a reduction in the ability of heat to enhance the cellular radiosensitivity. The data indicate that the mechanism leading to permanent resistance after repeated heating and the mechanism causing thermotolerance may share common features but are in part different.

Animals↗
PubMed2005

Quantification of the heat exchange of chicken eggs.

In the incubation process of domestic avian eggs, the development of the embryo is mainly influenced by the physical microenvironment around the egg. Only small spatiotemporal deviations in the optimal incubator air temperature are allowed to optimize hatchability and hatchling quality. The temperature of the embryo depends on 3 factors: (1) the air temperature, (2) the exchange of heat between the egg and its microenvironment and (3) the time-variable heat production of the embryo. Theoretical estimates on the heat exchange between an egg and its physical microenvironment are approximated using equations that assume an approximate spherical shape for eggs. The objective of this research was to determine the heat transfer between the eggshell and its microenvironment and then compare this value to various theoretical estimates. By using experimental data, the overall and the convective heat transfer coefficients were determined as a function of heat production, air humidity, air speed, and air temperature. Heat transfer was not affected by air humidity but solely by air temperature, embryonic heat generation, and air speed and flow around eggs. Also, heat transfer in forced-air incubators occurs mainly by convective heat loss, which is dependent on the speed of airflow. A vertical airflow is more efficient than a horizontal airflow in transferring heat from the egg. We showed that describing an egg as a sphere underestimated convective heat transfer by 33% and was, therefore, too simplistic to accurately assess actual heat transfer from real eggs.

Air Movements↗
PubMed1993

Heat loss during surgical skin preparation.

BACKGROUND: Hypothermia develops rapidly during the 1st h of anesthesia and results in part from evaporative heat loss during surgical skin preparation. The authors tested the hypothesis that evaporation of skin preparation solution contributes significantly to hypothermia. METHODS: Five healthy, unanesthetized volunteers were studied in a 22 +/- 0.4 degrees C environment. One thigh of each volunteer was washed for 10 min, using each of the following representative solutions: (1) water; (2) 50% ethanol in water (EtOH/H2O; similar to tincture of iodine); and (3) povidone-iodine gel. Water and EtOH/H2O each were tested at ambient temperature (cold), warmed to 40 degrees C before application (warm), and with radiant heating of the skin, and gel only at ambient temperatures, resulting in seven study states. Heat loss and skin temperatures on the washed thighs were measured using thermal flux transducers, and values compared with the data obtained from the contralateral unwashed thighs. Change in mean body temperature (per 70 kg) due to washing was calculated by integrating measured heat loss over time and multiplying by the specific heat of human tissue. A mathematical model was developed to predict cutaneous heat loss using only skin temperature, independent of the type and temperature of skin-preparation solution or the use of radiant heating during preparation. RESULTS: Heat loss from the unwashed thigh was approximately 14 kcal/m2 during radiant warming and approximately 39 kcal/m2 without warming. Net heat loss (increment produced by washing) was approximately 30 kcal/m2 with water and gel without radiant warming, but loss was larger with EtOH/H2O than with water under all study conditions. Radiant warming reduced total heat loss (increment produced by washing and environment) during both the EtOH/H2O and water trials, compared with warm or cold EtOH/H2O and water alone. The calculated decreases in mean body temperature per 70 kg ranged from -0.2 to -0.7 degree C/m2. The smallest decrease occurred during radiant warming and washing with water, and the largest decreases during warm or cold EtOH/H2O. CONCLUSIONS: Heat loss was significantly less with water-based than with alcohol-based solutions. Though heating the solutions and radiant warming decreased heat loss, such loss under each tested condition, even per square meter of washed surface, was small compared to other causes of perioperative hypothermia. Consequently, the authors recommend that efforts to maintain intraoperative normothermia be directed elsewhere.

Adult↗