Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “COLD”

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 91 records · Page 5Linked to original sources
PubMed2002

Effect of immobilization, cold and cold-restraint stress on liver monooxygenase activity and lipid peroxidation of influenza virus-infected mice.

The present study provides a direct experimental evidence that the combination of influenza A/Aichi/2/68 (H3N2) infection with different models of "oxidative stress", such as immobilization, cold and cold-restraint, is associated with graduated oxidative disturbances in the liver of mice, despite the absence of virus and inflammation in this tissue. It was found that experimental influenza virus infection is accompanied with a significant increase of lipid peroxidation products, a decrease of natural antioxidants (vitamin E, glutathione) and cytochrome P-450, an inhibition of cytochrome c reductase and liver monooxygenases (analgin- N-demethylase and amidopyrine- N-demethylase). Immobilization and cold stress, applied separately or in combination (cold-restraint), did not influence significantly any of the analysed parameters compared to those of the control group of non-infected mice. Preliminary exposure of mice to immobilization or cold stress and subsequent inoculation of influenza virus resulted in a significant increase of lipid peroxidation products and a significant decrease of vitamin E and reduced glutathione, compared with levels in control (non-infected) animals. Compared to influenza virus-infected and non-stressed animals, the changes in all these parameters were negligible. Immobilization or cold stress, applied in combination with influenza virus infection, partially prevented the suppressive effect of influenza virus on cytochrome P-450 and liver monooxygenases. A tendency towards normalization of these parameters to the control levels was observed. However, after application of cold-restraint plus influenza virus infection, the level of cytochrome P-450 and activity of cytochrome c reductase stayed markedly lower than in infected and non-stressed animals. The activities of liver monooxygenases were slightly increased compared with those of infected and non-stressed animals, but stayed relatively low compared to control (non-infected) mice. Combination of cold-restraint and influenza virus infection resulted in a greater synergistic increase of lipid peroxidation products and a greater synergistic decrease of vitamin E and reduced glutathione compared to controls, as well as to influenza virus-infected and non-stressed animals.

Aminopyrine N-Demethylase↗
PubMed2004

In vivo and in vitro rapid cold-hardening protects cells from cold-shock injury in the flesh fly.

The capacity to undergo rapid the cold-hardening response (RCH) has been documented in diverse groups of insects and functions to protect against non-freezing cold injury and to preserve physiological performance in response to environmental cooling. The RCH response is remarkable for the rapidity of its induction; however the mechanism by which insects perceive cold and transduce this input at the cellular level has received little attention. To test the hypothesis that cells from isolated tissues can undergo RCH in response to cold, we assessed cell viability in four tissues that had undergone either RCH (0 degree C, 2 h followed by -8 degrees C, 2 h) or cold-shock (-8 degrees C, 2 h) both in vivo and in vitro from the adult flesh fly Sarcophaga crassipalpis (Diptera: Sarcophagidae) using fluorescent probes. Adult flies showed a significantly higher survival rate in the RCH group than in the cold-shocked group. Similarly, in all tissues tested, both in vivo and in vitro, RCH significantly improved cell survival compared with the respective cold-shocked groups. To our knowledge this is the first report to demonstrate that isolated cells and tissues from insects can undergo RCH. These results indicate that insect cells are capable of cold-sensing without neuroendocrine mediation; direct induction at the cellular level also helps to explain the swiftness of the RCH response.

Acclimatization↗
PubMed1994

Different effects of cold exposure and cold acclimation on rat liver mitochondrial fatty acid oxidation and ketone bodies production.

1. We have studied fatty acid oxidation and ketone bodies production in liver mitochondria from rats exposed to cold for 10 days and in rats adapted to cold for 40 days. We have examined State 3 respiration and ketone bodies production with palmitoylcarnitine as substrate in isolated mitochondria, together with mitochondrial protein mass and hepatocyte oxygen consumption. 2. Mitochondrial protein mass increases both in cold exposed and in cold adapted rats. 3. State 3 respiration and hepatocyte respiration increase only in cold exposed rats. 4. Ketone bodies production increases in cold adapted rats. 5. Taken together, our results suggest that the increased hepatic mitochondrial protein mass and the increased fatty acid oxidation subserve two different roles: an increase in ATP production in cold exposed rats and an increase in ketone bodies production in cold adapted rats.

Acclimatization↗
PubMed1987

Heterogeneity of cold-stable and cold-labile tubulin in axon- and soma-enriched portions of the adult mouse brain.

Microtubules from the optic nerve (axonal tubulin) and lateral geniculate nucleus (cell tubulin) were separated by cold treatment and the cold-soluble fraction was purified in the presence of Taxol. Isoforms of cold-stable and cold-soluble tubulin were resolved by the use of high-resolution isoelectric focusing. The cold-soluble fraction of axonal tubulin has only 14 of the 20 isotypes seen in the same fraction of cell tubulin. The two cold-stable fractions have 20 isotypes but axonal tubulin has a specific pattern of isotypes 1, 2 and 5. Cold-stable fractions of both axonal and cell tubulin display the existence of an intensely stained alpha-isotype, isotype 7, which seems associated with the property of cold stability. Our results highly favor the hypothesis of a physiological role of the heterogeneity of tubulin in neuronal microtubules.

Animals↗
PubMed2006

Rapid cold-hardening increases membrane fluidity and cold tolerance of insect cells.

The rapid cold-hardening (RCH) response not only confers dramatic protection against cold-shock (non-freezing) injury, but also "instantaneously" enhances organismal performance. Since cold-shock injury is associated with damage to the cell membrane, we investigated the relationship between RCH and changes in cold tolerance and membrane fluidity at the cellular level. None of the adult flies (Sarcophaga bullata) in the cold-shocked treatment group survived direct transfer to -8 degrees C for 2 h; in contrast, 64.5% of flies in the RCH group survived exposure to -8 degrees C. Differences between the treatment groups also were reflected at the cellular level; only 21.3% of fat body cells in the cold-shocked group survived compared to 68.5% in the RCH group. Using 31P solid-state NMR spectroscopy, we determined that membrane fluidity increased concurrently with rapid cold-hardening of fat body cells. This result suggests that membrane characteristics may be modified very rapidly to protect cells against cold-shock injury.

Adaptation, Physiological↗
PubMed1979

Effects of noradrenaline and carbachol on temperature regulation of cold-stressed and cold-acclimated rats.

1 Noradrenaline (20 micrograms) and carbachol (1 microgram) injected into the anterior hypothalamus of rats at an ambient temperature of 23 degrees C evoked significant falls in core temperature and increases in tail temperature. 2 When rats were cold-stressed (4 degrees C for 90 min) or cold-acclimated (4 degrees C for 4 weeks) and the above amine injections repeated, only carbachol evoked significant falls in core temperature and neither amine increased tail temperature. 3 Central injections of noradrenaline and carbachol also evoked increases in plasma glucose concentrations but not plasma non-esterified fatty acid (NEFA) concentrations in control, acutely cold-stressed and cold-acclimated rats. 4 Although concentrations of plasma glucose and blood lactate of rats were unaffected by cold exposure to 4 degrees C for 1 to 28 days, glucose oxidation rate of both cold-stressed and cold-acclimated rats was significantly greater than in rats at 23 degrees C. Concentrations of plasma NEFA were increased after 1 to 28 days of cold exposure.

Acclimatization↗
PubMed2005

Heat stroke with multiple organ failure treated with cold hemodialysis and cold continuous hemodiafiltration: a case report.

A 23-year-old comatose man was presented in the emergency room. He had been working inside a building under construction on a hot summer's day. His core body temperature was 42.1 degrees C and he was diagnosed with heat stroke. Urgent cooling procedures, including applying cold vapor to the patient's skin, a gastric lavage with cold water and an intravenous cold saline infusion, were not completely successful and his body temperature remained above 40 degrees C. Because his high temperature was refractory to conventional cooling procedures and we suspected that acute renal failure (ARF) by rhabdomyolysis would develop, we applied hemodialysis (HD) using cold dialysate (initially 30 degrees C and later 35 degrees C), followed by continuous hemodiafiltration (CHDF) with cold dialysate (35 degrees C) at a high flow rate of 18,000 mL per hour. The patient's body temperature fell below 38.0 degrees C within 3 h and was kept below 38.0 degrees C. Continuous hemodiafiltration was continued for one week. During the first week, the patient suffered from multiple organ failure (MOF) involving renal failure, as well as the failure of heart, liver, lung, and central nervous systems. Disseminated intravascular coagulation also developed. However, by virtue of cold CHDF, he almost recovered 3 weeks after the onset, except for remaining mild liver and renal dysfunction. In severe heat stroke, cold HD and high flow, cold CHDF should be a therapeutic choice for cooling and treatment of MOF. Considering mild liver and renal dysfunction still remained, this case suggested these procedures should be initiated at the very beginning of the treatment of severe heat stroke.

Adult↗
PubMed1999

Pathogenic Yersinia species carry a novel, cold-inducible major cold shock protein tandem gene duplication producing both bicistronic and monocistronic mRNA.

Inverse PCR was used to amplify major cold shock protein (MCSP) gene families from a diverse range of bacteria, including the psychrotolerant Yersinia enterocolitica, which was found to have two almost identical MCSP coding regions (cspA1 and cspA2) located approximately 300 bp apart. This tandem gene duplication was also found in Y. pestis, Y. pseudotuberculosis, and Y. ruckeri but not in other bacteria. Analysis of the transcriptional regulation of this MCSP gene in Y. enterocolitica, performed by using both reverse transcriptase-PCR and Northern blot assays, showed there to be two cold-inducible mRNA templates arising from this locus: a monocistronic template of approximately 450 bp (cspA1) and a bicistronic template of approximately 900 bp (cspA1/A2). The former may be due to a secondary structure between cspA1 and cspA2 causing either 3' degradation protection of cspA1 or, more probably, partial termination after cspA1. Primer extension experiments identified a putative transcriptional start site (+1) which is flanked by a cold-box motif and promoter elements (-10 and -35) similar to those found in Escherichia coli cold-inducible MCSP genes. At 30 degrees C, the level of both mRNA molecules was negligible; however, upon a temperature downshift to 10 degrees C, transcription of the bicistronic mRNA was both substantial (300-fold increase) and immediate, with transcription of the monocistronic mRNA being approximately 10-fold less (30-fold increase) and significantly slower. The ratio of bicistronic to monocistronic mRNA changed with time after cold shock and was higher when cells were shocked to a lower temperature. High-resolution, two-dimensional protein gel electrophoresis showed that synthesis of the corresponding proteins, both CspA1 and CspA2, was apparent after only 10 min of cold shock from 30 degrees C to 10 degrees C. The data demonstrate an extraordinary capacity of the psychrotolerant Y. enterocolitica to produce major cold shock proteins upon cold shock.

Amino Acid Sequence↗
PubMed1987

Stress- and cold-induced adrenocortical responses in repetitively immobilized or cold-acclimated rats.

To evaluate the role of adrenocortical hormones in stress- or cold-induced nonshivering thermogenesis, plasma corticosterone (CS) and deoxycorticosterone (DOCS) were measured with the aid of HPLC under various conditions. Repetitive immobilization stress (3 h/day, for 1 or 4 weeks) elevated the resting level (24 h after the last immobilization) of CS, but not DOCS. Acute stress (immobilization for 30 min) or cold exposure (-5 degrees C for 15 min) caused marked increases of CS and DOCS in both nonstressed naive controls and repetitively stressed rats. Four weeks, but not 1 week, of repetitive immobilization stress potentiated the responsiveness of CS to both acute stress and cold, and that of DOCS to acute stress, but not to cold. Cold acclimation (5 degrees C, 4 weeks) significantly elevated both corticosteroids but did not affect the resting levels (18 h after being transferred to 25 degrees C) or the responsiveness of both CS and DOCS to either acute stress or cold. These results suggest that repetitive immobilization stress, but not cold acclimation, could enhance nonshivering thermogenesis, at least in part, through an improvement in the responsiveness of adrenocortical hormone secretion to acute stress or cold.

Acclimatization↗
PubMed1986

Human thermoregulatory responses to cold air are altered by repeated cold water immersion.

The effects of repeated cold water immersion on thermoregulatory responses to cold air were studied in seven males. A cold air stress test (CAST) was performed before and after completion of an acclimation program consisting of daily 90-min cold (18 degrees C) water immersion, repeated 5 times/wk for 5 consecutive wk. The CAST consisted of resting 30 min in a comfortable [24 degrees C, 30% relative humidity (rh)] environment followed by 90 min in cold (5 degrees C, 30% rh) air. Pre- and postacclimation, metabolism (M) increased (P less than 0.01) by 85% during the first 10 min of CAST and thereafter rose slowly. After acclimation, M was lower (P less than 0.02) at 10 min of CAST compared with before, but by 30 min M was the same. Therefore, shivering onset may have been delayed following acclimation. After acclimation, rectal temperature (Tre) was lower (P less than 0.01) before and during CAST, and the drop in Tre during CAST was greater (P less than 0.01) than before. Mean weighted skin temperature (Tsk) was lower (P less than 0.01) following acclimation than before, and acclimation resulted in a larger (P less than 0.02) Tre-to-Tsk gradient. Plasma norepinephrine increased during both CAST (P less than 0.002), but the increase was larger (P less than 0.004) following acclimation. These findings suggest that repeated cold water immersion stimulates development of true cold acclimation in humans as opposed to habituation. The cold acclimation produced appears to be of the insulative type.

Acclimatization↗
PubMed1989

Decreased releasability of basophils from patients with cold urticaria after cold exposure.

Histamine release from peripheral blood basophils challenged with C5a, f-met-peptides and calcium ionophore was studied in patients with cold urticaria before and after exposure to low environmental temperatures. Compared to healthy controls, stimulated mediator release before cold exposure was increased in 7 of 11 patients. When challenged by cold exposure mediator release from in vitro-stimulated basophils was decreased. This decrease was more pronounced after stimulation with receptor-mediated stimuli (e.g. C5a) as compared to receptor-unrelated stimuli, e.g. calcium ionophore. In 4 of 11 patients stimulated mediator release before cold exposure was moderately increased. Also after cold exposure only a weak decrease of stimulated histamine release was seen. Levels of activated complement components (C3a) before and after cold exposure failed to provide evidence for complement activation in vivo. Also the number of circulating basophils as well as their cellular histamine content remained normal after cold exposure. The results show that in these patients release of histamine is altered before and after cold exposure. These changes in basophil responsiveness are not due to complement activation in vivo.

Basophils↗
PubMed2000

Changes in cold-induced vasodilatation, pain and cold sensation in fingers caused by repeated finger cooling in a cool environment.

To examine how repeated cooling of fingers with a rest pause schedule at work affects cold-induced vasodilatation (CIVD), pain and cold sensation in fingers, six healthy men aged 21 to 23 years immersed their left index fingers six times in stirred water at 10 degrees C for 10 minutes. After each cold-water immersion of the fingers, 5-minute rest pause was taken to observe the recovery process of the indicators. This cold-water immersion/rest pause test was carried out in a range of three ambient temperature conditions: 30 degrees C (warm), 25 degrees C (thermoneutral), and 20 degrees C (cool) as experienced in daily life. At the ambient temperatures of 30 degrees C and 25 degrees C, marked CIVD response occurred and the CIVD reactivity did not significantly change upon repetition of cold-water immersion. The lowered finger skin temperature also tended to recover quickly to the pre-immersion level during each post-immersion rest period. At the ambient temperature of 20 degrees C, however, the CIVD response weakened continuously upon repetition of immersion and almost disappeared during the final immersion. The recovery of finger skin temperature during each post-immersion rest was gradually delayed upon repetition of immersion. At every ambient temperature, finger pain and cold sensation induced by each cold-water immersion significantly decreased upon repetition of immersion and completely disappeared during each post-immersion rest period. Oral temperature during the experiment showed no significant change at the ambient temperatures of 25 degrees C and 30 degrees C, but it decreased significantly at the ambient temperature of 20 degrees C. These results suggest that in a cool work environment where the body core temperature is liable to decrease, repeated finger cooling may weaken CIVD reactivity and delay the recovery of finger temperature during post-immersion rest periods. In such lower ambient temperature work conditions, subjective judgements such as the decrease in finger pain and cold sensation during repeated finger cooling and the absence of them during post-immersion rest may not be reliable indicators for monitoring the risk of progressive tissue cooling and frostbite formation.

Adult↗
PubMed1975

[Role of thyroid hormone in cold adaptation. 2. Increase of food consumption and fecal excretion of thyroxine during cold exposure (author's transl)].

In order to clarify the relationship between food consumption and excretion of thyroxine during cold exposure, 131I-thyroxine was injected to 1w- and 3w-cold exposed rats and the radioactivity of 131I in the feces and urine was counted over the first 24 hr and the next same period of time following the injection. The percentage of a dose of radioactive thyroxine excreted into the feces over the first 24 hr was the highest in 1w-cold exposed rats, whereas in 3w-cold exposed rats the excretion of radioactive thyroxine did not differ from the values in warm adapted rats. Since the correlation curve between fecal excretion of thyroxine and fecal weight was linearly positive and food consumption increased during the early stage of cold exposure, larger fecal thyroxine observed in the first week after cold exposure was inferred to be result from increased food consumption as well as fecal volume in this period. Nevertheless, since the increment of fecal excretion of thyroxine in 1w-cold exposed rats was only 30% as compared with the value of control group, it is impossible to explain 2-3 fold increase in thyroxine requirement during early stage of cold exposure by the increase in fecal excretion of thyroxine.

Acclimatization↗
PubMed1992

Blood histamine levels following graded cold challenge in atypical acquired cold urticaria.

Acquired cold urticaria with a negative cold stimulation test has been described in seven patients in whom the standard ice cube test did not induce localized urticaria. Subsequent total body cold exposure induced a generalized urticaria. A patient with this syndrome is presented where blood histamine levels rose from 9 to 60 micrograms/dL after a negative local cold stimulation test and from 60 to 90 micrograms/dL after total body cold exposure. Urticaria occurred only after generalized cold exposure. Blood histamine levels following the ice cube test may represent a sensitive method to diagnose this form of atypical acquired cold urticaria, without subjecting the patient to the risk of anaphylaxis reported following total body cold exposure.

Adult↗
PubMed1989

Ergonomic aspects of cold stress and cold adaptation.

In contrast to the simplified, unvarying, and rigidly controlled conditions that characterize laboratory studies of human responses to cold, normal work in cold regions is characterized by a complex and unstable thermal environment, intermittent cold exposure and exercise, and the freedom to adjust clothing and activity for comfort. These "ergonomic" aspects profoundly modify the impact of a cold environment on people's health, comfort, and performance. A review of recent field studies in the Antarctic shows that the supposed "tropical microclimate" of clothed people in the cold is an over-simplification. People tend to be alternately chilled and overheated, and the accompanying exercise of the vascular responses provides a potential stimulus for vasomotor adaptation. Significant and substantial changes in men's responses to standardized whole-body cold exposures, observed on eight Antarctic expeditions, show that general acclimatization to cold develops as an increase in tissue insulation, which is mediated by an enhanced vascular response to cold.

Acclimatization↗
PubMed1988

[Positive cross-adaptation between endurance physical training and general cold tolerance to acute cold exposure in rats].

This investigation suggested that a series of endurance physical training in rats could cause an improved cold tolerance in rats. The warm-acclimated control group was kept in a thermally neutral environment (25 +/- 1 degrees C). The trained group was subjected to forced physical training on a treadmill, exercising once 1 hour daily, and five times per week for the periods of 3 to 13 weeks. The cold-acclimated group was exposed to an ambient temperature of 5.0 +/- 0.5 degrees C for 12 weeks. Improved endurance physical fitness was suggested by a cardiac hypertrophy. The positive correlation was shown between the amount or intensity of training and the enhanced thermogenesis to acute cold exposure. However, no effect of endurance training was observed on the metabolic responses to noradrenaline and adrenaline. It was inferred that the acute cold exposure caused greater utilization of blood glucose in the trained rats than in the warm controls, but did not FFA in the latter. The increases in oxygen consumption and colonic temperature were caused by hexamethonium injection during cold exposure in the trained rats, but not in the warm and cold-acclimated rats. The increased metabolic rate to acute cold exposure was improved by the prolonged physical training. The development of greater metabolic rate during acute cold exposure in the trained rats was indicated to be associated with increased noradrenaline and adrenaline-independent non-shivering thermogenesises as well as enhanced resting metabolic rate at 25 degrees C ambient temperature.

Adaptation, Physiological↗
PubMed2000

Expression of cold-adapted beta-tubulins confer cold-tolerance to human cellular microtubules.

Isolated microtubule proteins from the cold-adapted fish, Atlantic cod (Gadus morhua), assemble at temperatures between 8 and 30 degrees C, while avian and mammalian microtubules normally do not assemble at temperatures below 20 degrees C. Tubulin, the main component in microtubules, is expressed as many isotypes. Microtubules with different isotype composition have been shown to have different dynamic properties in vitro. Our hypothesis was that cold-tolerance of microtubules is caused by tubulin isotypes that differ in the primary sequence compared to mammalian tubulins. Here we show that transfection of human HepG2 cells with cod beta-tubulin induced cold-adaptation of the endogenous microtubules. Incorporation of one single tubulin isotype can induce cold-tolerance to cold-intolerant microtubules. Three cod beta-tubulin isotypes were tested and two of these (beta1 and beta2) transferred cold-tolerance to HepG2 microtubules, thus not all cod beta-tubulins were able to confer cold-stability.

Acclimatization↗
PubMed2004

Cold-water acclimation does not modify whole-body fluid regulation during subsequent cold-water immersion.

We investigated the impact of cold-water acclimation on whole-body fluid regulation using tracer-dilution methods to differentiate between the intracellular and extracellular fluid compartments. Seven euhydrated males [age 24.7 (8.7) years, mass 74.4 (6.4) kg, height 176.8 (7.8) cm, sum of eight skinfolds 107.4 (20.4) mm; mean (SD)] participated in a 14-day cold-water acclimation protocol, with 60-min resting cold-water stress tests [CWST; 18.1 (0.1) degrees C] on days 1, 8 and 15, and 90-min resting cold-water immersions [18.4 (0.4) degrees C] on intervening days. Subjects were immersed to the 4th intercostal space. Intracellular and extracellular fluid compartments, and plasma protein, electrolyte and hormone concentrations were investigated. During the first CWST, the intracellular fluid (5.5%) and plasma volumes were reduced (6.1%), while the interstitial fluid volume was simultaneously expanded (5.4%). This pattern was replicated on days 8 and 15, but did not differ significantly among test days. Acclimation did not produce significant changes in the pre-immersion distribution of total body water, or changes in plasma osmolality, total protein, electrolyte, atrial natriuretic peptide or aldosterone concentrations. Furthermore, a 14-day cold-water acclimation regimen did not elicit significant changes in body-fluid distribution, urine production, or the concentrations of plasma protein, electrolytes or the fluid-regulatory hormones. While acclimation trends were not evident, we have confirmed that fluid from extravascular cells is displaced into the interstitium during acute cold-water immersion, both before and after cold acclimation.

Acclimatization↗