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PubMed1977

Increased responsiveness of heart rate to beta-adrenergic stimulation in cold-adapted rats.

The responsiveness of heart rate of cold-adapted rats (10-12 weeks, 5degrees C.) to a specific beta-adrenergic agonist was studied. Two hours after removal from cold, s.c. administration of l-isoproterenol (4, 8, or 16 microng/kg body weight) to female rats was accompanied by a greater responsiveness in cold-treated animals. The increase in heart rate of cold-treated rats above that of warm-adapted controls was related linearly to the dose of isoproterenol administered. An increased sensitivity of heart rate to isoproterenol (8 microng/kg body weight, s.c.) was also observed in male, cold-treated rats. The results suggest that adaptation to cold air is accompanied by increased beta-adrenergic responsiveness in rats.

Adaptation, Physiological↗

PubMed1992

Evaluation of a cold-adapted influenza B/Texas/84 reassortant virus (CRB-87) vaccine in young children.

A cold-adapted (ca) influenza B reassortant virus vaccine that contained the six internal RNA segments from influenza B/Ann Arbor/1/66 ca virus and the neuraminidase and hemagglutinin genes from wild-type influenza B/Texas/1/84 virus was evaluated in children ranging in age from 8 months to 14 years. The children were vaccinated intranasally with doses ranging from 10(3.2) to 10(6.2) 50% tissue culture infective doses (TCID50). Thirty children were seropositive, and 26 were seronegative. Thirty-three children participated as unvaccinated controls. The vaccine was well tolerated by both seronegative and seropositive children. The amount of virus required to infect 50% of seronegative children was approximately 10(4.5) TCID50. Vaccine viruses recovered from airway secretions retained temperature-sensitive and cold-adapted characteristics. The results of this study indicate that the vaccine virus, influenza B/Texas/84 ca reassortant virus, is attenuated, immunogenic, and phenotypically stable when given to young seronegative children.

Adaptation, Biological↗

PubMed1992

Enhancement of cellular immune function during cold adaptation of BALB/c inbred mice.

The cell-mediated immune function of cold-adapted BALB/c inbred mice was studied in experiments of splenic lymphocyte blastogenesis, indicated by tritium-labeled deoxythymidine incorporation and SDS-PAGE autoradiography of synthetic proteins in lymphocytes. Male BALB/c inbred mice were randomly divided into two groups: control (living at 25 degrees C) and cold-exposed (living at 2 degrees C). Results are as follows: in contrast with the control group, there was an obvious fluctuation of cell-mediated immune function in the cold-exposed group at initial cold exposure because of transient stress to cold; then cell-mediated immune function gradually recovered to control level. From Day 15, the cell-mediated immune function of the cold-exposed group was remarkably enhanced. On Day 15, the lymphocyte blastogenesis rate was increased by 20.66% (P less than 0.05), which implies the onset of cold adaptation; on Days 21 and 31, the rates increased by 80.15% (P less than 0.05) and 40.36% (P less than 0.05), respectively. Two to six months later, with continuing cold exposure, the murine lymphocyte blastogenesis rate in the cold-exposed group remained higher than that in the control group. The lymphocyte protein synthesis of the cold-exposed group, indicated by tritium-labeled leucine incorporation, apparently increased on Day 15 and the stimulated rate was 101.47% (P less than 0.05). SDS-PAGE autoradiography of synthetic proteins in lymphocytes demonstrated that after 2 weeks of cold exposure, protein bands were enriched in both quantity and quality. These results are identical to the results obtained from lymphocyte blastogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1979

Changes induced by cold adaptation in the brown adipose tissue from several species of rodents, with special reference to the mitochondrial components.

(1) The effects of cold adaptation upon the brown adipose tissue have been studied in rats, hamsters, mice, and guinea pigs. (2) Striking effects were found for total tissue as well as at the mitochondrial level, e.g., increases in protein and phospholipid contents, changes in phospholipid fatty acid composition (a decrease in the percentage of palmitic and palmitoleic acids and an increase in stearic and linoleic acids), and a change in the mitochondrial polypeptide composition (a marked increase in a 32000 molecular weight polypeptide, except for hamsters). (3) In situations where animals exhibit a greatly enhanced capacity for nonshivering thermogenesis (cold adaptation for rats, mice, and guinea pigs, birth for guinea pigs, and hibernation ability for hamsters, dormice, and garden dormice), brown fat mitochondria are characterized by the occurrence of large amounts of the 32000 molecular weight polypeptide characteristic of these mitochondria.

Adaptation, Physiological↗

PubMed1978

Comparative measurements of in vitro thermogenesis of brown adipose tissue from control and cold adapted rats.

Heat output and oxygen uptake rates as well as caloric equivalents of O2 were measured in brown fat fragments from cold-adapted and control rats. Resting metabolic rate per unit wet weight was the same in both groups. Submaximal responses to noradrenaline were significantly lower in the cold-adapted than in the control group. Apparent maximal responses were the same for both groups. Caloric equivalents of O2 gave no evidence for anaerobic glycolysis even under conditions of oxygen limitation.

Acclimatization↗

PubMed1977

Evidence that fatty acid synthesis in the interscapular brown adipose tissue of cold-adapted rats is increased in vivo by insulin by mechanisms involving parallel activation of pyruvate dehydrogenase and acetyl-coenzyme A carboxylase.

Plasma insulin concentrations in cold-adapted rats were altered acutely by administration of glucose or anti-insulin serum. Rates of fatty acid synthesis in interscapular brown adipose tissue were determined from the incorporation of 3H from 3H2O into tissue lipid. Rates of synthesis were greatly elevated after glucose administration and markedly decreased after injection with anti-insulin serum. Parallel changes in the initial activities of both acetyl-CoA carboxylase and pyruvate dehydrogenase were observed under these conditions, but no changes in total activities were evident. The results suggest that this tissue is an important site of fatty acid synthesis in the cold-adapted rat and that this feature of the tissue is sensitive to changes in plasma insulin concentrations.

Acetyl-CoA Carboxylase↗

PubMedDate not supplied

[Differentiating markers of virulent and attenuated (cold-adapted) strains of influenza A virus].

A high sensitivity of influenza virus to replication at a high temperature and a reduction of the temperature optimum of the neuraminidase activity are important genetic markers correlating with the degree of attenuation for the man. Cold-adapted variants of influenza virus produced in the course of passages at a low (25-28 degrees C) temperature are thermo-sensitive. The passage of the viruses at the optimal temperature (32 degrees C) does not change the range of thermal sensitivity even in variants, harmless for adult persons. The interfering activity of influenza viruses with different levels of human virulence was studied. A considerable portion of the examined cold-adapted strains differs from the original virulent strains in the capacity to interfere with the challenge virus in chick embryo fibroblast cell culture. However some thermosensitive variants as well as original strains do not react in interference tests. This indicates the lack of complete correlation between the interfering activity, thermal sensitivity and human virulence of influenza virus.

Adaptation, Physiological↗

PubMedDate not supplied

Biological, genetic and biochemical characterization of a cold-adapted recombinant A/Victoria/3/75 virus and its evaluation in volunteers.

A recombinant virus AA-CR19 was produced that contains RNA segments coding for one polymerase protein, the nucleoprotein and the matrix protein of cold-adapted A/Ann Arbor/6/60, but HA, NA and two other genes coding for polymerase proteins from A/Victoria/3/75. The nonstructural protein gene is probably derived from A/Ann Arbor/6/60, but may contain a spontaneous mutation. Biological characterization of AA-CR19 showed that it possesses the gene(s) responsible for cold-adaptation and temperature-sensitivity of the A/Ann Arbor/6/60 parent. At a dose of 10(7.2) TCID/50. AA-CR19 was found to be immunogenic and attenuated for seronegative volunteers.

Adult↗

PubMed1977

Comparative studies of wild-type and 'cold-mutant' (temperature sensitive) influenza viruses: geneology of the matrix (M) and non-structural (NS) proteins in recombinant cold-adapted H3N2 viruses.

The matrix (M) protein of the H2N2 virus A/Ann Arbor/6/60 may be distinguished from M protein of several H3N2 viruses and A/New Jersey/76 (HSWINI) by SDS acrylamide gel electrophoresis using a discontinuous buffer system. The smallest RNA (RNA 8) of the A/Ann Arbor/6/60 virus may be distinguished from RNA 8 of several H3N2 viruses by acrylamide gel electrophoresis in 3% or 3-6% gels in the absence of urea, if electrophoresis is done at 30 to 36 degrees C or 20 degrees C respectively. Ten clones of conditionally-lethal temperature-sensitive (ts) mutants were studied, which derived their cold-adaption and ts genes from mutant A/Ann Arbor/6/60, and their haemagglutinin from the H3N2 virus A/Scotland/840/74. Each clone was found to derive its M protein from A/Ann Arbor/6/60 mutant, and its RNA 8 from A/Scotland/840/74. The only assignment of genes 7 and 8 consistent with these findings for the recombinants is that in each parent virus (and in the recombinants) gene 7 codes for M protein, and gene 8 for NS protein. Furthermore, it may be concluded from the results that the biologically important ts lesions in the A/Ann Arbor/6/60 mutant parent are not present in the NS gene. In addition to the recombinants of A/Ann Arbor/6/60 and A/Scotland/840/74, five independent ts/cold-adapted recombinants of A/Ann Arbor/6/60 mutant with H3N2 and HSWINI wild-type viruses were examined, and all were found to contain the M protein of the A/Ann Arbor/6/60 mutant parent. This is suggestive that M protein may be at least partially responsible for the cold-adaptation and/or ts properties of the A/Ann Arbor/6/60 mutant and the recombinants.

Adaptation, Biological↗

PubMed1975

Increased metabolism of iodothyronines in the rat after short-term cold adaptation.

The effect of 2 weeks of continuous exposure to 4C on the metabolism of iodothyronines in the rat was studied. Metabolic clearances of [131I]triiodothyronine ([131]t3) and [125I[-thyroxine ([125I]T4) were increased in exposed animals. Estimated absolute turnover of T4 was increased approximately 2-fold as a result of cold exposure. Urinary and fecal clearances of labeled hormones were elevated. Intracellular total radioiodine and iodothyronine radioiodine concentrations were reduced in liver and kidney 24 h after a single injection of tracer hromones. Plasma hormonal binding was not altered. Expanded tissue spaces of [125I]T4 (liver, 52.4%, kidney, 66,7%) were measured by analysis of composite plasma and tissue disappearance curves in subgroups of animals sacrificed 6-24 h after dose injection. Enlarged tissue spaces ot [131I]T4 (liver 8.3%, kidney 26.2%) were observed in the cold-adapted groups. Fractional disappearance rates of labeled iodothyronines from the total rat were accelerated as determined in individual exposed animals and by composite disappearance curve analysis. These investigations suggest that the observed altered kinetic parameters of iodothyronine disappearance from plasma, tissue and total body pools are due to increased hormone flux, owing to increased deiodinative and fecal hormone disposition. Moreover, the data demonstrate that alterations in the peripheral metabolism of T3 and T4 become manifest early in the adaptation process to cold.

Adaptation, Physiological↗

PubMed1979

Catecholamines in dogs during cold adaptation by repeated immersions.

Dogs were immersed in cold water 1 h/day for 30 consecutive days. During the first immersion, oxygen uptake increased approximately sevenfold and colonic temperature decreased; a large increase in plasma epinephrine and norepinephrine concentrations was found; plasma glucose, lactic acid, and free fatty acid (FFA) concentrations were also increased. An adaptative response to cold was evidenced during the 10th immersion by a further increase in oxygen uptake and a reduction in the fall of colonic temperature; plasma epinephrine, glucose, and lactic acid were diminished whereas FFA were higher. Consequently 10 h spent in cold are sufficient to induce an improved capacity for heat production. An enhanced ability to produce nonshivering thermogenesis mediated by epinephrine or norepinephrine is not obvious because after the 30th immersion no enhanced calorigenic response to epinephrine or norepinephrine infusion was found. In dogs mechanisms other than norepinephrine-enhanced sensitivity might be involved in this kind of cold adaptation.

Adaptation, Physiological↗

PubMed1979

[Changes in muscular thermogenesis in cold adapted rats following beta-adrenoreceptor blockade].

The administration of beta-adrenergic blocking agent propranolol to cold adapted rats entailed some decrease of the total metabolic reaction and body temperature as well as an additive (compensatory) increase of electrical muscle activity. The compensatory effect was more obvious in postural-tonic groups of muscles (m. trapezius, m. masseter) and in deeper portions of muscles (m. tibialis ant., m. trapezius), mainly presented by the red fibers. An adaptive increase of non-shivering thermogenesis and temperature effect of muscular contraction seem to be mainly controlled by beta-adrenergic mechanisms.

Adaptation, Physiological↗

PubMedDate not supplied

[The evaluation of the degree of attenuation of cold-adapted influenza A virus strains in CBA-strain mouse and Syrian hamster models].

The pattern of the infectious process induced by the epidemic A/Leningrad/134/57 (H2N2) virus and its cold-adapted (CA) variants in CBA mice and Syrian hamsters was studied. The strains under study inoculated into the animals under a mild ether anesthesia differed by virulence, reproductive capacity in the nasopharynx, trachea and lungs, as well as by the isolation rate from extrarespiratory organs of both mice and hamsters. Upon intranasal inoculation of mice without anesthesia, the CA strains were found to be incapable of dissemination into the lower parts of the respiratory tract with distinguished these viruses from the original epidemic strain A/Leningrad/134/57 as well as from the mouse-adapted strain A/PR/8/34 (H1N1) used as control. The experimental results show that both models are suitable for laboratory evaluation of the attenuation degree of human influenza viruses.

Adaptation, Physiological↗

PubMed1991

Thermoregulation in man during cold adaptation.

Permanent residence in a cold environment affects the thermoregulatory system and other related functions (Table 5). These changes are adaptive because they decrease the stress action of cold, maintain the energy cost of temperature homeostasis and make it possible to receive additional heat during muscular work in cold without drawing on such heat production sources as shivering.

Acclimatization↗

PubMed1975

The influence of the social thermoregulation on the cold-adaptive growth of BAT in hairless and furred mice.

When mice were living in groups they developed less brown adipose tissue (BAT) during cold adaptation as compared with single mice. This effect of social aggregation was more pronounced in genetically hairless mice than in furred mice. In both races of mice the most significant difference in BAT growth was found between single mice and pairs of mice, indicating that the formation of pairs causes the relatively most effective improvement of thermal balance.

Adaptation, Physiological↗

PubMed1975

[Role of thyroid hormone in cold adaptation. 1. Requirement of thyroxine during the course of cold acclimation as estimated by noradrenaline sensitivity (author's transl)].

The amount of thyroxine required for the development and maintenance of cold acclimation was investigated in the rat. Warm-adapted thyroidectomized rats could not survive at 5 degrees C. When thyroxine was replaced, these rats could survive and responded to noradrenaline with increased oxygen consumption in proportion to the dose of replaced thyroxine. Judged from the amount of thyroxine in thyroidectomized rats necessary to restore noradrenaline sensitivity to the same level as seen in intact controls, 30 degrees C-adapted rats were found to require 3.3 mug thyroxine/100 g b.w./day, while 5 degrees C-adapted rats required only 1.2 mug. It is concluded that the amount of thyroxine necessary to produce cold acclimation is much larger than that for the maintenance of cold acclimation.

Acclimatization↗

PubMed1992

The attenuation phenotype conferred by the M gene of the influenza A/Ann Arbor/6/60 cold-adapted virus (H2N2) on the A/Korea/82 (H3N2) reassortant virus results from a gene constellation effect.

A single gene reassortant (SGR) virus that derived its M gene from the attenuated influenza A/Ann Arbor/6/60 cold-adapted (CA) donor virus and the remaining genes from the A/Korea/82 (H3N2) wild type (WT) virus (designated A/Korea/82 CA M-SGR) was previously shown to be attenuated in mice, hamsters, ferrets, and humans. The attenuation (ATT) phenotype of this SGR virus could result directly from an altered function of the mutant M gene product of the A/Ann Arbor/6/60 CA virus, which differs from the M gene of the A/Ann Arbor/6/60 WT virus at only one amino acid or, indirectly from a gene constellation effect in which ATT results from an inefficient interaction between the products of the M gene of the A/Ann Arbor/6/60 virus and other genes of the A/Korea/82 virus. Several lines of evidence from the present study are consistent with our interpretation that the ATT phenotype of the A/Korea/82 CA M-SGR results from a gene constellation effect. First, the A/Korea/82 CA M-SGR and an A/Korea/82 SGR containing the A/Ann Arbor/6/60 WT M gene were each restricted in replication in the upper and lower respiratory tract of mice compared with the A/Korea/82 WT virus. Second, an A/Udorn/72 CA M-SGR containing the M gene from the A/Ann Arbor/6/60 CA donor virus in a background of other genes derived from the A/Udorn/72 (H3N2) WT virus was not attenuated in the respiratory tract of mice. These data suggest that the change in the amino acid sequence of the M gene product from the A/Ann Arbor/6/60 WT to CA virus is not responsible for the ATT phenotype of the A/Korea/82 CA M-SGR. In addition, evidence of the genetic instability of the A/Korea/82 CA M-SGR is presented, specifically, an extragenic mutation that results in loss of the ATT phenotype. The implications of these findings for the ATT phenotype of the live attenuated reassortant viruses derived from the A/Ann Arbor/6/60 CA donor virus are discussed.

Adaptation, Physiological↗

PubMed1977

Pilot studies on recombinant cold-adapted live type A and B influenza virus vaccines.

Recombinant live attenuated type A and B influenza virus vaccines derived from standardized cold-adapted parent strains were given singly and in combination to volunteers. The vaccine viruses were well tolerated, functioned as good antigens, and failed to spread to intimate household contacts. Thirty-nine isolates that were recovered after a single passage in humans appeared genetically stable. The results of histopathologic studies in ferrets encourage development of an animal model for attenuation of the virus.

Animals↗