Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An animal model for anticancer drug-induced hair loss has been developed using the Angora rabbit given i.v. doxorubicin, 2 mg/kg, twice weekly for 3 weeks. There was a 167% increase in the weight of hair collected by grooming between weeks 2 and 5, and a 72% inhibition of new hair growth at week 6 compared with non-treated animals. The hairs that grew in the doxorubicin treated rabbits did so at the same rate as in non-treated rabbits and appeared normal by light microscopy. Topical application of dimethylsulfoxide (DMSO), of 10% alpha-tocopherol in DMSO, of 0.5% naphthazoline hydrochloride in DMSO, of 0.1% fluocinolone acetonide in a propylene glycol base and local hypothermia did not provide any protection against doxorubicin-induced hair loss. Angora rabbits fed an alpha-tocopherol-deficient diet for 6 weeks showed decreased hair growth compared with animals fed a normal diet or a diet supplemented with 100 mg alpha-tocopherol acetate twice a week for 6 weeks. Some rabbits fed the alpha-tocopherol-deficient diet died when given doxorubicin. Rabbits fed the alpha-tocopherol-supplemented diet showed evidence of protection against doxorubicin-dependent inhibition of new hair growth.
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PMID:Doxorubicin-induced hair loss in the Angora rabbit: a study of treatments to protect against the hair loss. 369 Aug 2

Phorbol esters, in particular 12-O-tetradecanoyl-phorbol-13-acetate (TPA), have been shown to have profound effects on most biological systems including tumor promotion. Presented here are studies on the acute toxic effects of TPA, and the effects of phorbol esters on the in vivo and in vitro, T cell-dependent, antigen-specific antibody response in the mouse. The LD50 of a single i.v. dose of TPA in the mouse was 309 micrograms/kg. Acute toxic effects included lethargy, hypothermia and enlarged, hemorrhagic spleens at the higher doses. TPA was shown to be a potent inhibitor of the in vivo primary antibody response as measured by the IgM antibody-forming cell (AFC) response to sheep red blood cells (sRBC). The ED50 of a cumulative i.v. dose was 145 micrograms/kg administered the day before and the day of immunization (72.5 micrograms/kg/day). A cumulative dose of 500 micrograms/kg (250 micrograms/kg/day) resulted in a 100% suppression of the response. This in vivo exposure to TPA did not alter B cell/T cell ratio in the spleen. Phorbol ester analogs inactive in other biological systems were also inactive in the in vivo AFC response. The in vitro AFC assay was used to determine what cell type was being affected by TPA. Separation of the adherent spleen cells into B and T cell populations was done using nylon wool columns and anti-theta plus complement treatment. Experiments with these cell populations indicated that TPA produced suppression of the response due to an effect on the nylon wool adherent cell population.
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PMID:Suppression of the antibody response by phorbol esters in the mouse is due to an effect on the nylon wool adherent cell population. 387 72

Glucocorticoids (GC) are important for thermoregulatory responses to low environmental temperatures. Pretreatment of hamsters, which are capable of natural hibernation, with cortisone acetate has been demonstrated to improve carbohydrate homeostasis during hypothermia. The objectives of the current studies were to evaluate the effects of GC pretreatment of a nonhibernator, the rat, on (i) cooling time, (ii) carbohydrate homeostasis (in terms of liver and cardiac glycogen concentrations and plasma glucose concentration), and (iii) duration of survival in hypothermia. In addition, the effects of liver glycogen depletion on cooling times and survival were examined. Hypothermia was induced in rats by exposure to a helium:oxygen (80:20, Helox) atmosphere at 0 degree C. Pretreatment of rats with triamcinolone acetonide (1.5 mg/kg/day, sc, 48, 24, and 1 hr prior to induction) significantly (P less than 0.05) lengthened induction time, while fasting was associated with a significant decrement (25%). While liver and cardiac glycogen levels in control and GC-treated rats fell approximately 45% during cooling, this reduction occurred over a significantly greater period of time in treated rats and suggests a sparing of glycogen or increased capacity for its production in response to GC. Glycogen utilization was accompanied by a hyperglycemia in control, GC-treated, and fasted groups. Survival in hypothermia at a rectal temperature of 14-15 degrees C in GC-treated (9.5 +/- 1.2 hr) and fasted (10.9 +/- 0.9 hr) rats was not significantly different from control (10.5 +/- 1.1 hr) values. These findings suggest that treatment with GC can increase the thermogenic capacity of the rat (as evidenced by an increased induction time) and promote carbohydrate homeostasis, but does not contribute to an enhancement of survival in the hypothermic nonhibernator.
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PMID:Glucocorticoids and hypothermic induction and survival in the rat. 402 83

Results are reported of a comparative study in vivo of the metabolism of [2-(14)C]-glucose and [1-(14)C]acetate in brains of rats intoxicated with triethyltin sulphate. The incorporation of (14)C from glucose into glutamate, glutamine, gamma-aminobutyrate and aspartate was greatly decreased. The incorporation of (14)C from acetate into these amino acids was unaffected. The experimental data indicated that the main action of triethyltin was to decrease the rate at which pyruvate formed from glucose is oxidized. Glycolysis was not inhibited. Changes in glucose metabolism in the brain are shown not to be directly due to hypothermia. Some of the advantages of measuring the labelling of intermediates at very short time intervals after the injection of the labelled glucose are demonstrated.
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PMID:Selective inhibition of glucose oxidation by triethyltin in rat brain in vivo. 548 56

Several 9-substituted delta 8-tetrahydrocannabinol (delta 8-THC) analogues were synthesized and evaluated for biological activity in mice. Compounds with phenyl (2b) and butyl (2c) substituents were prepared by the addition of phenyllithium and n-butyllithium, respectively, to (-)-9-nor-9-oxohexahydrocannabinol (1), followed by dehydration, whereas, isopropyl (2d), PhCH2 (2e), and Ph(CH2)2 (2f) derivatives were synthesized via the Grignard reaction with subsequent dehydration. Compounds with C2H5CH(OH) (2g) and CH3CH(OH) (2h) substituents at C-9 were prepared from (-)-9-nor-9-formyl-delta 8-tetrahydrocannabinol acetate (3) by the reaction of ethyl and methyl Grignard reagents, respectively. Biological activity indicated that a methyl group at the C-9 position is, thus far, optimum for producing hypoactivity and hypothermia in mice. In addition, hydroxyethyl substitution at position 9 reduced and antinociceptive activity of delta 8-THC, in contrast to the increased activity reported for hydroxymethyl substitution.
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PMID:Synthesis and pharmacological activity of some 9-substituted delta 8-tetrahydrocannabinol analogues. 632 13

After adrenalectomy in obese mice the rate of weight gain parallels that in lean controls and falls progressively behind that in intact ob/ob mice. Food intake was reduced to normal, but the body temperature of adrenalectomized ob/ob mice was similar to that of intact ob/ob mice and remained below that of control lean mice. After exposure to an ambient temperature of 6 degrees C the body temperature in adrenalectomized ob/ob mice fell at the same rate as in intact ob/ob mice. The increase in tail length, brain weight, spleen weight, and muscle weight after adrenalectomy in ob/ob mice could not be duplicated by reducing the weight gain of ob/ob mice to that of the adrenalectomized mice. Similarly the induction of obesity with gold thioglucose significantly increased the weight of the gastrocnemius muscle and spleen rather than lowering it to levels found in ob/ob mice. Treatment of adrenalectomized ob/ob mice with cortisone acetate, but not with deoxycorticosterone acetate (DOCA), reduced muscle weight, spleen weight, brain weight, and the growth in tail length. Both cortisone and DOCA increased food intake, liver weight, growth rate, and the weight of the adipose tissue in ob/ob mice. These effects are significantly greater than observed in comparably treated lean animals and suggest that glucocorticoids of adrenal origin play an integral role in the phenotypic expression of genetic obesity. These data also indicate that the hypothermia is not a sufficient cause of the obesity in the ob/ob mice, since hypothermia persists in the adrenalectomized mice, but when food intake falls to normal there is no progression of the obesity.
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PMID:Adrenalectomy and food restriction in the genetically obese (ob/ob) mouse. 642 Nov 74

The effects of prostacyclin on whole blood platelet count, blood coagulation factors, and postoperative bleeding were investigated in 20 patients undergoing aorta-coronary bypass. Eleven patients received heparin 2 mg/kg and prostacyclin 50 ng/kg/min during cardiopulmonary bypass (CPB). Nine patients received only heparin 3 mg/kg. CPB was by roller pump and bubble oxygenator primed with Ringer's acetate. Hypothermia to 28 degrees C was induced. In the control group, platelet count, corrected for hemodilution, was 70% +/- 15% (mean +/- SD) of pre-CPB value after 30 minutes of bypass and remained at this level 1 hour after CPB. In the prostacyclin group, the platelet count after 30 minutes was 85% +/- 17%, after 120 minutes 111% +/- 20%, and 1 hour after CPB 92% +/- 17%. There was a significant difference between the groups (p less than 0.05) from 60 minutes of CPB up to 1 hour after CPB. Prostacyclin allowed reduction of the heparin dosage while retaining anticoagulation as measured by activated coagulation time (ACT), fibrinopeptide A, and fibrinogen determinations. The ACT was more than 900 seconds in the prostacyclin group after 30 minutes of CPB, as compared to 523 +/- 118 seconds (p less than 0.05) in the control group. This difference diminished later during CPB. In the prostacyclin group, arterial blood pressure was 30 mm Hg or less during the first hour of CPB and the systemic vascular resistance was half of that in the control group. All patients survived. There were no clinical signs of neurologic damage. Postoperative bleeding was 352 +/- 61 ml in the prostacyclin group and 550 +/- 338 ml (NS) in the control group.
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PMID:Prostacyclin infusion during extracorporeal circulation foe coronary bypass. 703 54

Advances in myocardial preservation have led to improved patient survival after open heart operations. However, few studies have detailed the nature of national or regional patterns of cardioplegia use. To determine the regional pattern, all open heart surgery programs in Missouri were surveyed. During 1 year, it was found that cardioplegia was administered to 8,382 patients by 61 cardiothoracic surgeons at ten academic affiliated hospitals and 16 nonteaching hospitals. All cardioplegic solutions were hospital produced. Of 13 crystalloid solutions, 11 differed from one another and eight were intracellular formulations. Of 28 multidose blood-based cardioplegic solutions, there were 23 different mixtures. Most crystalloid (69%) and blood-based (89%) solutions differed substantially from commonly reported formulations. The incidences of the various additives to crystalloid solutions were as follows: bicarbonate, 92%; glucose, 69%; lidocaine, 54%; mannitol, 46%; magnesium, 31%; calcium, 23%; methylprednisolone, 15%; heparin, 8%; and acetate, 8%. Of the common blood-based cardioplegic solution additives, the following incidences were observed: glucose, 79%; bicarbonate, 43%; trishydroxyaminomethane, 36%; acetate, 29%; magnesium, 29%; procaine (or lidocaine), 25%; citrate-phosphate-dextrose, 18%; mannitol/albumin, 14%; nitroglycerin, 11%; glutamate/aspartate, 11%; calcium, 7%; insulin, 3%; and methylprednisolone, 3%. No calcium channel blocker or high-energy phosphate additives were reported. We conclude that many different cardioplegic admixtures that have not been tested experimentally are used routinely in clinical practice, presumably with acceptable results. Because the salutary effects of induced cardiac arrest and hypothermia may mask suboptimal solutions, further study of customized cardioplegia should be considered, particularly with regard to high-risk patients.
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PMID:Lack of cardioplegia uniformity in clinical myocardial preservation. 814 36

The aim of this study was to investigate the relationship between the hypothermic effect induced by lead or cadmium chloride treatments and the cerebral metal levels attained. Mice were injected intraperitoneally with different doses of lead acetate or cadmium chloride at ambient temperatures of 22 degrees C and 35 degrees C, and rectal temperatures and brain metal levels were determined. At 22 degrees C, doses of lead acetate exceeding 25 mg/kg caused significant hypothermia and a rise of lead levels in the brain; this hypothermic effect was significantly inhibited at 35 degrees C. In mice repeatedly treated with 2 or 5 mg/kg lead acetate and exposed to 22 degrees C or 35 degrees C, no significant changes were observed in body temperature after the repeated exposure, although brain lead levels increased significantly. Cadmium chloride at 22 degrees C produced a significant fall in body temperature, and a rise in brain cadmium levels at doses of 2-4 mg/kg; the decrease in body temperature was partially inhibited at 35 degrees C. The results of the present study suggest that the hypothermic effect elicited by these heavy metals is related to both the level of metal absorbed by the brain and its rate of uptake.
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PMID:Effects of different factors in lead- and cadmium-induced hypothermia in mice. 822 66

A number of phorboid 20-homovanillates were prepared by condensation of phorbol 12,13-diesters and 12-dehydrophorbol 13-esters with Mem-homovanillic acid followed by removal of the protecting group with SnCl4 in THF. These compounds were evaluated for their ability to inhibit [3H]resiniferatoxin (RTX) binding to rat spinal cord membranes. Compounds bearing a lipophilic ester group on ring C were considerably active, but a surprising tolerance of the vanilloid receptor toward the location and the orientation of this ester group was disclosed. Unexpectedly, these ligands could also diminish, to a variable degree, the positive cooperativity which characterizes RTX binding to the vanilloid receptor. Phorbol 12-phenylacetate 13-acetate 20-homovanillate (PPAHV, 6a), a compound which abolished binding cooperativity, was further tested in a variety of in vivo assay used to characterize vanilloid-like activity. PPAHV showed only a marginal pungency and failed to induce a measurable hypothermia response at doses (up to 200 mg/kg) at which it effectively desensitized against neurogenic inflammation. These data suggest that the peculiar binding behavior of these ligands might be associated with a distinct spectrum of biological activity.
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PMID:Synthesis and evaluation of phorboid 20-homovanillates: discovery of a class of ligands binding to the vanilloid (capsaicin) receptor with different degrees of cooperativity. 875 33


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