Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085593 (chills)
 4,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous reports have indicated that a proportion of pigs, homozygous normal for the skeletal muscle ryanodine receptor gene (RYR1), was halothane sensitive, and this was associated with poor meat quality when pigs were handled aggressively. This study was conducted to evaluate halothane sensitivity in RYR1-normal pigs, managed under simulated commercial conditions, to ascertain the association of halothane sensitivity with growth rate and meat quality. A total of 363 pigs across four farrowing groups, from seven Landrace sires and 38 Yorkshire-Landrace F1 dams, were tested at 8 weeks of age for halothane sensitivity using a closed system that delivered 5% halothane at 2 l/min for 3 (group 1) or 2 (groups 2 to 4) min. After 1 min, limb rigidity, limb tremors and abdominal discoloration were evaluated on a binomial scale with 0 indicating no reaction and 1 indicating reaction. Testing was repeated 2 days later. At 10 weeks of age, pigs were moved to finishing pens and not moved again until marketing. Within farrowing group, pigs were harvested in one of two groups, and at marketing were moved a distance of 91 m, weighed, tattooed, loaded and transported a distance of 550 km to a commercial harvest plant. After overnight rest, pigs were harvested and the pH of the loin muscle was measured at 45 min (pH45) after stunning. After an 18-h chill, loin muscle pH (pHu), International Commission on Illumination (CIE) L*, a*, b*, color (1 to 6) and marbling (1 to 10) scores and fluid loss percent were collected. Generalized linear mixed models were used to estimate repeatabilities for response to halothane challenge. Repeatabilities for limb rigidity for the front right and left legs were 0.24 and 0.31, respectively, whereas rear right and left leg repeatabilities were 0.19 and 0.17, respectively. Repeatabilities for front right and left leg tremors were 0.16 and 0.20, respectively. Growth rate was not influenced by any measure of halothane sensitivity. Carcasses from pigs exhibiting limb rigidity tended to have lower pH45 (5.88 v. 5.97; P = 0.06), similar pHu (5.47 v. 5.49; P = 0.32), less pH decline from 45 min to 18 h (-0.40 v. -0.50; P = 0.04) and a tendency for greater fluid loss percent (5.01 v. 4.55; P = 0.08) than carcasses from pigs that did not exhibit limb rigidity during halothane challenge. A proportion of pigs normal for RYR1 did exhibit limb rigidity during halothane gas challenge, and subsequently tended to have lower 45 min pH and greater longissimus muscle fluid loss post harvest.
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PMID:Association of halothane sensitivity with growth and meat quality in pigs. 2303 27

When cooled, insects first lose their ability to perform coordinated movements (CTmin) after which they enter chill coma (chill coma onset, CCO). Both these behaviours are popular measures of cold tolerance that correlate remarkably well with species distribution. To identify and understand the neuromuscular impairment that causes CTmin and CCO we used inter- and intraspecific model systems of Drosophila species that have varying cold tolerance as a consequence of adaptation or cold acclimation. Our results demonstrate that CTmin and CCO correlate strongly with a spreading depolarization (SD) within the central nervous system (CNS). We show that this SD is associated with a rapid increase in extracellular [K+] within the CNS causing neuronal depolarization that silences the CNS. The CNS shutdown is likely to be caused by a mismatch between passive and active ion transport within the CNS and in a different set of experiments we examine inter- and intraspecific differences in sensitivity to SD events during anoxic exposure. These experiments show that cold adapted or acclimated flies are better able to maintain ionoregulatory balance when active transport is compromised within the CNS. Combined, we demonstrate that a key mechanism underlying chill coma entry of Drosophila is CNS shutdown, and the ability to prevent this CNS shutdown is therefore an important component of acute cold tolerance, thermal adaptation and cold acclimation in insects.
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PMID:Central nervous system shutdown underlies acute cold tolerance in tropical and temperate Drosophila species. 2973 33

When insects are cooled, they initially lose their ability to perform coordinated movements at their critical thermal minima (CTmin). At a slightly lower temperature, they enter a state of complete paralysis (chill coma onset temperature - CCO) and if they are returned to permissive temperatures they regain function after a recovery period which is termed chill coma recovery time (CCRT). These three phenotypes (CTmin, CCO, and CCRT) are all popular measures of insect cold tolerance and it is therefore important to characterize the physiological processes that are responsible for these phenotypes. In the present study we measured extracellular field potentials in the central nervous system (CNS) and muscle membrane potential (Vm) during cooling and recovery in three Drosophila species that have different cold tolerances. With these measurements we assess the role of the CNS and muscle Vm in setting the lower thermal limits (CTmin and CCO) and in delaying chill coma recovery (CCRT). The experiments suggest that entry into chill coma is primarily caused by the onset of a spreading depolarization in the CNS for all three species. In the two most cold-sensitive species we observed that the loss of CNS function was followed closely by a depolarization of muscle Vm which is known to compromise muscle function. When flies are returned to benign temperature after a cold exposure we observe a rapid recovery of CNS function, but functional recovery was delayed by a slower recovery of muscle polarization. Thus, we demonstrate the primacy of different physiological systems (CNS vs. muscle) as determinants of the most commonly used cold tolerance measures for insects (CTmin vs. CCRT).
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PMID:The central nervous system and muscular system play different roles for chill coma onset and recovery in insects. 3091 Jun 13