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Results for “Temperature environment”

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At least 19 recordsLinked to original sources
PubMed1989

Lysine requirements of growing turkeys in various temperature environments.

The lysine requirement of Large White male turkeys (Nicholas strain commercial cross) was determined in two experiments at different environmental temperatures for two age periods (8 to 12 and 16 to 20 wk of age). Response curves (segmented and exponential) were obtained by regressing body weight gain (grams/day) on dietary lysine concentration (percentage) or lysine intake (grams/day). Varying levels of dietary lysine were obtained by supplementing a corn-sesame meal diet with L-lysine.HCl. Temperature affected percentage lysine requirement as determined by the segmented (broken line) regression model during 8 to 12 wk of age in Experiment 1 (P less than .05) and in Experiment 2 (P less than .10). The requirements (mean +/- SE) by broken line regression for the 8 to 12-wk age period were: Experiment 1, 1.13 +/- .02 and 1.25 +/- .02% at 6 and 23 C, respectively, and Experiment 2, 1.10 +/- .03, and 1.23 +/- .04% at 7, 20, and 26 C, respectively. For the 16 to 20 wk age period the requirements for Experiment 1 were .75 +/- .02 and .77 +/- .03% at 8 and 24 C, respectively. For Experiment 2, requirements were .74 +/- .03, .72 +/- .02, and .78 +/- .02% at 7, 16, and 24 C, respectively. Percentage requirements by the exponential model showed the same patterns relative to temperature. Multiple regression analysis of gain on lysine intake and temperature indicated that variability in gain was primarily explained by intake (R2 ranged from .82 to .97) with deficient lysine intakes. Temperature environment also affected the gain response to lysine intake, resulting in different response curves at the different environmental temperatures.

Animals↗
PubMed1990

[Study of work efficiency under high temperature environment and reasonable arrangement of work time].

The significant relationship of water loss rate (WLR) to air temperature and work intensity when people work in hot environment was developed in the field study 4000 g of water loss for a working day and 500 g for a working hour was used as the upper limitation for heat exposure, then the Allowable Continuous Heat Exposure Time (ACHET) and Total Heat Exposure Time (THET) were calculated at different air temperature and work intensity. In order to confirm the ACHET derived from field study, WLR and some other physiological examinations were done to the subjects in lab study. And the necessary rest time after each ACHET was also estimated by way of observing the recovery of physiological indexes of subjects.

Adult↗
PubMed1992

Switches in fish myosin genes induced by environment temperature in muscle of the carp.

Fish are cold blooded animals and their muscle function is expected to be greatly affected by environmental temperature. Species that live in the Antarctic ocean have evolved a different contractile system to fish that live in the tropical waters. In the case of Antarctic fish they have a higher specific myofibrillar ATPase activity but 'the trade off' seems to be a lower thermal stability. They are thus capable of a greater muscle power output at low temperatures but the lower thermal stability means they are restricted to living at temperatures below +4 degrees C. Some species, however, experience a wide range of seasonal variations in temperature. We found that these species adapt by changing their myofibrillar apparatus so that they have a higher specific ATPase which physiological studies indicate is due to a different type of myosin crossbridge for low temperature swimming. This is reversible and they develop a contractile system with a greater thermal stability and a commensurate loss of ATPase activity when their environment warms up again. There were several possibilities by which this may be achieved including expression of different isoform genes or the post- translational processing of existing proteins. To elucidate the mechanism we made a carp genomic library and screened this for myosin heavy chain gene using mammalian cDNA sequences under moderate stringency conditions. The clones were restriction mapped which resulted in 28 non overlapping sequences. This indicated that the carp had a reasonably large family of myosin heavy chain genes that is about twice the size of that in mammals. Rather fortuitously the first sequence to be identified was from the gene that is predominantly expressed in white muscle at warm temperatures. This was done by extracting the RNA from red and white muscle of fish acclimated to different 25 degrees C, 18 degrees C or 8 degrees C and carrying out Northern analysis using the gene fragment as the probe. The time course for the expression of this gene when carp maintained at a low temperature were acclimated to a warm temperature was slightly in advance of the change in myofibrillar ATPase which suggested that this strategy for adaptation is regulated at the transcriptional level. Hence these species of fish can adapt to seasonal changes in temperature by expressing different myosin heavy chain isoform genes and rebuilding their myofibrils for either warm or cold temperature swimming. At the present time we are characterising the 5' regulatory (promoter) sequence of this gene to see how a temperature switch may operate.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed1977

Metabolic effect of high environment temperature on non-diabetic and diabetic rats.

Blood lipids and glucose were studied in streptozotocin diabetic rats during hyperthermia. Blood glucose, free fatty acids (F.F.A.) and glycerol of diabetic rats with a rectal temperature of 42 degrees C (hyperthermic) were elevated significantly above those values found in normothermic (TR = 38 degrees C) diabetic or normothermic non-diabetic rats as well as hyperthermic non-diabetic rats. Streptozotocin diabetes caused an elevation in blood triglycerides of normothermic rats, but this hypertriglyceridemia was depressed in diabetic rats during hyperthermia. As in the case of diabetic animals, hyperthermia also caused a depression in the blood triglycerides of non-diabetic rats. However, unlike in the diabetic animals, the blood F.F.A. of non-diabetic rats were depressed during hyperthermia. Although hyperthermia caused a significant increase in the blood glucose of the diabetic animals, no significant change in blood glucose was shown in the hyperthermic non-diabetic rats. Blood cholesterol did not change significantly in the non-diabetic or diabetic animals during hyperthermia. The blood changes of these "energy substrates" are discussed with respect to their possible role in the extreme sensitivity of diabetics to high environmental temperature and "heat stress".

Animals↗
PubMed1978

Environment, temperature and death rates.

Analysis of recorded monthly deaths in England and Wales shows a close association of death rates with external temperature in most diseases other than the cancers. Analysis of daily deaths in England and Wales and in New York shows the following relationships between temperature and deaths from myocardial infarction, strokes and pneumonia. Between -10 degrees and +20 degrees C mimimum temperature there is a nearly linear fall in deaths as the temperature rises. Above 20 degrees C deaths rise steeply as the temperature rises and below -10 degrees C rise steeply as temperature falls. These associations of deaths with temperature are much stronger in the elderly than in younger subjects. Detailed analysis of the daily deaths in England and Wales from myocardial infarction, strokes and pneumonia show that short-term (1--2 days) temperature changes have little effect on death rates but medium-term (7--10 days) and longer-term (three or more weeks) changes associated with very significant changes in death rates. The three diseases vary in the time relations between temperature change and change in death rates. In all three there is an interval between the change in temperature and death and this is shortest in the case of myocardial infarction (1--2 days before death), longest in the case of pneumonia (about a week before death) and intermediate in the case of strokes (about 3--4 days before death). At low temperatures death rates increase as the duration of temperature change increases, while at high temperatures (but below +20 degrees C) death rates decrease as the period of temperature change is longer. The implications of these findings are discussed and it is postulated that there is probably causal relationship between temperature change and deaths from a wide variety of diseases. A proximal link in the chain is probably a failure of autonomic control of body temperature in the elderly leading to a change in body temperature and some humoral change which in turn leads to death. It is not appropriate to concentrate on hypothermia as the relationship between temperature and death is seen at all temperatures.

Age Factors↗
PubMed1987

Hypothermia and poikilothermia induced by a kappa-agonist opioid and a neuroleptic.

When an opioid acting selectively at the kappa opioid receptor is administered subcutaneously to rats along with a neuroleptic at an ambient temperature of 20 degrees C a marked hypothermia ensues. The combination of U-50,488H (a kappa agonist) and chlorpromazine (a neuroleptic) caused a drop in body temperature amounting to as much as 11 degrees C, with all animals recovering after 24-48 h. Naloxone partially reversed the hypothermia. Similar, but less dramatic, decreases in body temperature occurred with other neuroleptics and weaker kappa agonists. The induction of poikilothermia was indicated when the body temperature approached the environment temperature and lethality resulted in 100% of the animals at ambient temperatures of 5 degrees C or 35 degrees C. The potential utility of this or similar combinations of drugs lies in such diverse applications as cardiac surgery, treatment of the near-drowning syndrome and space travel.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗