[On the correlation between the heat resistance of muscles and cholinesterase and the temperature environment of some fishes].
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The spinal cords and brains--comprising dorsal cortex (DC), medial cortex (MC) and diencephalon (Dien)--of juvenile turtles acclimated to warm temperature [27-30 degrees C; warm-acclimated turtles (WATs)] revealed higher density values of bromodeoxyuridine-labeled cells (BrdU-LCs) than those acclimated to a cooler environment [5-14 degrees C; cold-acclimated turtles (CATs)]. Both populations were under the influence of the seasonal daily light-dark rhythms. Pronounced differences between WATs and CATs (independent t-test; confidence level, P<0.01) were found in the central area of the spinal gray matter and in the ependymal epithelium lining the brain ventricles. Forebrain regions (DC, MC and Dien) also revealed significant differences between WATs and CATs (independent t-test; confidence level, P<0.01-0.05). Unexplored biological clocks that may be affecting cell proliferation were equalized by performing paired experiments involving one WAT and one CAT. Both animals were injected on the same day at the same time and both were sacrificed 24 h later. These experiments confirmed that a warm environment increased cell proliferation in the CNS of turtles. Double- and triple-labeling experiments involving anti-BrdU antibody together with anti-glial protein antibodies revealed that temperature modulates not only cell populations expressing glial markers but also other cells that do not express them. As expected, in the case of short post-injection (BrdU) surviving time points, no cells were found colabeling for BrdU and NeuN (neuronal marker). The probable direct effect of temperature on the cell division rate should be analyzed together with potential indirect effects involving increased motor activity and increased food intake. The fate of the increased BrdU-LCs (death, permanence as progenitor cells or differentiation following neuronal or glial lines) remains a matter for further investigation. Results are discussed in the light of current opinions concerned with post-natal neurogenesis in vertebrates.
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)
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All cultivated isolates of the bacterial order Thermotogales are either thermophiles or hyperthermophiles, but Thermotogales 16S rRNA gene sequences have been detected in many mesophilic anaerobic and microaerophilic environments, particularly within communities involved in the remediation of pollutants. Here we provide metagenomic evidence for the existence of Thermotogales lineages, which we informally call "mesotoga," that are adapted to growth at lower temperatures. Two fosmid clones containing mesotoga DNA, originating from a low-temperature enrichment culture that degrades a polychlorinated biphenyl congener, were sequenced. Phylogenetic analysis clearly puts this bacterial lineage within the Thermotogales order, with the rRNA gene trees and 21 of 58 open reading frames strongly supporting this relationship. An analysis of protein sequence composition showed that mesotoga proteins are adapted to function at lower temperatures than are their identifiable homologs from thermophilic and hyperthermophilic members of the order Thermotogales, supporting the notion that this bacterium lives and grows optimally at lower temperatures. The phylogenetic analysis suggests that the mesotoga lineage from which our fosmids derive has used both the acquisition of genes from its neighbors and the modification of existing thermophilic sequences to adapt to a mesophilic lifestyle.
Different evolutions of experimental trypanosomiasis are observed in Mice kept in a permanent 35 degrees C environment. Evolution depends on the individuality or the strain of the host animal. An experimental factor influence on the host mechanism defense rather than on the parasite multiplication rate is shown.
At the conclusion of a 31-day recovery period following a previous sorghum feeding trial (Sell et al., 1983), 128 White Leghorn hens were used in a subsequent 44-day study to investigate the effects of methionine supplementation of sorghum-soybean meal diets on laying hen performance. The hens were arrayed into four nutritional treatments in each of two constant environments (22 and 28 C) based on their egg production during the last 10 days of the recovery period within a previous treatment and environment so that equal numbers of hens from the previous treatments were represented in the new treatments. Nutritional treatments consisted of either low (RS610) or high (savanna) tannin sorghum-soybean meal diets containing 13% protein and supplemented with either .2% DL-methionine (Met) or an isonitrogenous level of L-glutamic acid (Glu). With both high (HTS) and low tannin sorghum (LTS) diets, Met supplementation resulted in greater egg production, egg weight, feed intake, and less hen weight loss as compared with Glu addition, but with the exception of hen weight loss, the magnitude of the response was much greater with HTS. Hens fed the HTS diet supplemented with Glu showed greatly reduced egg production and feed efficiency as compared with those fed LTS similarly supplemented. In contrast, little difference in egg production and feed efficiency was observed between hens fed HTS and LTS diets supplemented with Met. All parameters studied except hen weight appeared to be reduced slightly by the higher temperature.
Rats raised in the cold showed an unusual pattern of adipose tissue morphology. Male Sprague-Dawley rats were maintained in a 5 degrees C environment for up to 24 wk and the cellularity of their major adipose depots was determined. Normal age-related increases in adipocyte number were absent in two major fat depots (retroperitoneal and inguinal), whereas there was a supranormal increase in a third (epididymal). This pattern of hyperplasia contrasts sharply with that seen in rats fed highly palatable high-fat or high-carbohydrate diets in which retroperitoneal depots show the most hyperplasia and epididymal pads the least. Such variations of response across depots suggest that the features of adipose tissue responsible for adipocyte proliferation in the various depots may not be homogeneous both in their nature and in their distribution.
The use of NiTi shape memory alloys, introduced into orthodontics because of their ability to develop light continuous forces that prove more effective than heavy intermittent forces in the teeth movement, requires the mastering of the functional properties of NiTi wires. More specifically, the recovery force acting on the teeth is a sensitive function of temperature: knowledge of oral temperature modifications is therefore required to understand the stress state modification felt during orthodontic therapy. The temperature modifications induced by cold or hot drink intake in the oral cavity were investigated by using arch wires, fixed to removable Hawley retainers, similar to those currently used in orthodontic practice, by means of six temperature sensors placed in correspondence with specific teeth. Similarly, the temperature changes were detected on a metallic frame, fixed onto the palatal zone to a Hawley retainer, where a palatal expander was placed to correct unilateral or bilateral crossbites in deciduous or in early mixed dentition. The maximum temperature change was observed in the interincisor area: The temperature modification on other teeth depends on the modality of drink intake, with the highest temperature variations being detected in the palatal zone. Hence modifications in the stress state during orthodontic therapy with NiTi wires are to be expected.
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".
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.
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