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Relevant bibliographies by topics / Thermoprotection

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Academic literature on the topic 'Thermoprotection'

Author: Grafiati

Published: 22 February 2025

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Journal articles on the topic "Thermoprotection"

1

Malayer, Jerry R., John W. Pollard, and Peter J. Hansen. "Modulation of thermal killing of bovine lymphocytes and preimplantation mouse embryos by alanine and taurine." American Journal of Veterinary Research 53, no. 5 (May 1, 1992): 689–94. http://dx.doi.org/10.2460/ajvr.1992.53.05.689.

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Summary Addition of alanine and taurine blocked killing of lymphocytes caused by culture at 45 C. The optimal concentration for thermoprotection was achieved at 12.5 mM for l-alanine and 5 mM for taurine. Both d and l forms of alanine provided thermoprotection. The effect of these agents was not simply to increase osmolarity of the culture medium, because NaCl did not provide thermoprotection at comparable concentrations. Alanine and taurine were each tested at concentration of 50 mM for ability to block heat shock-induced killing and developmental retardation of 8- to 16-cell mouse embryos. Both agents enhanced embryo development after exposure to high temperature, though development remained less than that for embryos not exposed to high temperature. In one experiment, for example, 81% of embryos cultured at 38 C advanced in development during culture vs 0% at 42 C, 15% at 42 C with alanine, and 32% at 42 C with taurine. The beneficial effect of alanine at high temperature may have been partly attributable to effects independent of thermoprotection, because development of embryos cultured at 38 C was also improved by alanine.

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Barclay, J. W., and R. M. Robertson. "Heat-shock-induced thermoprotection of hindleg motor control in the locust." Journal of Experimental Biology 203, no. 5 (March 1, 2000): 941–50. http://dx.doi.org/10.1242/jeb.203.5.941.

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Functional neuromuscular connections are critical for appropriate behavioural responses, but can be negatively affected by increases in temperature. We investigated the effects of heat shock on the thermosensitivity of a neuromuscular pathway to the hindleg tibial extensor muscle of Locusta migratoria. We found that exposure to heat shock induced thermoprotection of both neuromuscular transmission and extensor muscle contraction by (i) increasing the upper temperature limit for failure, (ii) improving recovery following heat-induced failure and (iii) stabilizing excitatory junction potential amplitude and duration and extensor muscle contraction force at high temperatures. Furthermore, the heat-shock-induced thermoprotection of extensor muscle contraction was not attributable to a protective effect on intrinsic components of muscle contraction. Finally, the use of jumping as a locomotor strategy to avoid capture, a behavioural response dependent upon functionally competent neuromuscular connections at the hindleg tibial extensor muscle, became less sensitive to temperature following heat shock. We conclude that the natural stress response of the locust stabilizes neuromuscular signalling during temperature stress, and that this can underlie a thermoprotection of muscle contraction force and thus alter the thermosensitivity of an escape behaviour critical for survival.

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Klose, M. K. "Stress-Induced Thermoprotection of Neuromuscular Transmission." Integrative and Comparative Biology 44, no. 1 (February 1, 2004): 14–20. http://dx.doi.org/10.1093/icb/44.1.14.

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Caldas, Teresa, Nathalie Demont-Caulet, Alexandre Ghazi, and Gilbert Richarme. "Thermoprotection by glycine betaine and choline." Microbiology 145, no. 9 (September 1, 1999): 2543–48. http://dx.doi.org/10.1099/00221287-145-9-2543.

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Neal, Scott J., Shanker Karunanithi, Adrienne Best, Anthony Ken-Choy So, Robert M. Tanguay, Harold L. Atwood, and J. Timothy Westwood. "Thermoprotection of synaptic transmission in a Drosophila heat shock factor mutant is accompanied by increased expression of Hsp83 and DnaJ-1." Physiological Genomics 25, no. 3 (May 16, 2006): 493–501. http://dx.doi.org/10.1152/physiolgenomics.00195.2005.

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In Drosophila larvae, acquired synaptic thermotolerance after heat shock has previously been shown to correlate with the induction of heat shock proteins (Hsps) including HSP70. We tested the hypothesis that synaptic thermotolerance would be significantly diminished in a temperature-sensitive strain ( Drosophila heat shock factor mutant hsf4), which has been reported not to be able to produce inducible Hsps in response to heat shock. Contrary to our hypothesis, considerable thermoprotection was still observed at hsf4 larval synapses after heat shock. To investigate the cause of this thermoprotection, we conducted DNA microarray experiments to identify heat-induced transcript changes in these organisms. Transcripts of the hsp83, dnaJ-1 ( hsp40), and glutathione- S-transferase gstE1 genes were significantly upregulated in hsf4 larvae after heat shock. In addition, increases in the levels of Hsp83 and DnaJ-1 proteins but not in the inducible form of Hsp70 were detected by Western blot analysis. The mode of heat shock administration differentially affected the relative transcript and translational changes for these chaperones. These results indicate that the compensatory upregulation of constitutively expressed Hsps, in the absence of the synthesis of the major inducible Hsp, Hsp70, could still provide substantial thermoprotection to both synapses and the whole organism.

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PLATT, MARK W., MICHAEL D. RICH, and JAMES C. MCLAUGHLIN. "The Role of Chitin in the Thermoprotection of Vibrio cholerae." Journal of Food Protection 58, no. 5 (May 1, 1995): 513–14. http://dx.doi.org/10.4315/0362-028x-58.5.513.

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Vibrio cholerae has been shown to be able to survive short periods of boiling. The potential role of chitin in the thermoprotection of Vibrio cholerae was determined. When V. cholerae 6706 (OI E1 Tor) cells were incubated at 37°C in the presence of chitin, the bacteria were able to grow in the absence of any other energy source. In phosphate-buffered saline, growth was not supported. The ability of six pathogenic strains to survive at 60°C was investigated. None of the isolates tested was able to survive at 60°C for 10 min regardless of whether chitin was present. Further investigation revealed that isolate 6706 was able to withstand 50°C for a period of 10 min; pre-incubation with chitin decreased the survival time at this temperature. The data presented here show that chitin does not provide thermoprotection.

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Rodriguez, P. X., Y. Ono, Y. Sun, P. Hamet, S. N. Orlov, and J. Tremblay. "THERMOPROTECTION OF VASCULAR SMOOTH MUSCLE ION TRANSPORTERS." Journal of Hypertension 18 (June 2000): S183. http://dx.doi.org/10.1097/00004872-200006001-00634.

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Newman, Amy E. M., Chengfeng Xiao, and R. Meldrum Robertson. "Synaptic thermoprotection in a desert-dwellingDrosophila species." Journal of Neurobiology 64, no. 2 (2005): 170–80. http://dx.doi.org/10.1002/neu.20132.

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Kraus, K. W., E. M. Hallberg, and R. Hallberg. "Characterization of a Tetrahymena thermophila mutant strain unable to develop normal thermotolerance." Molecular and Cellular Biology 6, no. 11 (November 1986): 3854–61. http://dx.doi.org/10.1128/mcb.6.11.3854-3861.1986.

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For Tetrahymena thermophila cells to survive extended periods of time at 43 degrees C, they must continuously synthesize heat shock proteins. For its translational machinery to function at 43 degrees C, T. thermophila requires either prior nonlethal heat shock treatment or brief treatment with partially inhibiting doses of cycloheximide or emetine. We have identified and characterized a mutant strain of T. thermophila (MC-3) in which prior nonlethal heat shock does not prevent protein synthesis inactivation at 43 degrees C. In addition, treatment of MC-3 cells with either of the antibiotics that normally confer 43 degrees C thermoprotection on wild-type cells elicited no similar thermoprotective response in these cells. Despite these phenotypic characteristics, by other criteria MC-3 synthesized a normal, functional array of heat shock proteins at 40 degrees C, a nonlethal heat shock protein-inducing temperature. The mutation in MC-3 which prevents the thermostabilization of protein synthesis by nonlethal heat shock is, by genetic criteria, most likely the same one which prevents the induction of thermotolerance by drug treatments. We present evidence that this mutation may affect some ribosome-associated functions.

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Kraus, K. W., E. M. Hallberg, and R. Hallberg. "Characterization of a Tetrahymena thermophila mutant strain unable to develop normal thermotolerance." Molecular and Cellular Biology 6, no. 11 (November 1986): 3854–61. http://dx.doi.org/10.1128/mcb.6.11.3854.

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For Tetrahymena thermophila cells to survive extended periods of time at 43 degrees C, they must continuously synthesize heat shock proteins. For its translational machinery to function at 43 degrees C, T. thermophila requires either prior nonlethal heat shock treatment or brief treatment with partially inhibiting doses of cycloheximide or emetine. We have identified and characterized a mutant strain of T. thermophila (MC-3) in which prior nonlethal heat shock does not prevent protein synthesis inactivation at 43 degrees C. In addition, treatment of MC-3 cells with either of the antibiotics that normally confer 43 degrees C thermoprotection on wild-type cells elicited no similar thermoprotective response in these cells. Despite these phenotypic characteristics, by other criteria MC-3 synthesized a normal, functional array of heat shock proteins at 40 degrees C, a nonlethal heat shock protein-inducing temperature. The mutation in MC-3 which prevents the thermostabilization of protein synthesis by nonlethal heat shock is, by genetic criteria, most likely the same one which prevents the induction of thermotolerance by drug treatments. We present evidence that this mutation may affect some ribosome-associated functions.

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Dissertations / Theses on the topic "Thermoprotection"

1

Barclay, Jeffrey William. "Environmentally-induced thermoprotection of insect motor control." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ63403.pdf.

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Wu, Bernhard Shiaoyuen. "Environmental stress-induced thermoprotection of action potential signalling in Locusta migratoria." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63472.pdf.

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Koch, Guillaume. "Optimisation de la protection du nerf sciatique lors des ablathermies du bassin." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAD041.

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La thermoablation est une technique de destruction tumorale percutanée. Cette technique mini-invasive utilise des imageurs pour guider durant l’intervention les sondes de thermoablation jusqu’à la zone cible et pour guider la mise en place d’outils de protection des structures anatomiques sensibles. La thermoablation de lésion osseuse du bassin est une technique à risque par proximité du nerf sciatique. Sa protection est essentielle pour éviter une lésion nerveuse thermique iatrogène. L’hydrodissection du nerf sciatique est une technique de protection active par éloignement du nerf de la zone soumise à des températures extrêmes, et par régulation thermique autour du nerf.Le but de ce travail est de faire l’état de l’art de l’anatomie du nerf sciatique à sa sortie du bassin, de définir les rapports qu’il a avec le muscle piriforme et l’os iliaque. Une modélisation 3D de la région glutéale a été réalisée pour effectuer des simulations d’une hydrodissection du nerf lors d’ablathermies du bassin. Puis un dispositif d’injection motorisé contrôlé en température a été dessiné
Thermoablation is a percutaneous technique for tumor destruction. This minimally invasive technique uses medical imaging to guide the thermoablation probes to the target area during the procedure and to guide the tools to protect sensitive anatomical structures. Thermoablation of a pelvic bone lesion is a high-risk technique due to the proximity of the sciatic nerve. Its protection is essential to avoid iatrogenic thermal nerve injury. Hydrodissection of the sciatic nerve is an active protection technique that removes the nerve from the area exposed to extreme temperatures and regulates the temperature around the nerve.The aim of this study was to review the anatomy of the sciatic nerve as it exits the pelvis and to define its relationship with the piriformis muscle and the pelvic bone. A 3D model of the gluteal region was created to simulate hydrodissection of the nerve during pelvic ablathermy. A temperature-controlled motorized injection device was then designed

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Armstrong, GARY. "Cellular signalling pathways involved in thermoprotection of neural ciruit function in the locust." Thesis, 2009. http://hdl.handle.net/1974/5102.

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Environmental temperature is arguably one of the most important abiotic physical factors affecting insect behaviour. Temperature affects virtually all physiological processes including those that regulate nervous system function. It is therefore not surprising that animals have evolved adaptations that confer tolerance to heat stress and allow for continued behaviour as ambient temperature fluctuates. Most animals have central nervous system (CNS) responses to heat shock (HS) preconditioning which extend the thermal operating range of neural circuits during exposure to extreme heat. It is unclear how HS preconditioning confers CNS thermotolerance. I used the migratory locust (Locusta migratoria), an animal that inhabits environments that can have large fluctuations in ambient temperature daily, to examine how neuronal circuits cope with temperatures stress. Using the ventilatory central pattern generator (vCPG) as a model circuit I was able to address how the CNS switches on adaptations which provide protection against heat stress. vCPG thermotolerance was manifested as an increase in the thermal operating range and a decrease in the length of time required to recover vCPG activity when temperature stress was removed. I investigated the octopaminergic (OA/cAMP/PKA) and nitrergic (NO/cGMP/PKG) signalling pathways and tested their involvement in conferring thermotolerance to the vCPG during heat stress. I found that long applications of octopamine, or increased adenylate cyclase activity generated vCPG thermotolerance and was dependent upon transcription and translation. In addition I found that HS-treated locust had significantly reduced nitric oxide (NO) production during heat stress, and when I pharmacologically reduced PKG activity vCPG thermotolerance was generated. However, unlike octopamine treatment thermotolerance could be observed within minutes following PKG inhibition. Thus I conclude that the octopaminergic and nitrergic pathways coordinate long- and short-term protective modulation of the locust CNS.
Thesis (Ph.D, Biology) -- Queen's University, 2009-08-27 16:11:09.581

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Book chapters on the topic "Thermoprotection"

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Lin, Chu-Yung, Tsung-Luo Jinn, Ming-Hsiun Hsieh, and Yih-Ming Chen. "Class I low molecular weight heat shock proteins in plants: immunological study and thermoprotection against heat denaturation of soluble proteins." In Biochemical and Cellular Mechanisms of Stress Tolerance in Plants, 141–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79133-8_7.

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Conference papers on the topic "Thermoprotection"

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Zhestkov, B. Eu, I. V. Yegorov, W. P. P. Fischer, and J. Antonenko. "Windtunnel Catalyticity Evaluation for Thermoprotective Elements." In 31st International Conference On Environmental Systems. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2001. http://dx.doi.org/10.4271/2001-01-2384.

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Wei, Yanhong, and Chang Xu. "Automatic testing system for parameters of high-current thermoprotector." In Instruments (ICEMI). IEEE, 2009. http://dx.doi.org/10.1109/icemi.2009.5274812.

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Reports on the topic "Thermoprotection"

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Hansen, Peter J., and Zvi Roth. Use of Oocyte and Embryo Survival Factors to Enhance Fertility of Heat-stressed Dairy Cattle. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7697105.bard.

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The overall goal was to identify survival factors that can improve pregnancy success following insemination or embryo transfer in lactating dairy cows exposed to heat stress. First, we demonstrated that oocytes are actually damaged by elevated temperature in the summer. Then we tested two thermoprotective molecules for their effect on oocyte damage caused by heat shock. One molecule, ceramide was not thermoprptective. Another, insulin-like growth factor-1 (IGF) reduced the effects of heat shock on oocyte apoptosis and oocyte cleavage when added during maturation. We also used lactating cows exposed to heat stress to determine whether bovine somatotropin (bST), which increases IGF1 levels in vivo, would improve fertility in summer. Cows treated with bST received a single injection at 3 days before insemination. Controls received no additional treatment. Treatment with bST did not significantly increase the proportion of inseminated cows diagnosed pregnant although it was numerically greater for the bST group (24.2% vs 17.8%, 124–132 cows per group). There was a tendency (p =0.10) for a smaller percent of control cows to have high plasma progesterone concentrations (≥ 1 ng/ml) at Day 7 after insemination than for bST-treated cows (72.6 vs 81.1%). When only cows that were successfully synchronized were considered, the magnitude of the absolute difference in the percentage of inseminated cows that were diagnosed pregnant between bST and control cows was reduced (24.8 vs 22.4% pregnant for bST and control). Results failed to indicate a beneficial effect of bST treatment on fertility of lactating dairy cows. In another experiment, we found a tendency for addition of IGF1 to embryo culture medium to improve embryonic survival after embryo transfer when the experiment was done during heat stress but not when the experiment was done in the absence of heat stress. Another molecule tested, granulocyte-macrophage colony-stimulating factor (GM-CSF; also called colony-stimulating factor-2), improved embryonic survival in the absence of heat stress. We also examined whether heat shock affects the sperm cell. There was no effect of heat shock on sperm apoptosis (programmed cell death) or on sperm fertilizing ability. Therefore, effects of heat shock on sperm function after ejaculation if minimal. However, there were seasonal changes in sperm characteristics that indicates that some of the decrease in dairy cow fertility during the summer in Israel is due to using semen of inferior quality. Semen was collected from five representative bulls throughout the summer (August and September) and winter (December and January). There were seasonal differences in ion concentration in seminal plasma and in the mRNA for various ion channels known to be involved in acrosome reactions. Furthermore, the proportion of sperm cells with damaged acrosomes was higher in post-thaw semen collected in the summer than in its counterpart collected in winter (54.2 ± 3.5% vs. 51.4 ± 1.9%, respectively; P < 0.08Further examination is required to determine whether such alterations are involved in the low summer fertility of dairy cows.

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