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Journal articles on the topic 'Thermoprotection'

Author: Grafiati

Published: 22 February 2025

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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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Klose, Markus K., David Chu, Chengfeng Xiao, Laurent Seroude, and R. Meldrum Robertson. "Heat Shock–Mediated Thermoprotection of Larval Locomotion Compromised by Ubiquitous Overexpression of Hsp70 in Drosophila melanogaster." Journal of Neurophysiology 94, no. 5 (November 2005): 3563–72. http://dx.doi.org/10.1152/jn.00723.2005.

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Maintaining the competence of locomotor circuitry under stressful conditions can benefit organisms by enabling locomotion to more tolerable microhabitats. We show that prior heat shock protects locomotion and the locomotor central pattern generator of larval Drosophila against subsequent hyperthermic stress. We combined molecular genetic, electrophysiological, and behavioral techniques to investigate heat shock–mediated thermoprotection. Prior heat shock increased the distance traveled by larvae during hyperthermia before failure. The frequency of the rhythm of peristaltic locomotor contractions and the velocity of locomotion were both less thermosensitive after heat shock and were less susceptible to failure at high temperatures. Rhythmic coordinated motor patterns, recorded intracellularly as excitatory junction potentials in body wall muscles of dissected preparations, were centrally generated because patterns could still be generated in the absence of sensory feedback (sensory function disrupted with shibire). Prior heat shock protected central circuit operation during hyperthermic stress by increasing the temperature at which it failed. Overexpression of Hsp70 after a heat shock using transgenic flies ( traII) did not enhance thermoprotection, as expected, but had deleterious effects on parameters of behavior.

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12

Shabtay, A. "Ectothermy and endothermy: evolutionary perspectives of thermoprotection by HSPs." Journal of Experimental Biology 208, no. 14 (July 15, 2005): 2773–81. http://dx.doi.org/10.1242/jeb.01705.

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13

Reshetnikov, Igor S., Marina Yu Yablokova, and Nikolay A. Khalturinskij. "Influence of surface structure on thermoprotection properties of intumescent systems." Applied Surface Science 115, no. 2 (June 1997): 199–201. http://dx.doi.org/10.1016/s0169-4332(97)80205-x.

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14

Trejo, A. C., I. B. Abad, V. M. V. Meza, A. M. Villa, J. Z. Abad, M. C. Navarro-Maldonado, and D. G. Ambriz. "93 THE INVOLVEMENT OF E-CADHERIN IN THERMOPROTECTIVE FUNCTION OF INSULIN-LIKE GROWTH FACTOR-1 IN 4-CELL HAMSTER EMBRYOS." Reproduction, Fertility and Development 27, no. 1 (2015): 139. http://dx.doi.org/10.1071/rdv27n1ab93.

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Studies have demonstrated that the early pre-implantation embryo is very sensitive to effects of heat stress in vitro. Heat stress reduces the total cell number in blastocysts and increases apoptosis in blastomeres. Insulin-like growth factor-1 (IGF-1) has been widely studied as a thermoprotective agent for its anti-apoptotic actions. Addition of IGF-1 to the culture medium decreases the effects of heat stress on blastocysts but has no effects on 2-cell embryos. Molecular mechanisms by which IGF-1 decreases apoptosis involve activation of the PI3K/Akt pathway. It is also known that adherens junctions contribute to PI3K/AKT activation mediated by the transmembrane glycoprotein E-cadherin, which is involved in Ca2+-dependent cell-cell adhesion. Within 2- to 8-cell embryos, E-cadherin is mainly inactive and has cytoplasmic localization. 6-Dimethylaminopurine (6-DMAP) induces premature cell flattening and E-cadherin redistribution to adhesion sites in 4-cell embryos. The aim of this study was to induce E-cadherin redistribution in 4-cell hamster embryos and evaluate the thermoprotective function of IGF-1 in these embryos. Four-cell embryos were incubated in the presence of 6-DMAP to induce E-cadherin redistribution to adhesion sites and cultured for 24 h under conditions of heat stress and compared with controls without 6-DMAP. Culture medium was supplemented with IGF-1. At the end of culture, developmental stage and rate of apoptosis were determined and analysed by ANOVA using the General Linear Model (GLM) of SAS (SAS Institute Inc., Cary, NC, USA) procedure with statistical significance at P < 0.05. E-Cadherin redistribution induced by 6-DMAP increased development to the 6-cell stage after 24 h (63.57% v. 38.81%, respectively; P < 0.05) and reduced apoptosis (25% v. 33%, respectively; P < 0.05) under heat-stress conditions. In conclusion, we hypothesise a role for E-cadherin-mediated cell flattening in promoting IGF-1-mediated thermoprotection in pre-compact 4-cell hamster embryos. Further studies are required to confirm this link.

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15

Aréchiga, C. F., A. D. Ealy, and P. J. Hansen. "Efficacy of vitamin E and glutathione for thermoprotection of murine morulae." Theriogenology 41, no. 8 (January 1994): 1545–53. http://dx.doi.org/10.1016/0093-691x(94)90820-9.

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16

Barclay, J. W., and R. M. Robertson. "Role for calcium in heat shock-mediated synaptic thermoprotection inDrosophila larvae." Journal of Neurobiology 56, no. 4 (August 8, 2003): 360–71. http://dx.doi.org/10.1002/neu.10247.

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17

Garnon, Julien, Roberto Luigi Cazzato, Jean Caudrelier, Maud Nouri-Neuville, Pramod Rao, Emanuele Boatta, Nitin Ramamurthy, Guillaume Koch, and Afshin Gangi. "Adjunctive Thermoprotection During Percutaneous Thermal Ablation Procedures: Review of Current Techniques." CardioVascular and Interventional Radiology 42, no. 3 (October 11, 2018): 344–57. http://dx.doi.org/10.1007/s00270-018-2089-7.

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18

EALY, A., M. DROST, C. BARROS, and P. HANSEN. "Thermoprotection of preimplantation bovine embryos from heat shock by glutathione and taurine." Cell Biology International Reports 16, no. 2 (February 1992): 125–31. http://dx.doi.org/10.1016/s0309-1651(06)80106-2.

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19

Armstrong, Gary A. B., and R. Meldrum Robertson. "A role for octopamine in coordinating thermoprotection of an insect nervous system." Journal of Thermal Biology 31, no. 1-2 (January 2006): 149–58. http://dx.doi.org/10.1016/j.jtherbio.2005.11.022.

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20

Wu, Bernhard S., Virginia K. Walker, and R. Meldrum Robertson. "Heat shock-induced thermoprotection of action potentials in the locust flight system." Journal of Neurobiology 49, no. 3 (2001): 188–99. http://dx.doi.org/10.1002/neu.1074.

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21

Fernández, J., T. Soto, J. Vicente-Soler, J. Cansado, and M. Gacto. "Increased thermal stability of the enzyme content in permeabilized whole cells from the fission yeast Schizosaccharomyces pombe by exogenous trehalose and other compounds." Canadian Journal of Microbiology 41, no. 10 (October 1, 1995): 936–41. http://dx.doi.org/10.1139/m95-129.

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Cells of the fission yeast Schizosaccharomyces pombe were permeabilized by treatment with toluene–ethanol. The permeabilized cells lost the bulk of the internal trehalose pool while most of the alkaline phosphatase, invertase, α-glucosidase, or neutral trehalase activities located inside the cells remained unaffected. This system was used as an in situ assay to determine the involvement of trehalose in enzyme protection during thermal treatments. The addition of trehalose to suspensions of permeabilized cells resulted in a sugar-dependent thermoprotection of the internal marker enzymes. This approach demonstrates that in whole cells of the fission yeast trehalose plays a physiological role as a protective molecule against thermal denaturation of cellular enzymes.Key words: permeabilization, fission yeast, trehalose, thermal stability.

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22

MICHEL, Marcel R., Daniel FAVRE, Erwin STUDER, Andre-Patrick ARRIGO, and Christoph KEMPF. "Modulation of thermoprotection and translational thermotolerance induced by Semliki Forest virus capsid protein." European Journal of Biochemistry 223, no. 3 (August 1994): 791–97. http://dx.doi.org/10.1111/j.1432-1033.1994.tb19054.x.

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23

Garlick, Kristopher M., and R. Meldrum Robertson. "Cytoskeletal stability and heat shock-mediated thermoprotection of central pattern generation in Locusta migratoria." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 147, no. 2 (June 2007): 344–48. http://dx.doi.org/10.1016/j.cbpa.2006.10.044.

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24

Garnon, Julien, Matthias Fuerstner, Ishaq Fahmi Uri, Nitin Ramamurthy, and Klaus Hausegger. "Intramural Hydrodissection of an Adherent Bowel Loop during Renal Tumor Cryoablation: Complication or Thermoprotection?" Journal of Vascular and Interventional Radiology 29, no. 9 (September 2018): 1294–96. http://dx.doi.org/10.1016/j.jvir.2018.04.031.

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25

Klose, Markus K., Gary Armstrong, and R. Meldrum Robertson. "A role for the cytoskeleton in heat-shock-mediated thermoprotection of locust neuromuscular junctions." Journal of Neurobiology 60, no. 4 (2004): 453–62. http://dx.doi.org/10.1002/neu.20058.

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26

Bonilla, A. Q. S., L. J. Oliveira, M. Ozawa, E. M. Newsom, M. C. Lucy, and P. J. Hansen. "121 DEVELOPMENTAL CHANGES IN THERMOPROTECTIVE ACTIONS OF INSULIN-LIKE GROWTH FACTOR-1 ON THE PREIMPLANTATION BOVINE EMBRYO." Reproduction, Fertility and Development 23, no. 1 (2011): 165. http://dx.doi.org/10.1071/rdv23n1ab121.

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Insulin-like growth factor-1 (IGF1) is an important endocrine signal for regulation of early embryonic development. It increases the proportion of preimplantation embryos becoming blastocysts, alters blastocyst gene expression, improves resistance of embryos to various stresses and can enhance survival of embryos after transfer to recipients. The present study had 2 objectives. The first was to determine whether the thermoprotective actions of IGF1 on the preimplantation bovine embryo were developmentally regulated, with the 2-cell embryo being refractory to IGF1. The second was to determine the molecular basis for the improved competence of embryos treated with IGF1 to establish pregnancy after transfer to heat-stressed recipients. Heat shock at 41°C decreased (P < 0.005) the percentage of 2-cell embryos becoming a blastocyst at day 8 (39.5 v. 21% for 38.5 and 41°C, respectively), and treatment of embryos with 100 ng mL–1 IGF1 did not provide thermoprotection to 2-cell embryos heat shocked at 41°C (21 v. 21% for control and IGF1-treated embryos, respectively). Heat shock at 41°C had no effect on blastocyst development of day 5 embryos. However, exposure to 42°C reduced (P < 0.001) blastocyst development of day 5 embryos (87 v. 47.6% for 38.5 and 42°C, respectively). Furthermore, treatment of embryos with 100 ng mL–1 IGF1 reduced (P = 0.05) the effect of heat shock at 42°C on day 5 embryos (48 v. 66% control and IGF1-treated embryos, respectively). Failure of IGF1 to alter 2-cell embryo survival after heat shock was not associated with reduced expression of genes involved in IGF1 signaling (IGF1R, RAF1, PI3K, and MAPK), as shown by quantitative real-time RT-PCR assay, or in amounts of immunoreactive IGF1R protein. Treatment with IGF1 had little effect on the transcriptome at the blastocyst stage, with a total of 102 differentially expressed genes identified. Among the differentially expressed genes were several involved in apoptosis, protection against free radicals, and development. Changes in gene expression are consistent with IGF1 acting to induce an anti-apoptotic state and inhibit neurulation. In conclusion, thermoprotective actions of IGF1 are developmentally regulated. Failure of IGF1 to protect the 2-cell embryo from heat shock could reflect the fact that these embryos are maximally sensitive to damage caused by heat shock or reflect the quiescence of the embryonic genome at this early stage in development. Changes in gene expression at the blastocyst stage induced by IGF1 could contribute to the increased survival of IGF1-treated embryos when transferred during periods of heat stress. Support: USDA NRI 2007-35203-18070 and 2009-65203-05732.

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27

Vertrees, Roger A., Joseph B. Zwischenberger, Paul J. Boor, and Scot D. Pencil. "Oncogenic ras results in increased cell kill due to defective thermoprotection in lung cancer cells." Annals of Thoracic Surgery 69, no. 6 (June 2000): 1675–80. http://dx.doi.org/10.1016/s0003-4975(00)01421-1.

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28

Yoon, Jason T., Jared Nesbitt, Barry L. Raynor, Michael Roth, Colin C. Zertan, and Jack W. Jennings. "Utility of Motor and Somatosensory Evoked Potentials for Neural Thermoprotection in Ablations of Musculoskeletal Tumors." Journal of Vascular and Interventional Radiology 31, no. 6 (June 2020): 903–11. http://dx.doi.org/10.1016/j.jvir.2019.12.015.

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29

Padilha, M. M., J. Stephen Jones, K. Streator Smith, M. Zhou, E. Walker, and C. Magi-Galluzzi. "Prediction of prostate cancer to urethra distance by a pretreatment nomogram: urethral thermoprotection implication in cryoablation." Prostate Cancer and Prostatic Diseases 16, no. 4 (September 3, 2013): 372–75. http://dx.doi.org/10.1038/pcan.2013.32.

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30

Holtmann, Gudrun, and Erhard Bremer. "Thermoprotection of Bacillus subtilis by Exogenously Provided Glycine Betaine and Structurally Related Compatible Solutes: Involvement of Opu Transporters." Journal of Bacteriology 186, no. 6 (March 15, 2004): 1683–93. http://dx.doi.org/10.1128/jb.186.6.1683-1693.2004.

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ABSTRACT Bacillus subtilis possesses five osmotically regulated transporters (Opu) for the uptake of various compatible solutes for osmoprotective purposes. We have now found that compatible solutes also function as thermoprotectants for B. subtilis. Low concentrations of glycine betaine enhanced the growth of the B. subtilis wild-type strain JH642 at its maximal growth temperature (52°C) but did not allow an extension of the upper growth limit. A similar enhancement in the growth of B. subtilis was also observed by the addition of several other compatible solutes that are structurally related to glycine betaine or by the addition of proline. Each of these compatible solutes was taken up under heat stress by the cell through the same Opu transporters that are used for their acquisition under osmostress conditions. Northern blot analysis revealed a moderate increase in transcription of the structural genes for each of the Opu transport systems in cells that were propagated at 52°C. In contrast, the uptake level of radiolabeled glycine betaine was very low under high-temperature growth conditions but nevertheless allowed the buildup of an intracellular glycine betaine pool comparable to that found in cells grown at 37°C in the absence of salt stress. Although exogenously added glutamate has only a limited osmoprotective potential for B. subtilis, it was found to be a very effective thermoprotectant. Collectively, our data demonstrate thermoprotection by a variety of compatible solutes in B. subtilis, thus ascribing a new physiological function for this class of compounds in this microorganism and broadening the physiological role of the known osmoprotectant uptake systems (Opu).

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31

Wolfe, Gregory R., Clyde A. Smith, Donald L. Hendrix, and Michael E. Salvucci. "Molecular basis for thermoprotection in Bemisia: structural differences between whitefly ketose reductase and other medium-chain dehydrogenases/reductases." Insect Biochemistry and Molecular Biology 29, no. 2 (February 1999): 113–20. http://dx.doi.org/10.1016/s0965-1748(98)00114-3.

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32

Alswang, J., M. Moussa, G. Abiola, J. Honhart, S. Degerstedt, V. Ramalingam, and M. Ahmed. "Abstract No. 274 Utility of Intraoperative Neuromonitoring as a Method of Passive Thermoprotection in Musculoskeletal and Lymph Cryoablations." Journal of Vascular and Interventional Radiology 35, no. 3 (March 2024): S121. http://dx.doi.org/10.1016/j.jvir.2023.12.313.

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33

Gouesbet, Gwenola, Gwenael Jan, and Patrick Boyaval. "Two-Dimensional Electrophoresis Study of Lactobacillus delbrueckii subsp. bulgaricus Thermotolerance." Applied and Environmental Microbiology 68, no. 3 (March 2002): 1055–63. http://dx.doi.org/10.1128/aem.68.3.1055-1063.2002.

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ABSTRACT The response of Lactobacillus delbrueckii subsp. bulgaricus cells to heat stress was studied by use of a chemically defined medium. Two-dimensional electrophoresis (2-DE) analysis was used to correlate the kinetics of heat shock protein (HSP) induction with cell recovery from heat injury. We demonstrated that enhanced viability, observed after 10 min at 65°C, resulted from the overexpression of HSP and from mechanisms not linked to protein synthesis. In order to analyze the thermoadaptation mechanisms involved, thermoresistant variants were selected. These variants showed enhanced constitutive tolerance toward heat shock. However, contrary to the wild-type strain, these variants were poorly protected after osmotic or heat pretreatments. This result suggests that above a certain threshold, cells reach a maximum level of protection that cannot be easily exceeded. A comparison of protein patterns showed that the variants were able to induce more rapidly their adaptive mechanisms than the original strain. In particular, the variants were able to express constitutively more HSP, leading to the higher level of thermoprotection observed. This is the first report of the study by 2-DE of the heat stress response in L. delbrueckii subsp. bulgaricus.

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34

Brown, M. A., R. P. Upender, L. E. Hightower, and J. L. Renfro. "Thermoprotection of a functional epithelium: heat stress effects on transepithelial transport by flounder renal tubule in primary monolayer culture." Proceedings of the National Academy of Sciences 89, no. 8 (April 15, 1992): 3246–50. http://dx.doi.org/10.1073/pnas.89.8.3246.

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35

Tongden, C., and Usha Chakraborty. "Heat acelimation and chemical pre-treatments induccd thermotolerancc in chickpea." NBU Journal of Plant Sciences 3, no. 1 (2009): 43–47. http://dx.doi.org/10.55734/nbujps.2009.v03i01.008.

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Induced heat-tolerance triggered by heat acclimation treatment and foliar application of salicylic acid and abscisic acid were evaluated in three different genotypes of chickpea (Cicer arietinum L.) distinctly differing in their sensitivity to heat stress. Seedlings pre-treated with 100uM salicylic acid (SA) and 50 uM abscisic acid (ABA) showed improved heat tolerance to a lethal temperature of 46°C than the untreated control seedlings. Heat stress increased lipid peroxidation of membranes and reduced plant survival. Protein and proline contents increased significantly in pre-treated seedlings. Cell membrane stability also increased remarkably in pre-treated seedlings of all three genotypes. Changes in activities of antioxidative enzymes like peroxidase, ascorbate peroxidase in pre-treated seedlings revealed increase in enzymatic activities which declined sharply at lethal temperuturc. Quantum of increase in enzymatic activity was however higher in thermotolerant genotype in comparison to heat susceptible genotype. Thermotolerant genotype also exhibited constitutively higher antioxidative activities. Catalase activity, in contrast, showed a significant decrease in its activity in pre-treated seedlings following exposure to lethal temperature. These results indicate that heat acclimation treatment and application of SA and ABA show great potential in inducing heat tolerance in chickpea seedlings and these can be further analyzed to understand their role in thermoprotection.

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Lamosa, Pedro, Luï¿½s G. Gonï¿½alves, Marta V. Rodrigues, Lï¿½gia O. Martins, Neil D. H. Raven, and Helena Santos. "Occurrence of 1-Glyceryl-1-myo-Inosityl Phosphate in Hyperthermophiles." Applied and Environmental Microbiology 72, no. 9 (September 2006): 6169–73. http://dx.doi.org/10.1128/aem.00852-06.

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ABSTRACT The accumulation of compatible solutes was studied in the hyperthermophilic bacterium Aquifex pyrophilus as a function of the temperature and the NaCl concentration of the growth medium. Nuclear magnetic resonance analysis of cell extracts revealed the presence of α- and β-glutamate, di-mannosyl-di-myo-inositol phosphate, di-myo-inositol phosphate, and an additional compound here identified as 1-glyceryl-1-myo-inosityl phosphate. All solutes accumulated by A. pyrophilus are negatively charged at physiological pH. The intracellular levels of di-myo-inositol phosphate increased in response to supraoptimal growth temperature, while α- and β-glutamate accumulated in response to osmotic stress, especially at growth temperatures below the optimum. The newly discovered compound, 1-glyceryl-1-myo-inosityl phosphate, appears to play a double role in osmo- and thermoprotection, since its intracellular pool increased primarily in response to a combination of osmotic and heat stresses. This work also uncovered the nature of the unknown compound, previously detected in Archaeoglobus fulgidus (L. O. Martins et al., Appl. Environ. Microbiol. 63:896-902, 1997). The curious structural relationship between diglycerol phosphate (found only in Archaeoglobus species), di-myo-inositol phosphate (a canonical solute of hyperthermophiles), and the newly identified solute is highlighted. This is the first report on the occurrence of 1-glyceryl-1-myo-inosityl phosphate in living systems.

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Fitzsimmons, Liam F., Stevenson Flemer, A. Sandy Wurthmann, P. Bruce Deker, Indra Neil Sarkar, and Matthew J. Wargo. "Small-Molecule Inhibition of Choline Catabolism in Pseudomonas aeruginosa and Other Aerobic Choline-Catabolizing Bacteria." Applied and Environmental Microbiology 77, no. 13 (May 20, 2011): 4383–89. http://dx.doi.org/10.1128/aem.00504-11.

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ABSTRACTCholine is abundant in association with eukaryotes and plays roles in osmoprotection, thermoprotection, and membrane biosynthesis in many bacteria. Aerobic catabolism of choline is widespread among soil proteobacteria, particularly those associated with eukaryotes. Catabolism of choline as a carbon, nitrogen, and/or energy source may play important roles in association with eukaryotes, including pathogenesis, symbioses, and nutrient cycling. We sought to generate choline analogues to study bacterial choline catabolismin vitroandin situ. Here we report the characterization of a choline analogue, propargylcholine, which inhibits choline catabolism at the level of Dgc enzyme-catalyzed dimethylglycine demethylation inPseudomonas aeruginosa. We used genetic analyses and13C nuclear magnetic resonance to demonstrate that propargylcholine is catabolized to its inhibitory form, propargylmethylglycine. Chemically synthesized propargylmethylglycine was also an inhibitor of growth on choline. Bioinformatic analysis suggests that there are genes encoding DgcA homologues in a variety of proteobacteria. We examined the broader utility of propargylcholine and propargylmethylglycine by assessing growth of other members of the proteobacteria that are known to grow on choline and possess putative DgcA homologues. Propargylcholine showed utility as a growth inhibitor inP. aeruginosabut did not inhibit growth in other proteobacteria tested. In contrast, propargylmethylglycine was able to inhibit choline-dependent growth in all tested proteobacteria, includingPseudomonas mendocina,Pseudomonas fluorescens,Pseudomonas putida,Burkholderia cepacia,Burkholderia ambifaria, andSinorhizobium meliloti. We predict that chemical inhibitors of choline catabolism will be useful for studying this pathway in clinical and environmental isolates and could be a useful tool to study proteobacterial choline catabolismin situ.

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Liossis, S. N., X. Z. Ding, J. G. Kiang, and G. C. Tsokos. "Overexpression of the heat shock protein 70 enhances the TCR/CD3- and Fas/Apo-1/CD95-mediated apoptotic cell death in Jurkat T cells." Journal of Immunology 158, no. 12 (June 15, 1997): 5668–75. http://dx.doi.org/10.4049/jimmunol.158.12.5668.

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Abstract To investigate whether the protective effects of the 70-kDa heat shock protein (hsp70) extend to the apoptotic mode of cell death, we transfected Jurkat T cells with the gene for the human hsp70 and challenged the cells with an anti-Fas mAb or with two different murine anti-CD3 mAbs. The anti-Fas mAb-triggered apoptotic cell death and the anti-CD3 mAb-mediated activation-induced cell death were significantly enhanced in the gene-transfected Jurkat cells overexpressing hsp70 compared with the unmanipulated and the vector-transfected cells. On the other hand, the well-established protective effect that this protein offers to the cells was unaffected, as determined by enhanced viability of gene-transfected cells exposed to a lethal heat shock. To investigate the mechanisms that are responsible for the increased susceptibility of the gene-transfected cells to apoptotic death, we studied the TCR/CD3-initiated events that showed a significant down-regulation of the protein tyrosine phosphorylation levels and the cytoplasmic free Ca2+ responses. As for the Fas/Apo-1/CD95-mediated early events, the activity of protein serine/threonine phosphatases was markedly increased in the cells overexpressing hsp70. Our study demonstrates that hsp70 overexpression offers thermoprotection but enhances TCR/CD3- and the Fas-induced apoptotic cell death. This phenomenon is associated with a down-regulation of the Ag receptor-initiated early signal transduction pathways and with an up-regulation of Fas-mediated early metabolic events.

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Lanciloti, Daniel F., Christopher Cwik, and Mark R. Brodl. "Heat shock proteins do not provide thermoprotection to normal cellular protein synthesis, alpha-amylase mRNA and endoplasmic reticulum lamellae in barley aleurone layers." Physiologia Plantarum 97, no. 3 (July 1996): 513–23. http://dx.doi.org/10.1111/j.1399-3054.1996.tb00511.x.

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40

Lanciloti, Daniel F., Christopher Cwik, and Mark R. Brodl. "Heat shock proteins do not provide thermoprotection to normal cellular protein synthesis, alpha-amylase mRNA and endoplasmic reticulum lamellae in barley aleurone layers." Physiologia Plantarum 97, no. 3 (July 1996): 513–23. http://dx.doi.org/10.1034/j.1399-3054.1996.970314.x.

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41

Borges, Nuno, Rie Matsumi, Tadayuki Imanaka, Haruyuki Atomi, and Helena Santos. "Thermococcus kodakarensis Mutants Deficient in Di-myo-Inositol Phosphate Use Aspartate To Cope with Heat Stress." Journal of Bacteriology 192, no. 1 (October 30, 2009): 191–97. http://dx.doi.org/10.1128/jb.01115-09.

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ABSTRACT Many of the marine microorganisms which are adapted to grow at temperatures above 80°C accumulate di-myo-inositol phosphate (DIP) in response to heat stress. This led to the hypothesis that the solute plays a role in thermoprotection, but there is a lack of definitive experimental evidence. Mutant strains of Thermococcus kodakar ensis (formerly Thermococcus kodakaraensis), manipulated in their ability to synthesize DIP, were constructed and used to investigate the involvement of DIP in thermoadaptation of this archaeon. The solute pool of the parental strain comprised DIP, aspartate, and α-glutamate. Under heat stress the level of DIP increased 20-fold compared to optimal conditions, whereas the pool of aspartate increased 4.3-fold in response to osmotic stress. Deleting the gene encoding the key enzyme in DIP synthesis, CTP:inositol-1-phosphate cytidylyltransferase/CDP-inositol:inositol-1-phosphate transferase, abolished DIP synthesis. Conversely, overexpression of the same gene resulted in a mutant with restored ability to synthesize DIP. Despite the absence of DIP in the deletion mutant, this strain exhibited growth parameters similar to those of the parental strain, both at optimal (85°C) and supraoptimal (93.7°C) temperatures for growth. Analysis of the respective solute pools showed that DIP was replaced by aspartate. We conclude that DIP is part of the strategy used by T. kodakarensis to cope with heat stress, and aspartate can be used as an alternative solute of similar efficacy. This is the first study using mutants to demonstrate the involvement of compatible solutes in the thermoadaptation of (hyper)thermophilic organisms.

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García-Estepa, Raúl, Montserrat Argandoña, Mercedes Reina-Bueno, Nieves Capote, Fernando Iglesias-Guerra, Joaquín J. Nieto, and Carmen Vargas. "The ectD Gene, Which Is Involved in the Synthesis of the Compatible Solute Hydroxyectoine, Is Essential for Thermoprotection of the Halophilic Bacterium Chromohalobacter salexigens." Journal of Bacteriology 188, no. 11 (June 1, 2006): 3774–84. http://dx.doi.org/10.1128/jb.00136-06.

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ABSTRACT The halophilic bacterium Chromohalobacter salexigens synthesizes and accumulates compatible solutes in response to salt and temperature stress. 13C-nuclear magnetic resonance analysis of cells grown in minimal medium at the limiting temperature of 45°C revealed the presence of hydroxyectoine, ectoine, glutamate, trehalose (not present in cells grown at 37°C), and the ectoine precursor, Nγ-acetyldiaminobutyric acid. High-performance liquid chromatography analyses showed that the levels of ectoine and hydroxyectoine were maximal during the stationary phase of growth. Accumulation of hydroxyectoine was up-regulated by salinity and temperature, whereas accumulation of ectoine was up-regulated by salinity and down-regulated by temperature. The ectD gene, which is involved in the conversion of ectoine to hydroxyectoine, was isolated as part of a DNA region that also contains a gene whose product belongs to the AraC-XylS family of transcriptional activators. Orthologs of ectD were found within the sequenced genomes of members of the proteobacteria, firmicutes, and actinobacteria, and their products were grouped into the ectoine hydroxylase subfamily, which was shown to belong to the superfamily of Fe(II)- and 2-oxoglutarate-dependent oxygenases. Analysis of the ectoine and hydroxyectoine contents of an ectABC ectD mutant strain fed with 1 mM ectoine or hydroxyectoine demonstrated that ectD is required for the main ectoine hydroxylase activity in C. salexigens. Although in minimal medium at 37°C the wild-type strain grew with 0.5 to 3.0 M NaCl, with optimal growth at 1.5 M NaCl, at 45°C it could not cope with the lowest (0.75 M NaCl) or the highest (3.0 M NaCl) salinity, and it grew optimally at 2.5 M NaCl. The ectD mutation caused a growth defect at 45°C in minimal medium with 1.5 to 2.5 M NaCl, but it did not affect growth at 37°C at any salinity tested. With 2.5 M NaCl, the ectD mutant synthesized 38% (at 37°C) and 15% (at 45°C) of the hydroxyectoine produced by the wild-type strain. All of these data reveal that hydroxyectoine synthesis mediated by the ectD gene is thermoregulated and essential for thermoprotection of C. salexigens.

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43

Hallberg, R. L., K. W. Kraus, and E. M. Hallberg. "Induction of acquired thermotolerance in Tetrahymena thermophila: effects of protein synthesis inhibitors." Molecular and Cellular Biology 5, no. 8 (August 1985): 2061–69. http://dx.doi.org/10.1128/mcb.5.8.2061-2069.1985.

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When Tetrahymena thermophila cells growing at 30 degrees C are shifted to either 40 or 43 degrees C, the kinetics and extent of induction of heat shock mRNAs in both cases are virtually indistinguishable. However, the cells shifted to 40 degrees C show a typical induction of heat shock protein (HSP) synthesis and survive indefinitely (100% after 24 h), whereas those at 43 degrees C show an abortive synthesis of HSPs and die (less than 0.01% survivors) within 1 h. Cells treated at 30 degrees C with the drugs cycloheximide or emetine, at concentrations which are initially inhibitory to protein synthesis and cell growth but from which cells can eventually recover and resume growth, are after this recovery able to survive a direct shift from 30 to 43 degrees C (ca. 70% survival after 1 h). This induction of thermotolerance by these drugs is as efficient in providing thermoprotection to cells as is a prior sublethal heat treatment which elicits the synthesis of HSPs. However, during the period when drug-treated cells recover their protein synthesis ability and simultaneously acquire the ability to subsequently survive a shift to 43 degrees C, none of the major HSPs are synthesized. The ability to survive a 1-h, 43 degrees C heat treatment, therefore, does not absolutely require the prior synthesis of HSPs. But, as extended survival at 43 degrees Celsius depends absolutely on the ability of cells to continually synthesize HSPs, it appears that a prior heat shock as well as the recovery from protein synthesis inhibition elicits a change in the protein synthetic machinery which allows the translation of HSP mRNAs at what would otherwise be a nonpermissive temperature for protein synthesis.

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44

Hallberg, R. L., K. W. Kraus, and E. M. Hallberg. "Induction of acquired thermotolerance in Tetrahymena thermophila: effects of protein synthesis inhibitors." Molecular and Cellular Biology 5, no. 8 (August 1985): 2061–69. http://dx.doi.org/10.1128/mcb.5.8.2061.

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When Tetrahymena thermophila cells growing at 30 degrees C are shifted to either 40 or 43 degrees C, the kinetics and extent of induction of heat shock mRNAs in both cases are virtually indistinguishable. However, the cells shifted to 40 degrees C show a typical induction of heat shock protein (HSP) synthesis and survive indefinitely (100% after 24 h), whereas those at 43 degrees C show an abortive synthesis of HSPs and die (less than 0.01% survivors) within 1 h. Cells treated at 30 degrees C with the drugs cycloheximide or emetine, at concentrations which are initially inhibitory to protein synthesis and cell growth but from which cells can eventually recover and resume growth, are after this recovery able to survive a direct shift from 30 to 43 degrees C (ca. 70% survival after 1 h). This induction of thermotolerance by these drugs is as efficient in providing thermoprotection to cells as is a prior sublethal heat treatment which elicits the synthesis of HSPs. However, during the period when drug-treated cells recover their protein synthesis ability and simultaneously acquire the ability to subsequently survive a shift to 43 degrees C, none of the major HSPs are synthesized. The ability to survive a 1-h, 43 degrees C heat treatment, therefore, does not absolutely require the prior synthesis of HSPs. But, as extended survival at 43 degrees Celsius depends absolutely on the ability of cells to continually synthesize HSPs, it appears that a prior heat shock as well as the recovery from protein synthesis inhibition elicits a change in the protein synthetic machinery which allows the translation of HSP mRNAs at what would otherwise be a nonpermissive temperature for protein synthesis.

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45

Chuykova, Polina, Sergii Shtrygol’, Andrii Taran, Tetiana Yudkevych, Iryna Lebedinets, and Denys Oklei. "Acute heat trauma model in rats, gender-dependent thermoresistance, and screening of potential thermoprotectors." ScienceRise: Pharmaceutical Science, no. 2 (48) (April 30, 2024): 4–11. http://dx.doi.org/10.15587/2519-4852.2024.301620.

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Heat trauma (HT) is an urgent medical and social problem. Heat damage is a widespread effect of the environment on humans, driven by global warming, military conflicts, technological disasters, work in hot environments, and engagement in extreme sports and tourism. The aim of the study: to propose a model of acute HT in rats that does not cause the death of animals, to determine the dependence of thermoresistance on gender, and to compare the effectiveness of the thermoprotective effects of a range of non-steroidal anti-inflammatory drugs (NSAIDs), paracetamol, and glucosamine hydrochloride in this model. Materials and Methods: The experiment was conducted on adult white rats of both genders. Acute HT was modelled by using a specially developed method involving heat exposure to animals at +55 °C for 30 minutes, followed by a recovery period of 60 minutes. Rectal temperature was measured every 15 minutes. The degree of hyperthermia in males and females was determined. The presence and intensity of the thermoprotective effect of glucosamine hydrochloride (G h/ch), diclofenac sodium, acetylsalicylic acid (ASA), nimesulide, etoricoxib, celecoxib, and paracetamol were evaluated through intragastric administration 60 minutes before heat exposure. The results were analyzed using the STATISTICA 12.0 program. Results: It was established that heat exposure at +55 °C for 30 minutes effectively replicates acute HT in rats without causing animal fatalities, adhering to bioethical requirements. Body temperature increases by 10-13 %, characterized as a heat stroke. Occasionally, thermoresistant animals are encountered, where the temperature increase during the first 15 minutes of exposure is less than 1 °C. These animals should not be used for further modelling of heat trauma. Male rats are more sensitive to the effect of high environmental temperatures than females, exhibiting greater hyperthermia (temperature increase of 5.03±0.39°C compared to 3.72±0.22 °C in females, p<0.01). The thermoprotective effect of glucosamine hydrochloride depends on gender, being more pronounced in males. Among the 6 tested COX inhibitors, the most significant thermoprotective effect was observed in the highly selective COX-2 inhibitor celecoxib and the weakly selective central inhibitor paracetamol, warranting in-depth research into their impact on organ and system states following heat trauma, as well as the mechanisms of their thermoprotective action. The thermoprotective effect is not associated with selectivity towards COX (cyclooxygenase): it is not observed in the highly selective COX-2 inhibitor etoricoxib and moderately selective COX-2 inhibitor nimesulide, as well as in non-selective COX inhibitors such as diclofenac sodium and aspirin, which also slows down the recovery of body temperature after heat exposure. Conclusions: A convenient and simple model of acute HT in rats is proposed, demonstrating higher thermosensitivity and a more pronounced thermoprotective effect of glucosamine hydrochloride in males. A significant thermoprotective effect was identified in celecoxib and paracetamol, surpassing other investigated NSAIDs. The mechanism and specific features of this effect require further clarification

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Khanov, A. M., L. D. Sirotenko, L. P. Shingel’, and E. O. Trofimov. "Internal grinding of thermoprotective rubber coatings." Russian Engineering Research 36, no. 7 (July 2016): 599–602. http://dx.doi.org/10.3103/s1068798x16070091.

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47

Pennarossa, G., S. Maffei, M. M. Rahman, A. Vanelli, G. Berruti, T. A. L. Brevini, and F. Gandolfi. "4 IDENTIFICATION AND FUNCTIONAL CHARACTERIZATION OF HEAT SHOCK PROTEIN 40 IN PIG OVARY." Reproduction, Fertility and Development 23, no. 1 (2011): 108. http://dx.doi.org/10.1071/rdv23n1ab4.

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Decreased fertility during the hot season is a common problem in pigs. Maternal hyperthermia reduces oocyte fertilizability and increases embryonic mortality. Cell biochemical thermoprotection mechanisms involve members of the heat shock protein (Hsp) family. Hsp40, also known as Mammalian Relative of DnaJ (MRJ) protein, plays a pivotal role as co-chaperone after heat shocks. This protein binds Hsp70 and, through ATP hydrolysis, induces the conformational changes needed by Hsp70 to bind and release heat unfolded proteins. However, no information is available on the role of Hsp40 in mammalian ovary. Here we investigate a) the expression and localization of Hsp40 in pig ovaries; b) its response to heat stress in oocytes and cumulus cells. To identify Hsp40 in pig, we extracted RNA from ovaries, granulosa cells and from pools of 5 oocytes. cDNA was amplified using primers specifically designed for Hsp40, based on sequence data available in other species. The amplified products were sequenced and aligned using ClustalW. The nucleotide sequence showed an homology of 95% with the human, 92% with the bovine and 84% with the mouse orthologs. A polyclonal antibody was raised against the mouse GST/MSJ1(145–242) homologue protein in New Zealand rabbits and serum was affinity-purified using a GST-coupled Affigel-10 column. Whole ovary proteins were separated by SDS PAGE, immunoblotted and stained with the Hsp40 antibody. The protein displayed a MW of 38 KDa, in agreement with results obtained in other species. Immunofluorescence studies showed that Hsp40 is found in oocytes, granulosa and theca cells of follicle at all developmental stages. Pig ovaries, collected at the slaughterhouse, were exposed to 42°C for 1 h, to verify whether Hsp40 has a functional response to heat stress in this specie. Transcript level was compared with the control group, maintained at 38.5°C. mRNA was extracted from cumulus cells and pools of 5 oocytes, isolated from follicles of 3 to 5 mm. Semi-quantitative analysis was performed in the exponential phase of PCR amplification, using 28S as endogenous control. Data were analyzed with Quantity One (Bio-Rad) and Student-t statistical analysis was performed. Exposure of porcine ovaries to 42°C for 1 h resulted in a significant increase (P ≤ 0.05) of Hsp40 mRNA levels (2.4 ± 0.35 fold) in oocytes, while no significant raise was detected in cumulus cells. To our knowledge, this is the first demonstration that Hsp40 is expressed and responds to a thermal stress in pig ovary. Since this co-chaperone acts upstream to other heat shock protein-such as Hsp70- and it is specifically up regulated in the oocytes, our findings suggest that it may play an important protective role against heat stress infertility.

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Donzelli, Joseph, John P. Leonetti, Richard Bergstrom, Robert Wurster, and M. Rita I. Young. "Thermoprotective Mechanisms of Irrigation During Bipolar Cautery." Otolaryngology–Head and Neck Surgery 117, no. 2 (August 1997): P103—P104. http://dx.doi.org/10.1016/s0194-59989780164-7.

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DONZELLI, J., J. LEONETTI, R. BERGSTROM, R. WURSTER, M. RITA, and I. YOUNG. "Thermoprotective mechanisms of irrigation during bipolar cautery." Otolaryngology - Head and Neck Surgery 117, no. 2 (August 1997): P103—P104. http://dx.doi.org/10.1016/s0194-5998(97)80164-7.

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50

Angelescu, Nicolae, Dan Nicolae Ungureanu, and Florin Toma. "Special Refractories Resistant to the Melt Metals and Slags Attack." Scientific Bulletin of Valahia University - Materials and Mechanics 17, no. 16 (May 1, 2019): 28–31. http://dx.doi.org/10.2478/bsmm-2019-0004.

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Abstract The paper is an attempt to present and evaluate of the some monolithic refractory materials, originating from our research activity, with potential to be used as the thermoprotective linings for the nonferrous metals and ferrous alloys manufacturing installations in foundries and steelworks.

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