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PubMed1969

Fixed-interval schedules of electric shock presentation: extinction and recovery of performance under different shock intensities and fixed-interval durations.

In squirrel monkeys responding under a schedule in which responding postponed the delivery of electric shock, the presentation of response-dependent shock under a fixed-interval (FI) schedule increased the rate of responding. When the schedule of shock-postponement was eliminated, so that the only shocks delivered were those produced by responses under the FI schedule, a pattern of positively accelerated responding developed and was maintained over an extended period. When responses did not produce shocks (extinction), responding decreased. When shocks were again presented under the FI schedule, the previous pattern of responding quickly redeveloped. In general, response rates were directly related to the intensity of the shock presented, and inversely related to the duration of the fixed-interval. These results raise fundamental questions about the traditional classification of stimuli as reinforcers or punishers. The basic similarities among FI schedules of food presentation, shock termination, and shock presentation strengthen the conclusion that the schedule under which an event is presented and the characteristics of the behavior at the time the event is presented, are of overriding importance in determining the effect of that event on behavior.

Journal Article↗
PubMed2006

[Shock absorption of mouthguard materials--influence of temperature conditions and shore hardness on shock absorption].

PURPOSE: To consider changes in the physical properties of mouthguard materials with the change of temperature, shock-absorbing examination and Shore hardness measurement of existing MG materials and other elastic materials were carried out. METHODS: Both examinations were done under two temperature conditions: at room temperature (25 degrees C) and simulated intraoral temperature (37 degrees C). In addition, a comparative study of the relation between Shore hardness and shock absorption of the materials was made. A self-made drop impact machine was used for the shock-absorbing examination. The thickness of a sample was assumed to be 3 mm. The loading was applied by dropping 3 kinds of steel ball, phi 10 mm (4.0 g), phi 15 mm (13.7 g), and phi 20 mm (32.6 g) from a height of 60 cm. The shock absorption of all materials was compared by the maximum impact force. Shore hardness was measured based on the JIS standard. RESULTS: The shock absorption of each material showed a different tendency depending on the loading condition. Furthermore, the shock absorption of the same material showed different results depending on the temperature condition. Shore hardness measurements tended to show low values with the condition of 37 degrees C for all materials. CONCLUSION: From the relation between shock absorption and Shore hardness, it was confirmed that there is a correlation between hardness and the maximum impact force in the materials that showed shock absorption by elastic deformation. Some materials showed high shock absorption compared with existing MG materials.

Hardness↗
PubMed2000

Heat shock-induced actin polymerization, SAPK/JNK activation, and heat-shock protein expression are mediated by genistein-sensitive tyrosine kinase(s) in K562 cells.

Upon exposure to elevated growth temperatures, mammalian cells exhibit a variety of cellular responses, such as the expression of heat-shock proteins (HSPs) and the activation of stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK). In this study, we show that heat shock transiently induces morphological change (cell elongation) and polymerization of actin, but not of microtubules, in human erythroleukaemic K562 cells. Pretreatment with actinomycin D or cycloheximide did not prevent the heat shock-induced cell elongation and actin reorganization, indicating that gene transcription and protein synthesis are not required for this phenomenon. The alterations in cell morphology and actin structure in response to heat shock were specifically inhibited by genistein, a tyrosine kinase inhibitor, but not by other kinase inhibitors, including tyrosine kinase inhibitors (herbimycin and tyrphostin) and protein kinase C inhibitors (staurosporine and H7). The activities of genistein-sensitive tyrosine kinase (GTK) and c-Src were enhanced by heat-shock treatment. In addition, a 75 kDa protein was highly phosphorylated in its tyrosine residues(s) by heat shock, and the phosphorylation was prevented by genistein pretreatment. Genistein also inhibited the heat-shock-induced SAPK/JNK activation and HSP expression. In contrast, while colchicine, a microtubule-disrupting agent, was able to induce actin polymerization and SAPK/JNK activation, these events were not inhibited by genistein. These results suggest that the heat-shock-induced actin polymerization, HSP expression, and SAPK/JNK activation may be mediated by the specific signal pathway involving GTK(s), while colchicine-induced actin polymerization and SAPK/JNK activation is regulated in a different manner.

Actins↗
PubMed1995

Estrogen dependent expression of heat shock transcription factor: implications for uterine synthesis of heat shock proteins.

Transcriptional induction of heat shock protein genes is generally mediated by binding of heat shock transcription factor(s) to the heat shock element present in the promoters of heat shock genes. Although the steady-state levels of heat shock factor mRNAs vary among different tissues, at present virtually nothing is known regarding the cellular signals responsible for their synthesis and hence the observed variations. In this report we demonstrate that the heat shock transcription factor (HSTF or HSF) is under positive regulation by estrogen. The effect of estrogen was observed with both types of heat shock factors (HSF-1 and HSF-2) and occurred at both the mRNA and protein level. Immunolocalization studies emphasized the potential biological importance of these observations whereby the increase in uterine HSF-1 and HSF-2 due to estrogen was found to be associated with the endometrium, the primary tissue component which is targeted for estrogen action. This is the first demonstration of a cellular factor which can regulate HSF-1 and HSF-2 gene expression. The implications of these findings to uterine heat shock protein gene expression are discussed.

Animals↗
PubMed1996

The heat shock factor and mitochondrial Hsp70 are necessary for survival of heat shock in Saccharomyces cerevisiae.

A heat shock recovery assay on solid medium (Nwaka et al. (1995) J. Biol. Chem. 270, 10193-10198) as well as the classical cell counting method were used to investigate the function of some heat shock proteins in thermotolerance. We show that expression of intact heat shock factor protein (HSF), which regulates the stress induced expression of heat shock proteins (HSPs), is necessary for recovery from heat shock. A HSF1 mutant (hsf1-m3) which does not induce the expression of some heat shock proteins at heat stress (37-40 degrees C) is defective in recovery after heat shock at 50-52 degrees C compared to a corresponding wild-type strain in both stationary and exponentially growing cells. Using two temperature sensitive mutants of the mitochondrial Hsp70 (ssc1-2 and ssc1-3) encoded by the SSC1 gene, we show that the ssc1-3 mutant, which has a mutation in the ATPase domain, is defective in recovery after heat shock in contrast to the ssc1-2 mutant, which has a mutation in the peptide binding domain. Different binding capacities for unfolded proteins are shown to be the molecular reason for the observed phenotypes. The thermotolerance defect of the hsf1-m3 and ssc1-3 mutants is demonstrated for both glucose and glycerol media.

Adaptation, Physiological↗
PubMed2004

Heat shock and cold shock in Deinococcus radiodurans.

On the basis of acquired thermotolerance and cryotolerance, the optimal heat shock and cold shock temperatures have been determined for Deinococcus radiodurans. A heat shock at 42 degrees C maximized survival at the lethal temperature of 52 degrees C and a cold shock at 20 degrees C maximized survival after repeated freeze-thawing. Enhanced survival from heat shock was found to be strongly dependent on growth stage, with its greatest effect shortly after phase. Increased synthesis of a total of 67 proteins during heat shock and 42 proteins during cold shock were observed by two-dimensional polyacrylamide gel electrophoresis (2D PAGE) and autoradiography. Eight of the most highly induced heat shock proteins shown by 2D PAGE were identified by MALDI-MS as Hsp20, GroEL, DnaK, SodA, Csp, Protease I, and two proteins of unknown function.

Autoradiography↗
PubMed1987

Plasma kallikrein-kinin system in patients with uncomplicated sepsis and septic shock--comparison with cardiogenic shock.

Alterations of the kallikrein-kinin system consistent with activation and increased consumption have been reported in septic patients and it has been suggested that this activation could contribute to the development of septic shock. The aim of this work was to confirm these alterations in septic patients and to investigate the possible existence of similar changes in subjects developing cardiogenic shock secondary to myocardial infarction as a model of non septic shock. Patients with septic shock, especially in fatal cases, showed a highly significant decrease in levels of factor XII, prekallikrein, high molecular weight kininogen (HMW-kininogen), alpha 2-macroglobulin (alpha 2-M) and antithrombin III (AT-III). C1-esterase inhibitor (C1-INH) activity was increased in uncomplicated sepsis but came back to normal or was slightly decreased in septic shock. Components and inhibitors of the kallikrein-kinin system were within normal limits in patients with cardiogenic shock. Our findings support the idea of a contribution of the kallikrein-kinin system to the development of septic shock though this system does not seem to play a significant role in the pathogenesis of cardiogenic shock or seem to be altered as a consequence of it.

Adolescent↗
PubMed2004

Developmentally dictated expression of heat shock factors: exclusive expression of HSF4 in the postnatal lens and its specific interaction with alphaB-crystallin heat shock promoter.

The molecular cascade of stress response in higher eukaryotes commences in the cytoplasm with the trimerization of the heat shock factor 1 (HSF1), followed by its transport to the nucleus, where it binds to the heat shock element leading to the activation of transcription from the down-stream gene(s). This well-established paradigm has been mostly studied in cultured cells. The developmental and tissue-specific control of the heat shock transcription factors (HSFs) and their interactions with heat shock promoters remain unexplored. We report here that in the rat lens, among the three mammalian HSFs, expression of HSF1 and HSF2 is largely fetal, whereas the expression of HSF4 is predominantly postnatal. Similar pattern of expression of HSF1 and HSF4 is seen in fetal and adult human lenses. This stage-specific inverse relationship between the expression of HSF1/2 and HSF4 suggests tissue-specific management of stress depending on the presence or absence of specific HSF(s). In addition to real-time PCR and immunoblotting, gel mobility shift assays, coupled with specific antibodies and HSE probes, derived from three different heat shock promoters, establish that there is no HSF1 or HSF2 binding activity in the postnatal lens nuclear extracts. Using this unique, developmentally modulated in vivo system, we demonstrate 1) specific patterns of HSF4 binding to heat shock elements derived from alphaB-crystallin, Hsp70, and Hsp82 promoters and 2) that it is HSF4 and not HSF1 or HSF2 that interacts with the canonical heat shock element of the alphaB-crystallin gene.

Animals↗
PubMed2000

Activation of Akt is induced by heat shock and involved in suppression of heat-shock-induced apoptosis of NIH3T3 cells.

Heat shock exposure to NIH3T3 cells for 15 min at 45 degrees C activated Akt, which is mediated by PI3-kinase, as evidenced by the significant inhibition of heat-shock-induced phosphorylation by specific inhibitors of PI3-kinase. The phosphorylated Akt was gradually decreased to the basal level within 9 h after heat shock. This resulted in growth arrest, but cell growth could be recovered within 24 h accompanied with a high rate of proliferation. However, heat shock for 60 min failed to activate Akt, resulting in apoptosis. The recovery of cell growth after heat-shock-inducing activation of Akt was completely blocked by wortmannin. Moreover, overexpression of a dominant-negative Akt mutant significantly inhibited the apoptosis-suppressive effect of heat shock, indicating the direct involvement of heat-shock-induced Akt activation in the apoptosis suppression. The results indicate that a signal transduction pathway, namely, PI3-kinase/Akt, may contribute to an apoptosis-suppressive function after heat shock in NIH3T3 cells.

3T3 Cells↗
PubMed2003

[Special features of intensive care of toxic shock syndrome. Review and case report of a TSST-1 associated toxic-shock syndrome with adult respiratory distress syndrome and multiple organ failure from a staphylococcal panaritium].

Toxic-shock-syndrome (TSS) is an acute febrile, exanthematous illness caused by toxins such as toxic-shock-syndrome-toxine-1 (TSST-1) and other endotoxines from staphylococcus aureus with an incidence of 0,5 per 100.000 inhabitants. Patients with menstrual toxic-shock-syndrome (menstrual-TSS) usually have TSS associated with menstruation and use of a vaginal device such as tampons. Other patients with non-menstrual toxic-shock-syndrome (non-menstrual-TSS) have a focus of staphylococcal infection such as a surgical wound infection or soft tissue abscess. TSS usually presents with fever, pharyngitis, diarrhoea, vomiting, myalgia and may progress rapidly (within hours) to signs of hypovolaemic hypotension and shock. In some cases TSS is associated with multisystem failure including shock, renal failure, myocardial failure and adult respiratory distress syndrome. In its acute phase the diagnosis of TSS is often uncertain because of its initial symptoms are non-specific and numerous conditions need to be considered in the differential diagnosis. But obviously less incidence, the signs and symptoms of toxic-shock-syndrome should be recognised early to permit successful therapy. The site of infection should be adequately drained and treated with antimicrobial therapy. Possible complications including ARDS and myocardial failure require a thorough understanding of its underlying pathophysiology to ensure appropriate intensive-care treatment. Only if appropriate therapy is instituted as early as possible, most of patients will be able to survive their toxic-shock-syndrome. In other cases TSS can be a rapidly progressive and perhaps lethal ending disease because of possible multiple organe failure such as ARDS.

Adolescent↗
PubMed2006

Lethal endotoxic shock using alpha-galactosylceramide sensitization as a new experimental model of septic shock.

The effect of alpha-galactosylceramide (alpha-GalCer) on lipopolysaccharide (LPS)-mediated lethality was examined. Administration of LPS killed all mice pretreated with alpha-GalCer, but not untreated control mice. The lethal shock in alpha-GalCer-sensitized mice was accompanied by severe pulmonary lesions with marked infiltration of inflammatory cells and massive cell death. On the other hand, hepatic lesions were focal and mild. A number of cells in pulmonary and hepatic lesions underwent apoptotic cell death. alpha-GalCer sensitization was ineffective for the development of the systemic lethal shock in Valpha14-positive natural killer T cell-deficient mice. Sensitization with alpha-GalCer led to the circulation of a high level of interferon (IFN)-gamma and further augmented the production of tumor necrosis factor (TNF)-alpha in response to LPS. The lethal shock was abolished by the administration of anti-IFN-gamma or TNF-alpha antibody. Further, the lethal shock did not occur in TNF-alpha-deficient mice. Taken together, alpha-GalCer sensitization rendered mice very susceptible to LPS-mediated lethal shock, and IFN-gamma and TNF-alpha were found to play a critical role in the preparation and execution of the systemic lethal shock, respectively. The LPS-mediated lethal shock using alpha-GalCer sensitization might be useful for researchers employing experimental models of sepsis and septic shock.

Adjuvants, Immunologic↗
PubMed2004

Heat-shock treatment-mediated increase in transduction by recombinant adeno-associated virus 2 vectors is independent of the cellular heat-shock protein 90.

Recombinant adeno-associated virus 2 (AAV) vectors transduction efficiency varies greatly in different cell types. We have described that a cellular protein, FKBP52, in its phosphorylated form interacts with the D-sequence in the viral inverted terminal repeat, inhibits viral second strand DNA synthesis, and limits transgene expression. Here we investigated the role of cellular heat-shock protein 90 (HSP90) in AAV transduction because FKBP52 forms a complex with HSP90, and because heat-shock treatment augments AAV transduction efficiency. Heat-shock treatment of HeLa cells resulted in tyrosine dephosphorylation of FKBP52, led to stabilization of the FKBP52-HSP90 complex, and resulted in approximately 6-fold increase in AAV transduction. However, when HeLa cells were pre-treated with tyrphostin 23, a specific inhibitor of cellular epidermal growth factor receptor tyrosine kinase, which phosphorylates FKBP52 at tyrosine residues, heat-shock treatment resulted in a further 18-fold increase in AAV transduction. HSP90 was shown to be a part of the FKBP52-AAV D-sequence complex, but HSP90 by itself did not bind to the D-sequence. Geldanamycin treatment, which disrupts the HSP90-FKBP52 complex, resulted in >22-fold increase in AAV transduction in heat-shock-treated cells compared with heat shock alone. Deliberate overexpression of the human HSP90 gene resulted in a significant decrease in AAV-mediated transduction in tyrphostin 23-treated cells, whereas down-modulation of HSP90 levels led to a decrease in HSP90-FKBP52-AAV D-sequence complex formation, resulting in a significant increase in AAV transduction following pre-treatment with tyrphostin 23. These studies suggest that the observed increase in AAV transduction efficiency following heat-shock treatment is unlikely to be mediated by HSP90 alone and that increased levels of HSP90, in the absence of heat shock, facilitate binding of FKBP52 to the AAV D-sequence, thereby leading to inhibition of AAV-mediated transgene expression. These studies have implications in the optimal use of recombinant AAV vectors in human gene therapy.

Benzoquinones↗
PubMed1986

Induction of B2 RNA polymerase III transcription by heat shock: enrichment for heat shock induced sequences in rodent cells by hybridization subtraction.

When hybridization subtraction was used to enrich for sequences induced by heat shock in Chinese hamster cells, B2 sequences were found to be one of the major sequences enriched. With cloned B2 probes, we found that the level of the short, 0.1 to 0.6 kb, polyadenylated RNA polymerase III transcripts of this repetitive genetic element increased approximately 10 to 20 fold after heat shock. Transcription of B2 RNA by RNA polymerase III was rapidly induced after heat shock based on time course studies and nuclear runoff experiments. The induction of B2 RNA was not a nonspecific response to lethality or cellular injury because maximum B2 RNA induction was observed with even nontoxic heating while no induction occurred with other agents such as UV or X-radiation. Since B2 RNA increased after heat shock in several different Chinese hamster and mouse cell lines, induction of B2 RNA by heat shock is probably common in rodent cells. B2 RNA may also be the most abundant transcript induced by heat shock because the level of B2 RNA was substantially higher than several other abundant transcripts induced by heat shock including a rodent HSP70. Our finding of the induction of high levels of RNA polymerase III B2 transcripts in different rodent cells raise the possibility of a role in the heat shock response.

Animals↗
PubMed1981

Suppression of centrineurogenic shock lung by Dilantin (DPH) administered early in established hemorrhagic shock.

Centrineurogenic shock lung following acute hemorrhage was prevented by Dilantin (DPH) given preshock. Nineteen anemia (Hct = 30 +/- 5%) dogs were divided into five groups: one control (no anesthesia, no shock); one of three with 4 hours of anesthesia alone; and of 15 dogs with hemorrhagic shock, eight were without DPH, two with preshock DPH, and five received DPH 15 min after shock was established. Shock animals were rapidly bled to 40 mm Hg which was maintained for 2 hours, and all shed blood was reinfused. One hour later, all animals were sacrificed, the lungs fixed with formalin instilled at 15 cm H2O intratracheal pressure, the trachea cross-clamped, the lungs excised, photographed, and sent for gross and histopathologic study. Shock animals without DPH had grossly hemorrhagic lungs with diffuse interstitial and alveolar congestion, hemorrhage, and edema. Neither of the DPH-treated groups developed gross changes and showed minimal to no histopathology. Dilantin given early in established hemorrhagic shock prevents shock lung.

Animals↗
PubMed1999

An imperfect heat shock element and different upstream sequences are required for the seed-specific expression of a small heat shock protein gene.

Chimeric constructs containing the promoter and upstream sequences of Ha hsp17.6 G1, a small heat shock protein gene, reproduced in transgenic tobacco (Nicotiana tabacum) its unique seed-specific expression patterns previously reported in sunflower. These constructs did not respond to heat shock, but were expressed without exogenous stress during late zygotic embryogenesis coincident with seed desiccation. Site-directed mutagenesis of its distal and imperfect heat shock element strongly impaired in vitro heat shock transcription factor binding and transgene expression in seeds. Deletion analyses of upstream sequences indicated the contribution of additional cis-acting elements with either positive or negative effects on transgene expression. These results show differences in the transcriptional activation through the heat shock element of small heat shock protein gene promoters in seeds compared with the heat shock response. In addition, they suggest that heat shock transcription factors and other distinct trans-acting factors cooperate in the regulation of Ha hsp17.6 G1 during seed desiccation.

Gene Expression Regulation, Plant↗
PubMed1991

Heat shock in cultured neurons and astrocytes: correlation of ultrastructure and heat shock protein synthesis.

Cultured cerebral cortical neurons and astrocytes were compared after a brief shock. Morphological findings were correlated with the synthesis of the 68 kD heat shock protein (HSP68). Heat shocked neurons demonstrated many severe morphological changes after exposure to temperatures of 43 degrees C for 15 min and 45 degrees C for 10 min. Nuclear membrane 'blebbing' with lysis of the membrane, chromatin clumping, and disappearance of the nucleolus were prominent after both conditions. Lysis of the cell membrane was noted in severely injured neurons; this was more prominent at the higher temperature. In addition, alterations to polyribosomes, Golgi apparatus, rough endoplasmic reticulum and mitochondria were noted in the cytoplasm of neurons after heat shock. In contrast, no significant changes were noted in either the nucleus or cytoplasm of heat shocked astrocytes. The severity of morphological changes in neurons directly correlated with the low level of induction of HSP68 in neurons. Neurons synthesized much less 68 kD heat shock protein than similarly heat shocked astrocytes. We conclude that cultured cerebral cortical neurons are more susceptible to injury after heat shock than heat resistant astrocytes and that one possible mechanism of injury is failure to synthesize adequate amounts of HSP68 after injury.

Animals↗
PubMed1990

DNA binding of heat shock factor to the heat shock element is insufficient for transcriptional activation in murine erythroleukemia cells.

The heat shock response is among the most highly conserved examples of regulated gene expression, being present in all cellular organisms. Transcriptional activation of heat shock genes by increased temperature or other cellular stresses is mediated by the binding of a heat shock factor (HSF) to a conserved nucleotide sequence (the heat shock element) present in the promoter of heat-inducible genes. Despite the high degree of conservation of this response, embryonic stages of development are characterized by the absence of a heat shock response. Murine erythroleukemia (MEL) cells also lack this response, and we report here a detailed characterization of this defect for one of the most highly conserved of these genes, hsp70. Surprisingly, heat-induced transcriptional activation of this gene does not occur, despite the induction of a protein with the binding specificity of murine HSF. However, the MEL HSF differs slightly in apparent size from the HSF in 3T3 cells, which exhibit a normal heat shock response. These data suggest that activation of mammalian HSF by heat requires at least two separate steps: an alteration of binding activity followed by further modification that activates transcription. MEL cells do not respond to heat shock because they lack the ability to perform this secondary modification. These cells provide a useful system for characterizing heat shock activation in mammals.

Animals↗
PubMed1986

Large changes in intracellular pH and calcium observed during heat shock are not responsible for the induction of heat shock proteins in Drosophila melanogaster.

Heat shock caused significant changes in intracellular pH (pHi) and intracellular free calcium concentration [( Ca2+]i) which occurred rapidly after temperature elevation. pHi fell from a resting level value at 25 degrees C of 7.38 +/- 0.02 (mean +/- standard error of the mean, n = 15) to 6.91 +/- 0.11 (n = 7) at 35 degrees C. The resting level value of [Ca2+]i in single Drosophila melanogaster larval salivary gland cells was 198 +/- 31 nM (n = 4). It increased approximately 10-fold, to 1,870 +/- 770 nM (n = 4), during a heat shock. When salivary glands were incubated in calcium-free, ethylene glycol-bis(beta-aminoethyl ether)-N,N',N'-tetraacetic acid (EGTA)-buffered medium, the resting level value of [Ca2+]i was reduced to 80 +/- 7 nM (n = 3), and heat shock resulted in a fourfold increase in [Ca2+]i to 353 +/- 90 nM (n = 3). The intracellular free-ion concentrations of Na+, K+, Cl-, and Mg2+ were 9.6 +/- 0.8, 101.9 +/- 1.7, 36 +/- 1.5, and 2.4 +/- 0.2 mM, respectively, and remained essentially unchanged during a heat shock. Procedures were devised to mimic or block the effects of heat shock on pHi and [Ca2+]i and to assess their role in the induction of heat shock proteins. We report here that the changes in [Ca2+]i and pHi which occur during heat shock are not sufficient, nor are they required, for a complete induction of the heat shock response.

Animals↗