Home About us Contact
|
Home About us Contact | ||
|
|
||
Shock Treatment (shock + treatment)
Kinds of Shock Treatment Selected AbstractsACID TOLERANCE OF ESCHERICHIA COLI FOLLOWING COLD SHOCK TREATMENTJOURNAL OF FOOD SAFETY, Issue 2 2003GREG BLANK ABSTRACT The effect of an initial cold shock treatment (2 h at 10C), following an abrupt downshift in temperature from 37 to 10C, on the subsequent growth and survival of Escherichia coli strains O157:H7 and MY20 (Biotype 1) in acidified Trypticase soy broth (TSB) and fruit juices (orange, apple) was investigated. Overall, no difference in growth at 37C was observed between each cold shocked and noncold shocked E. coli strain when cultured in TSB adjusted with either acetic acid (pH 6.0)or malic, citric and tartaric acid (each adjusted to: pH 4.5, 5.0, 5.5, 6.0). However, significant (P ± 0.05) differences in survival were observed between cold shocked and noncold shocked populations in TSB acidified with acetic acid (pH 5.0) or citric, malic and tartaric acid (pH 4.0). For strain MY20, survivor levels for cold shocked cells in TSB acidified with acetic acid citric, malic and tartaric acid at 8C were significantly (P ± 0.05) higher than in noncold shocked populations. Also, at 37C survival levels for cold shocked cells were significantly (P ± 0.05) higher than noncold shocked cells in TSB acidified with either malic or tartaric acid (pH 4.0). For the O157:H7 strain, survivor levels were higher (P ± 0.05) for cold shocked cells when maintained in TSB at 37C regardless of acid type. At 8C, cold shock treatment only increased (P ± 0.05) the survival of the O157:H7 strain in TSB adjusted with acetic acid (pH 6.0). Acid cross protection induced by cold shocking, as evidenced by enhanced survival, was not apparent for either E. coil strain in apple (pH 3.5) or orange juice (pH 3.8) maintained at 8C. [source] The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticityDEVELOPMENTAL NEUROBIOLOGY, Issue 5 2010Eero Castrén Abstract Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 2010 [source] ACID TOLERANCE OF ESCHERICHIA COLI FOLLOWING COLD SHOCK TREATMENTJOURNAL OF FOOD SAFETY, Issue 2 2003GREG BLANK ABSTRACT The effect of an initial cold shock treatment (2 h at 10C), following an abrupt downshift in temperature from 37 to 10C, on the subsequent growth and survival of Escherichia coli strains O157:H7 and MY20 (Biotype 1) in acidified Trypticase soy broth (TSB) and fruit juices (orange, apple) was investigated. Overall, no difference in growth at 37C was observed between each cold shocked and noncold shocked E. coli strain when cultured in TSB adjusted with either acetic acid (pH 6.0)or malic, citric and tartaric acid (each adjusted to: pH 4.5, 5.0, 5.5, 6.0). However, significant (P ± 0.05) differences in survival were observed between cold shocked and noncold shocked populations in TSB acidified with acetic acid (pH 5.0) or citric, malic and tartaric acid (pH 4.0). For strain MY20, survivor levels for cold shocked cells in TSB acidified with acetic acid citric, malic and tartaric acid at 8C were significantly (P ± 0.05) higher than in noncold shocked populations. Also, at 37C survival levels for cold shocked cells were significantly (P ± 0.05) higher than noncold shocked cells in TSB acidified with either malic or tartaric acid (pH 4.0). For the O157:H7 strain, survivor levels were higher (P ± 0.05) for cold shocked cells when maintained in TSB at 37C regardless of acid type. At 8C, cold shock treatment only increased (P ± 0.05) the survival of the O157:H7 strain in TSB adjusted with acetic acid (pH 6.0). Acid cross protection induced by cold shocking, as evidenced by enhanced survival, was not apparent for either E. coil strain in apple (pH 3.5) or orange juice (pH 3.8) maintained at 8C. [source] Opposing Actions of Phosphatidylinositol 3-Kinase and Glycogen Synthase Kinase-3, in the Regulation of HSF-1 ActivityJOURNAL OF NEUROCHEMISTRY, Issue 6 2000Gautam N. Bijur Abstract: Elevated temperatures activate the survival promoters Aktand heat shock factor-1 (HSF-1), a transcription factor that induces theexpression of heat shock proteins (HSPs), such as HSP-70. Because neuronalmechanisms controlling these responses are not known, these were investigatedin human neuroblastoma SH-SY5Y cells. Heat shock (45°C) rapidly activatedAkt, extracellular signal-regulated kinases 1 and 2 (ERK1/2), and p38, butonly Akt was activated in a phosphatidylinositol 3-kinase (PI-3K)-dependentmanner, as the PI-3K inhibitors LY294002 and wortmannin blocked Aktactivation, but not ERK1/2 or p38 activation. Akt activation was not blockedby inhibition of p38 or ERK1/2, indicating the independence of these signalingsystems. Heat shock treatment also caused a rapid increase in HSF-1 DNAbinding activity that was partially dependent on PI-3K activity, as both thePI-3K inhibitors attenuated this response. Because Akt inhibits glycogensynthase kinase-3, (GSK-3,), an enzyme that facilitates cell death,we tested if GSK-3, is a negative regulator of HSF-1 activation.Overexpression of GSK-3, impaired heat shock-induced activation of HSF-1,and also reduced HSP-70 production, which was partially restored by theGSK-3, inhibitor lithium. Thus, heat shock-induced activation of PI-3Kand the inhibitory effect of GSK-3, on HSF-1 activation and HSP-70expression imply that Akt-induced inhibition of GSK-3, contributes to theactivation of HSF-1. [source] Deletion of tau attenuates heat shock-induced injury in cultured cortical neuronsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2010Yanying Miao Abstract The microtubule-associated protein tau has been implicated in ,-amyloid- and glutamate-induced neurotoxicity. However, the potential role of tau in response to other insults to neurons remains unclear. In this study, we examined whether deletion of tau would change cell injury induced by heat shock in primary cultures of cortical neurons. After 30 min of a 45°C heat shock, lactate dehydrogenase (LDH) release increased, reaching a peak at 6 hr in wild-type (WT) neurons. A significantly lower LDH release, with a peak delayed by 24 hr, was detected in tau knockout (TKO) neurons. After heat shock treatment, MAP-2 and tubulin staining of the processes of WT neurons revealed more dramatic abnormalities than in TKO neurons. Both WT and TKO neurons exhibited a similar elevation of HSP70 level but different time courses of Akt phosphorylation. In contrast to an early, brief response in WT neurons, TKO neurons displayed a late, but long-lasting increase in phosphorylation of Akt and its downstream target, glycogen synthase kinase 3,. Additionally, inhibition of Akt activity aggravated the cell morbidity caused by heat shock exposure in both WT and TKO neurons, indicating a protective role of Akt against cell injury. In conclusion, our results demonstrate that deletion of tau attenuated heat shock-induced neuronal injury. Enhanced Akt response in the absence of endogenous tau is suggested to represent a compensatory mechanism for regulating cell reactions to stress stimuli. © 2009 Wiley-Liss, Inc. [source] Effects of 2-hydroxypropyl-,-cyclodextrin and cholesterol on porcine sperm viability and capacitation status following cold shock or incubationMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 5 2006Hannah L. Galantino-Homer Abstract Porcine sperm are extremely sensitive to the damaging effects of cold shock. It has been shown that cholesterol-binding molecules, such as 2-hydroxypropyl-,-cyclodextrin (HBCD), improve post-cooling porcine sperm viability when added to an egg yolk-based extender, but also enhance sperm capacitation in other species. The objective of this study was to determine the effects of HBCD and cholesterol 3-sulfate (ChS) on porcine sperm viability and capacitation following cold shock or incubation under conditions that support capacitation using a defined medium. We report here that porcine sperm incubated in medium containing both HBCD and ChS have significantly improved viability following cold shock (10 min at 10°C) when compared to sperm incubated without HBCD or ChS, or with either component alone. Treatment with HBCD plus ChS also completely inhibited the increase in protein tyrosine phosphorylation induced by the cold shock treatment or by incubation for 3 hr under conditions that support capacitation. Two assays of sperm capacitation, the rate of calcium ionophore-induced acrosome reactions and chlortetracycline (CTC) staining, were not significantly altered by HBCD and ChS following cold shock. However, 3-hr incubation with HBCD plus ChS or with 1 mM ChS alone decreased the percentage of sperm undergoing the induced acrosome reaction without significantly affecting viability when compared to the control. These results indicate that the manipulation of sperm plasma membrane cholesterol content affects porcine sperm viability and capacitation status and could therefore be useful to protect sperm from cold shock during cryopreservation by improving viability without promoting premature capacitation. Mol. Reprod. Dev. © 2006 Wiley-Liss, Inc. [source] Basic characterization of 90 kDa heat shock protein genes HSP90AA1, HSP90AB1, HSP90B1 and TRAP1 expressed in Japanese quail (Coturnix japonica)ANIMAL SCIENCE JOURNAL, Issue 4 2010Kohji NAGAHORI ABSTRACT In the current study, we describe four novel members of the 90 kDa heat shock protein (HSP90) family expressed in Japanese quail, Coturnix japonica. The coding regions of the genes, CjHSP90AA1, CjHSP90AB1, CjHSP90B1 and CjTRAP1, exhibited more than 94% similarity to their related genes in chicken. The putative proteins encoded by these quail genes contained motifs considered essential for HSP90 gene function. In addition, the predicted proteins were more similar to HSP90AA1, HSP90AB1, HSP90B1 and TRAP1 proteins expressed in vertebrates than they were to other members of the HSP90 family. Exon numbers of CjHSP90AA1 (11), CjHSP90AB1 (12) or CjTRAP1 (18) are the same as the chicken and mammalian orthologs. Furthermore, gene order in the regions surrounding CjHSP90AB1 and CjTRAP1 has been preserved, providing evidence that the genomic regions were orthologous to HSP90-containing regions in the chicken genome. The promoter regions of the genes also contained conserved motifs identified in related genes of chicken. However, the nucleotide sequences of the 5,-flanking region of these genes were highly polymorphic. We also found that CjHSP90AA1 exhibited a robust response to heat shock treatment. Taken together, the data suggest that CjHSP90AA1, CjHSP90AB1, CjHSP90B1 and CjTRAP1 encode orthologs of HSP90AA1, HSP90AB1, HSP90B1 and TRAP1, respectively. [source] Cytological studies on induced meiogynogenesis in Japanese flounder Paralichthys olivaceus (Temminck et Schlegel)AQUACULTURE RESEARCH, Issue 6 2009Jilun Hou Abstract The cytological process of induced gynogenetic development and subsequent chromosome duplication by a cold shock treatment was observed in Japanese flounder Paralichthys olivaceus (Temminck et Schlegel). Mature eggs were at the metaphase of the second meiosis when inseminated with ultraviolet (UV)-irradiated sperm of red sea bream Pagrus major. After the beginning of cold shock treatment, the previously visible spindle became invisible, probably due to the side effect caused by cold shock treatment. The chromosomes at the centre of the metaphase plate were condensed. This condition continued during the duration of the cold shock treatment and several minutes after it. The release of the second polar body was blocked and it developed into a female-like pronucleus. Then, it fused with the female pronucleus to generate a diploid zygotic nucleus, and the egg exhibited the first mitosis. Consequently, the haploid female chromosome set of the egg was doubled by the inhibition of the second polar body release. There was a significant delay in developmental time in the gynogenetic eggs when compared with that in the normal eggs. From the time of insemination to early cleavage, the UV-irradiated heterospecific sperm nucleus remained condensed. [source] Synthetic small interfering RNA targeting heat shock protein 105 induces apoptosis of various cancer cells both in vitro and in vivoCANCER SCIENCE, Issue 7 2006Seiji Hosaka We previously reported that heat shock protein 105 (HSP105), identified by serological analysis of a recombinant cDNA expression library (SEREX) using serum from a pancreatic cancer patient, was overexpressed in various human tumors and in the testis of adult men by immunohistochemical analysis. In the present study, to elucidate the biological function of the HSP105 protein in cancer cells, we first established NIH3T3 cells overexpressing murine HSP105 (NIH3T3-HSP105). The NIH3T3-HSP105 cells acquired resistance to apoptosis induced by heat shock or doxorubicin. The small interfering RNA (siRNA)-mediated suppression of HSP105 protein expression induced apoptosis in human cancer cells but not in fibroblasts. By a combination of siRNA introduction and doxorubicin or heat shock treatment, apoptosis was induced synergistically in a human colon cancer cell line, HCT116. In vivo, siRNA inoculation into the human gastric cancer cell line KATO-3 established in the flank of an NOD SCID mouse suppressed the tumor growth. This siRNA-induced apoptosis was mediated through caspases, but not the p53 tumor suppressor protein, even though the HSP105 protein was bound to wild-type p53 protein in HCT116 cells. These findings suggest that the constitutive overexpression of HSP105 in cancer cells is involved in malignant transformation by protecting tumor cells from apoptosis. HSP105 may thus be a novel target molecule for cancer therapy and a treatment regimen using synthetic siRNA to suppress the expression of HSP105 protein may provide a new strategy for cancer therapy. (Cancer Sci 2006; 97: 623,632) [source] 915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci in human lymphocytes from hypersensitive and healthy personsBIOELECTROMAGNETICS, Issue 3 2005Igor Y. Belyaev Abstract We used exposure to microwaves from a global system for mobile communication (GSM) mobile phone (915 MHz, specific absorption rate (SAR) 37 mW/kg) and power frequency magnetic field (50 Hz, 15 ,T peak value) to investigate the response of lymphocytes from healthy subjects and from persons reporting hypersensitivity to electromagnetic field (EMF). The hypersensitive and healthy donors were matched by gender and age and the data were analyzed blind to treatment condition. The changes in chromatin conformation were measured with the method of anomalous viscosity time dependencies (AVTD). 53BP1 protein, which has been shown to colocalize in foci with DNA double strand breaks (DSBs), was analyzed by immunostaining in situ. Exposure at room temperature to either 915 MHz or 50 Hz resulted in significant condensation of chromatin, shown as AVTD changes, which was similar to the effect of heat shock at 41 °C. No significant differences in responses between normal and hypersensitive subjects were detected. Neither 915 MHz nor 50 Hz exposure induced 53BP1 foci. On the contrary, a distinct decrease in background level of 53BP1 signaling was observed upon these exposures as well as after heat shock treatments. This decrease correlated with the AVTD data and may indicate decrease in accessibility of 53BP1 to antibodies because of stress-induced chromatin condensation. Apoptosis was determined by morphological changes and by apoptotic fragmentation of DNA as analyzed by pulsed-field gel electrophoresis (PFGE). No apoptosis was induced by exposure to 50 Hz and 915 MHz microwaves. In conclusion, 50 Hz magnetic field and 915 MHz microwaves under specified conditions of exposure induced comparable responses in lymphocytes from healthy and hypersensitive donors that were similar but not identical to stress response induced by heat shock. Bioelectromagnetics 26:173,184, 2005. © 2005 Wiley-Liss, Inc. [source] | ||||||||||