Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SHOCK”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources
PubMed1986

Non-menstrual toxic shock syndrome. A case report and a review of non-menstrual toxic shock syndrome in Western Europe.

Having been confronted with a post-operative toxic shock syndrome, we made a study of European literature and were struck by the more favorable course the disease promptly took when penicillinase-resistant antibiotics were used. We suggest that a new case, based on bacteriological analysis and phagotyping of the offending organism and wound appearance, was prevented by us when immediate antibiotic treatment was given.

Adult↗
PubMedDate not supplied

Heat shock cellular stress on aged gut-associated lymphocytes; mRNA expression of inducible heat shock protein gene and protooncogenes.

To investigate the effects of senescence and cellular stress on gut mucosal lymphocytes, we used heat shock (HS) to determine the mRNA expression of an inducible HSP70-family gene (HSP68) and two nuclear protooncogenes (c-fos and c-myc) from gut-associated (GA) lymphocytes of aged (> or = 24 month) and young (3-4 month) mice. First, with temperatures of 37-44 degrees C, the maximal HS effect on expression of inducible HSP68 mRNA was at 41 degrees C, and that of c-fos and c-myc at 42 degrees C; with HS durations of 0-6 h at 42 degrees C, the maximal effect was at 1 or 2 h in the young GA lymphocytes. Second, without HS (37 degrees C), inducible HSP68 mRNA was not expressed in the GA lymphocytes of both age groups. The expression of c-fos and c-myc mRNA was greater in the aged GA lymphocytes than in the young, and c-myc mRNA was more highly expressed than c-fos mRNA in both age groups. Third, with HS (42 degrees C) for 30 min to 6 h, followed by recovery (37 degrees C) for up to 6 h, the peak expression of inducible HSP68 mRNA in the aged GA lymphocytes was reduced, but occurred at the same time as seen in the young (2 h) and declined faster during the recovery period. The peak expression of c-fos mRNA in the aged GA lymphocytes was earlier than that of the HSP68 mRNA in both age groups (1 h); the intensity of expression was decreased at all time points in the aged and declined more rapidly during the recovery period, whereas the peak expression of c-myc mRNA in the aged GA lymphocytes after HS was retarded in time (2 h) but also reduced in amount, when compared to that of the young, and during recovery the expression declined more rapidly in the aged than in the young. However, the recovery kinetics of the above three mRNAs remained unaltered in the lymphocytes from two different ages. To summarize our conclusions: First, prior to HS cellular stress, aged GA lymphocytes did not show mRNA expression of HSP68 but augmented mRNA expression of the nucleoprotooncogenes c-fos and c-myc. These findings suggest that senescent lymphocytes are more active metabolically in vivo than are young ones without significant activation of an inducible HSP70 family gene.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1993

Demonstration of selective protein complexes of p53 with 73 kDa heat shock cognate protein, but not with 72 kDa heat shock protein in human tumor cells.

It has been demonstrated that p53, especially, mutant p53 (mp53), makes protein complexes with major heat shock proteins hsp72/hsc73. However, there is no direct evidence showing whether hsp72 or hsc73 could bind preferentially to p53. In the present study, using TYKnu human ovarial carcinoma cells and monoclonal antibodies reacting specifically to hsp72/hsc73, we were able to find the selective protein complex formation with p53, presumably mp53, and hsc73, but not in the case of p53 and hsp72. The p53-hsc73 protein complexes dissociate with the addition of ATP, indicating that the dissociation is dependent upon the ATP-hydrolysis. These data suggest that hsc73 rather than hsp72 plays an important role in the yet undefined mechanism of disregulated cell growth control by mp53.

Adenosine Triphosphate↗
PubMed1994

Dual infections with Staphylococcus aureus and Streptococcus pyogenes causing toxic shock syndrome. Possible synergistic effects of toxic shock syndrome toxin 1 and streptococcal pyrogenic exotoxin C.

We describe a 35-year-old woman with clinical, microbiologic, and serologic findings suggesting that the patient developed toxic shock syndrome as a result of dual infections caused by toxin-producing strains of Staphylococcus aureus and Streptococcus pyogenes. Certain aspects of the pathogenesis of this toxin-related syndrome are reviewed.

Adult↗
PubMed1997

Isolation of six low molecular weight heat shock proteins and partial characterization of heat shock protein 29 from mung bean hypocotyl.

Heat shock protein (HSP29) together with five other low-M(r) HSPs have been isolated from mung bean hypocotyls by preparative continuous elution SDS-PAGE. Autoradiography and immunochemical analysis of 2D electrophoretograms of the radiolabelled HSP29 revealed that it consists of seven isotypes, two of which are constitutive while the other five are heat-inducible. The pI values of the seven isotypes range from 4.6 to 6.6. A monoclonal antibody raised against the HSP29 isolate reacted with six of the seven isotypes. When HSP29 was subjected to partial proteolysis by V8 Staphylococcus aureus protease (EC 3.4.21.19), two fragments of 12 and 17 kDa were identified, neither of which was recognized by the antibody.

Antibodies, Monoclonal↗
PubMed2001

Serum heat shock protein and anti-heat shock protein antibody levels in aging.

We have previously reported the presence of Hsp60 and Hsp70 in the peripheral circulation of normal individuals. Given that the capacity to generate stress proteins declines with age, this study measured Hsp60 and Hsp70 levels in the sera of 60 individuals aged between 20 and 96 years. Levels of anti-human Hsp60, anti-human Hsp70 and anti-mycobacterial Hsp65 antibody were also measured. Senieur-approximated elderly subjects were well and randomly selected from the Belfast Elderly Longitudinal Free-living Aging STudy (BELFAST). Samples from younger individuals were obtained from the Northern Ireland Blood Transfusion Service. Hsp60, anti-Hsp60, anti-Hsp70 and anti-mycobacterial Hsp65 antibodies were detected in all samples, whereas Hsp70 was detectable in only 46 of the samples analysed (77%). Regression analysis revealed a progressive decline in Hsp60 (759ng/ml < 40 years; 294ng/ml > or = 90 years) and Hsp70 (400ng/ml < 40 years; 20ng/ml > or = 90 years) levels with age whereas no relationship was apparent for anti-Hsp60 and Hsp65 antibody levels. Hsp70 antibody levels tended to increase with age (115U/ml < 40 years; 191U/ml > or = 90 years). This study in Senieur-approximated subjects demonstrates an apparent decrease in Hsp60 and Hsp70 with increasing age that does not appear to be related to anti-heat shock protein antibody status. These findings support in vitro work that demonstrates an age-related reduced ability to respond to stress. Further studies are required to understand the basis for declining serum Hsp60 and Hsp70 levels in aging and to elucidate their origin and role in the maintenance of homeostasis and resistance to environmental challenges.

Adult↗
PubMed1996

Oxygen transport and oxygen metabolism in shock and critical illness. Invasive and noninvasive monitoring of circulatory dysfunction and shock.

The common underlying physiologic problem in shock is low flow from hypovolemia or maldistributed microcirculatory flow from uneven vasoconstriction, leading to inadequate tissue perfusion (hypoxia), often in the face of increased metabolic demands. Noninvasive monitoring which was found to provide similar information to that of invasive monitoring, was used in the earliest period of time shortly after admission to the emergency department to provide objective physiologic criteria as therapeutic goals for each of the three major circulatory components: cardiac, pulmonary, and tissue perfusion functions. A clinical algorithm or branch-chain decision tree for high-risk surgical patients was developed from decision rules based on survivor and nonsurvivor patterns, outcome predictors, prospective controlled clinical trials of the oxygen delivery/oxygen consumption (DO2/VO2) concept, and the DO2/VO2 responses of a wide variety of therapeutic agents.

Decision Trees↗
PubMed1997

Heat shock and proinflammatory stressors induce differential localization of heat shock proteins in human monocytes.

Heat shock (HS) proteins (HSP) are a family of molecular chaperones induced by environmental stresses such as oxidative injury, and contribute to protection from and adaptation to cellular stress. We investigated in human monocytes the expression and subcellular distribution of hsp70 and hsc70 after HS and inflammation-related stresses leading to generation of reactive oxygen species by these cells, such as the phorbol ester PMA and erythrophagocytosis (E phi). By combining immunofluorescent staining and Western blot on subcellular fractions, we found that all three stress factors resulted in an increased hsp70 expression, however the subcellular distribution pattern was different depending on the type of stress. While HS induced a rapid translocation of hsp70 into the nucleus, no nuclear translocation of hsp70 was observed after PMA or E phi. Neither of the examined stresses induced membrane expression of hsp70. The observed differences in subcellular distribution pattern might relate to distinct regulation and specific functions of hsp70 in inflammation.

Biological Transport↗
PubMed2002

Lack of muco-cutaneous signs of toxic shock syndrome when T cells are absent: S. aureus shock in immunodeficient adults with multiple myeloma.

Staphylococcal toxic shock syndrome (TSS) is an acute life threatening disease. The diagnosis can be made clinically based on diagnostic criteria. The clinical manifestations are caused in large part by there lease of high levels of T-cell-derived cytokines as a result of potent toxins, also called superantigens (SAg), produced by Staphylococcus aureus, but it is not clear which clinical symptoms/signs are strictly T-cell dependent. Here, we report on three adults with multiple myeloma (MM) presenting with S.aureus sepsis/shock, and two patients with typical TSS. The MM patients had compromised humoral immunity because of depression of normal immunoglobulin (Ig) levels at the expense of the M protein. In addition, their T cells were absent due to high dose chemotherapy initiated for bone marrow trans-plantation. The MM cases lacked mucosal hyperemia, erythroderma and desquamation, but were otherwise indistinguishable from the TSS cases. All patients grew S. aureus and in each case, SAg genes were detected by PCR. In several cases, the plasma contained biological SAg activity resulting in VP specific proliferation of indicator T cells in vitro. The same specific activity was observed with the supernatant fluids of S. aureus broth cultures from the respective bacterial isolates. This confirms the presence of bio-active toxins in the plasma but did not lead to full blown TSS when T cells were lacking.Thus, S. aureus sepsis/shock can be clinically distinguished from typical TSS, and we suggest that mucocutaneous manifestations of TSS are the most telling signs of massive T-cell-dependent cytokine release.

Adult↗
PubMed2000

Natural autoantibodies against heat-shock proteins hsp70 and gp96: implications for immunotherapy using heat-shock proteins.

Immunization of mice with cognate cancer-derived heat-shock protein (hsp) preparations leads to protection from cancer growth. As hsp used for vaccination or therapy are derived from autologous cancers, questions of pathological autoimmunity are of immense significance for the ongoing translation of this approach to therapy of human cancer. Employing the sera of normal adult mice as the first antibody, highly sensitive immunoblotting revealed the presence of anti-hsp natural autoantibodies in healthy animals. Natural autoantibodies of the immunoglobulin D (IgD) isotype bind to gp96, whereas hsp70 was recognized by IgD and IgM autoantibodies. Neither hsp was recognized by the IgA, IgE or IgG immunoglobulins contained in the serum. The antigen-antibody recognition was titratable and dependent on the integrity of the IgD molecule. Sera from only a subset of the animals tested were found to be positive for autoantibodies against gp96 and hsp70, and individual and strain-specific variations were detected. Injection of gp96 into healthy mice did not show sustained or consistent anti-gp96 IgD antibody response, class switching, toxicity or pathological autoimmunity. IgD autoantibodies against gp96 and hsp70 were also not detected in the autoimmune lpr mice. These observations show the existence of a measured and tightly regulated natural immune response to hsp.

Animals↗
PubMed1999

Heat shock protein 70 overexpression protects LLC-PK1 tubular cells from heat shock but not hypoxia.

BACKGROUND: Overexpression of the 70 kDa heat shock protein (Hsp70) protects myocytes and neural cells from hypoxic injury. In contrast, Hsp70 induction in the kidney after ischemic or thermal preconditioning does not correlate well with protection from hypoxic injury. Herein, we directly tested if Hsp70 overexpression protects LLC-PK1 porcine tubular epithelial cells from hypoxic or thermal injury. METHODS: LLC-PK1 cells were either cotransfected with an Hsp70 and a luciferase expression vector or singly transfected with the luciferase expression vector. Loss of intracellular luciferase activity was used to assess injury after exposure to hypoxia or hyperthermia and after recovery under normal growth conditions. RESULTS: Overexpression of Hsp70 decreased loss of and improved restoration of intracellular luciferase activity in LLC-PK1 cells exposed to hyperthermia. In contrast, Hsp70 overexpression did not decrease the loss of or improve restoration of luciferase activity in cells exposed to hypoxia. CONCLUSIONS: These results suggest that Hsp70 overexpression is sufficient to protect LLC-PK1 proximal tubular cells from hyperthermia but is not sufficient for protection from hypoxia.

Animals↗
PubMedDate not supplied

[The mechanical effects of shock waves in extracorporeal shock wave treatment of calcific tendinitis--an in vitro model].

OBJECTIVE: Various studies have shown the benefit of the extracorporal shock wave therapy in the treatment of the calcific tendinitis. It was the aim of this study to examine the energy needed to disintegrate a calcific deposit. METHOD: By using the in vitro model of the pig shoulder the mechanical effects of different energy levels and impulse rates on the calcifying deposits are investigated. RESULTS: The results are showing the energy- and impulse-depending effect of the shockwaves. The disintegration of the implanted "bonn-stones" with development of an large amount of fragments smaller then 1000 microns requires an energy of 0.42 mJ/mm2 and between 2000 and 3000 impulses. CONCLUSIONS: According to the experimental results a instant mechanical effect on the calcifying deposits using the ordinary parameter is unlikely. The absorption of the calcifying deposits in likely induced through cellular clearing function. Clinical trials confirmed the good therapeutical results after two sessions with at least 1500 pulses and an energy of 0.28-0.30 mJ/mm2.

Animals↗
PubMed2000

A non-toxic heat shock protein 70 inducer, geranyl-geranyl-acetone, restores the heat shock response in gastric mucosa of protein-malnourished rats.

Acute gastric mucosal lesions caused by stress or noxious stimuli are important to consider in the management of critically or chronically ill patients. Protein malnutrition has been implicated as a risk factor for stress ulcer and subsequent complications in those patients. When male Wistar rats fed a 5% or 20% casein diet for 3 weeks were exposed to restraint and water-immersion stress, the low-protein diet significantly increased the ulcer index. The low-protein diet did not change the level of heat shock factor 1 (HSF1) in gastric mucosa but it did attenuate the HSF1 activation after exposure to the stress, resulting in the inhibition of HSP70 mRNA expression and HSP70 induction in gastric mucosa. HSP70 is crucial for the maintenance of cell integrity during pathophysiologic conditions; therefore the impaired HSP70 induction appeared to at least in part aggravate stress ulcer. We also tested whether a non-toxic HSP70 inducer, geranyl-geranyl-acetone (GGA), effectively improved the mucosal integrity by stimulating HSP70 induction under protein malnutrition. Intragastric administration of GGA (200 mg/kg twice a day) to the protein-malnourished rats for up to 1 week failed to stimulate the HSP70 induction. However, the administration of GGA (200 mg/kg twice a day) for 3 weeks restored HSP70 induction and induced higher resistance against stress ulcer as compared with results in vehicle-treated, normally nourished rats. Our results suggest that GGA may have a potential benefit for the prevention of stress ulcer in chronically or critically ill patients with protein malnutrition.

Animals↗
PubMed2000

Role of c-jun expression increased by heat shock- and ceramide-activated caspase-3 in HL-60 cell apoptosis. Possible involvement of ceramide in heat shock-induced apoptosis.

Ceramide has emerged as a lipid mediator in apoptosis induced by a variety of stresses. As we previously showed that the activation of AP-1, a nuclear transcription factor was indispensable to ceramide-induced apoptosis in human leukemia HL-60 cells (Sawai, H., Okazaki, T., Yamamoto, H., Okano, H., Takeda, Y., Tashima, M., Sawada, H., Okuma, M., Ishikura, H., Umehara, H., and Domae, N. (1995) J. Biol. Chem. 270, 27326-27331), the role and mechanism of heat shock (HS)-increased c-jun expression in apoptosis was here investigated. HS increased morphological changes compatible with apoptosis in human leukemia HL-60 cells, and induced ceramide generation and sphingomyelin hydrolysis with an increase of neutral magnesium-dependent sphingomyelinase activity. When HS failed to induce apoptosis in HS-resistant HL-60 cells, ceramide generation was not detected, suggesting that ceramide was involved in downstream signals required for HS-induced apoptosis. Both HS and N-acetylsphingosine (C(2)-ceramide) increased the expression of c-jun/c-fos mRNAs with the peak 2 h after treatment. When we examined whether the inhibition of c-jun expression by its antisense oligodeoxynucleotides (AS) blocked HS- or C(2)-ceramide-induced apoptosis, AS of c-jun gene inhibited apoptotic morphological changes and DNA fragmentation whereas did not sense oligodeoxynucleotides. Moreover, a synthetic tetrapeptide, acetyl-Asp-Met-Gln-Asp-aldehyde (DMQD-CHO), which inhibited the formation of active form of caspase-3 more efficiently than those of caspase-4, -6, -7, and -8, blocked both caspase-3 like activity, c-jun expression and apoptosis induced by HS or C(2)-ceramide, although DMQD-CHO did not affect HS-induced ceramide generation. These results suggested that the ceramide was generated through sphingomyelin hydrolysis by HS-activated neutral, magnesium-dependent sphingomyelinase and that subsequent c-jun expression through activation of caspase-3 played a role in HS-induced HL-60 cell apoptosis.

Apoptosis↗
PubMed2003

Interactions between small heat shock protein subunits and substrate in small heat shock protein-substrate complexes.

Small heat shock proteins (sHSPs) are dynamic oligomeric proteins that bind unfolding proteins and protect them from irreversible aggregation. This binding results in the formation of sHSP-substrate complexes from which substrate can later be refolded. Interactions between sHSP and substrate in sHSP-substrate complexes and the mechanism by which substrate is transferred to ATP-dependent chaperones for refolding are poorly defined. We have established C-terminal affinity-tagged sHSPs from a eukaryote (pea HSP18.1) and a prokaryote (Synechocystis HSP16.6) as tools to investigate these issues. We demonstrate that sHSP subunit exchange for HSP18.1 and HSP16.6 is temperature-dependent and rapid at the optimal growth temperature for the organism of origin. Increasing the ratio of sHSP to substrate during substrate denaturation decreased sHSP-substrate complex size, and accordingly, addition of substrate to pre-formed sHSP-substrate complexes increased complex size. However, the size of pre-formed sHSP-substrate complexes could not be reduced by addition of more sHSP, and substrate could not be observed to transfer to added sHSP, although added sHSP subunits continued to exchange with subunits in sHSP-substrate complexes. Thus, although some number of sHSP subunits within complexes remain dynamic and may be important for complex structure/solubility, association of substrate with the sHSP does not appear to be similarly dynamic. These observations are consistent with a model in which ATP-dependent chaperones associate directly with sHSP-bound substrate to initiate refolding.

Adenosine Triphosphate↗
PubMed1996

Effect of acute heat stress on heat shock protein 70 messenger RNA and on heat shock protein expression in the liver of broilers.

1. The synthesis of heat shock protein 70 (Hsp70) mRNA and the expression of Hsp70 in the liver of broiler chickens submitted to acute heat stress (35 degrees C for 5 h) was investigated. 2. Hsp70 expression was detected by SDS-PAGE and Western blot analysis using a polyclonal antiserum against Hsp70 of Blastocladiella emersonii. The specific signal of Hsp70 mRNA was analysed by Northern blot using as probe a Hsp70 cDNA of B. emersonii. 3. An increase in the amount of Hsp70 was detected from the first up to the fifth hour of acute heat exposure. This increase in the amount of Hsp70 was accompanied by an increase in Hsp70 mRNA which peaked at 3 h. 4. This study shows that the heat induced increase in Hsp70 mRNA and protein in broiler liver, in vivo, are time dependent, similar to that in mammals.

Animals↗
PubMed2003

Effects of total body irradiation and cyclosporin a on the lethality of toxic shock syndrome toxin-1 in a rabbit model of toxic shock syndrome.

Toxic shock syndrome (TSS) may be mediated by superantigen-activated T cells, a theory we tested in rabbits, which are more susceptible to the lethal effects of superantigens, such as TSS toxin-1 (TSST-1), than are mice. Rabbits exposed to 10 cGy of total body irradiation exhibited T cell deficiency, with profound depletion of splenic lymphocytes and circulating CD4(+) lymphocytes, as well as an inability to manifest delayed-type hypersensitivity. Nevertheless, these rabbits remained completely susceptible to TSST-1, indicating that TSS can occur in the setting of marked immunosuppression.

Animals↗
PubMedDate not supplied

Passive protection of rabbits infected with toxic shock syndrome-associated strains of Staphylococcus aureus by monoclonal antibody to toxic shock syndrome toxin 1.

The effectiveness of passive immunization was assessed in an infection model of toxic shock syndrome (TSS) in which monoclonal antibody to TSS toxin 1 (TSST-1) was administered intravenously to rabbits. Previously implanted infection chambers were inoculated with Staphylococcus aureus strains RN4710 and D4508. The former strain carries the TSST-1 gene on plasmid pRN6201; the latter is a TSST-1-negative clinical isolate obtained from a patient with nonmenstrual TSS. Purified monoclonal antibody, MAb 8-5-7 (IgG), was administered in two doses of approximately 1.25 mg each 24 hours before and 24 hours after infection. MAb 8-5-7 provided complete protection against both the TSS-like syndrome and the mortality that occurred in unprotected rabbits infected with strain RN4710 but did not provide complete protection in rabbits infected with strain D4508; three of the five rabbits either displayed signs of illness or died despite treatment. Western-blot analyses of the extracellular proteins produced by strains RN4710 and D4508 that used MAb 8-5-7 as a probe revealed that only TSST-1 produced by RN4710 reacted with the antibody. Thus, if MAb 8-5-7 partially protected animals against infections with strain D4508, the protection appears to have been nonspecific.

Animals↗