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At least 685 records · Page 38Linked to original sources
PubMed1995

Detection of antibodies to 65 KD heat shock protein and to human superoxide dismutase in autoimmune hepatitis-molecular mimicry between 65 KD heat shock protein and superoxide dismutase.

The antibody to 65 KD mycobacterial heat shock protein (HSP65) and antibody to human superoxide dismutase (H-SOD) were measured by ELISA in patients with autoimmune hepatitis (AIH), and results were compared with those of patients with chronic active hepatitis C (CAH-C) or systemic lupus erythematosus (SLE) and normal subjects (NS). Patients with AIH had significantly higher OD values of anti-HSP65 antibody and anti-H-SOD antibody compared with those of patients with CAH-C or SLE and NS. OD values of anti-HSP65 antibody were correlated with those of anti-SOD antibody. Affinity-purified anti-SOD antibody reacted with HSP65. Analysis of the amino acid sequence of human SOD showed that 7 segments, corresponding to r to 25 amino acid residues, exhibited 50 to 71% homology with that of my mycobacterial HSP65.

Amino Acid Sequence↗
PubMed1995

Regulation of heat shock protein 70 synthesis by heat shock in the preimplantation murine embryo.

Induced thermotolerance in murine embryos occurs at the 8-cell stage when embryos are maintained in vitro but not until the blastocyst stage if development proceeds in vivo. Present results indicate that ability of embryos to undergo induced thermotolerance is not limited by heat shock protein 70 (HSP70) synthesis. Exposure of 8-cell embryos to 40 degrees C enhanced synthesis of 2 constitutive HSP70 proteins (HSC70 and HSC72) and induced another protein, HSP68; exposure of 43 degrees C was required to induce similar responses in expanded blastocysts. Unlike induced thermotolerance, increased synthesis of HSP70 molecules did not depend on whether embryos were cultured or developed in vivo. Thus, other biochemical mechanisms in addition to HSP70 confer thermotolerance in the preimplantation-stage murine embryo. The observation that the temperature threshold for induction of HSP70 synthesis increased from the 8-cell to the blastocyst stage is indicative of these other biochemical processes.

Journal Article↗
PubMedDate not supplied

Heat shock protection against induction of chromatid aberrations is dependent on the time span between heat shock and clastogen treatment of Vicia faba root tip meristem cells.

Variation of the time span between heat shock (hs) and clastogen treatment of V. faba root tip meristems showed that hs protection is a very quick response (effective after less than 10 min) and lasting for up to 240 min in the case of induction of chromatid aberrations by maleic hydrazide (MH). Analogous protective responses are significantly slower and shorter when TEM is used for aberration induction. This, together with absence of 'clastogenic cross-adaptation' to these agents and differential effects of benzamide (BA, an inhibitor of poly-ADP-ribosylation) pretreatment before hs on hs protection, suggests that hs before clastogen treatment triggers at least 2 clastogen-specific, protective functions which eventually result in protection against these 2 clastogens.

Chromosome Aberrations↗
PubMed1985

Utility of military anti-shock trousers (MAST) in anaphylactic shock--a case report.

A 49-year-old man with severe anaphylactic hypotension deteriorated and developed an unmeasurable blood pressure despite vigorous intravenous (IV) fluid and epinephrine administration. Application of the lower body compression garment known as MAST (Military Anti-Shock Trousers) improved the patient's blood pressure and helped to stabilize it until additional fluids and vasopressors were administered; he survived without sequellae. We propose that augmentation of preload and afterload by MAST is a useful adjunct in severely hypotensive anaphylactic patients who do not respond initially to IV fluids and epinephrine.

Aminophylline↗
PubMed1992

Extracorporeal shock wave lithotripsy retreatment ("stir-up") promotes discharge of persistent caliceal stone fragments after primary extracorporeal shock wave lithotripsy.

A prospective randomized study was performed to compare the results of piezoelectric extracorporeal shock wave lithotripsy (ESWL) retreatment versus surveillance only in 50 patients with persistent caliceal stone fragments after primary ESWL for renal calculi. After a 3-month followup significant decreases in residual debris were observed in the retreated group, while changes in the control group were negligible. Considering the low morbidity of outpatient ESWL with a pain-free, second generation lithotriptor, ESWL retreatment of completely fragmented but persistent stone debris appears to be justified to render the kidney stone-free.

Adult↗
PubMed1994

Chlordiazepoxide microinjected into the region of the dorsal raphe nucleus eliminates the interference with escape responding produced by inescapable shock whether administered before inescapable shock or escape testing.

Systemic administration of benzodiazepines before exposure to inescapable shock (IS) blocks the enhanced fear conditioning and escape learning deficits that follow exposure to IS, whereas administration before the subsequent behavioral testing eliminates the enhanced fear but not the interference with escape. The failure of benzodiazepines to reduce the IS-produced escape learning deficit when given before testing is inconsistent with a recent proposal that interference with escape is mediated by an IS-induced sensitization of dorsal raphe nucleus (DRN) activity. The present experiments demonstrate that chlordiazepoxide will block both the enhancement of fear and interference with escape responding when given before either IS or testing if microinjected in the region of the DRN. This suggests that systemic benzodiazepines fail to block escape deficits when given before testing because action at a site distant from the DRN counters the effect of the drug at the DRN.

Animals↗
PubMed1996

Purification and identification of a major activator for p38 from osmotically shocked cells. Activation of mitogen-activated protein kinase kinase 6 by osmotic shock, tumor necrosis factor-alpha, and H2O2.

A stress-activated, serine/threonine kinase, p38 (also known as HOG1 or MPK2) belongs to a subgroup of mitogen-activated protein kinase (MAPK) superfamily molecules. An activity to activate p38 (p38 activator activity) as well as p38 activity itself were greatly stimulated by hyperosmolar media in mouse lymphoma L5178Y cells. The activator activity has been purified by sequential chromatography. A 36-kDa polypeptide that was coeluted with the activity in the final chromatography step was identified as MAPK kinase 6 (MAPKK6) by protein microsequencing analysis. Monoclonal and polyclonal antibodies raised against recombinant MAPKK6 recognized specifically the 36-kDa MAPKK6 protein but did not cross-react with MKK3 proteins. The use of these anti-MAPKK6 antibodies revealed that two major peaks of the p38 activator activity in the first chromatography step reside in the activated MAPKK6. Using a genetic screen in yeast, we isolated MKK3b, an alternatively spliced form of MKK3. Like MKK3 and MAPKK6, MKK3b was shown to be a specific activator for p38 and was activated by osmotic shock when expressed in COS7 cells. Immunoblotting analysis revealed that MAPKK6 is expressed highly in HeLa and KB cells and scarcely in PC12 cells, whereas MKK3 and MKK3b are expressed in all cells examined. Immunodepletion of MAPKK6 from the extracts obtained from L5178Y cells and KB cells exposed to hyperosmolar media depleted them of almost all of the p38 activator activity, indicating that MAPKK6 is a major activator for p38 in an osmosensing pathway in these cells. In addition, MAPKK6 was activated strongly by tumor necrosis factor-alpha, H2O2, and okadaic acid and moderately by cycloheximide in KB cells. Thus, there are at least three members of p38 activator, MKK3, MKK3b, and MAPKK6, and MAPKK6 may function as a major activator for p38 when expressed.

Amino Acid Sequence↗
PubMed2004

Physical and functional interactions among RNase E, polynucleotide phosphorylase and the cold-shock protein, CsdA: evidence for a 'cold shock degradosome'.

Escherichia coli contains at least five ATP-dependent DEAD-box RNA helicases which may play important roles in macromolecular metabolism, especially in translation and mRNA decay. Here we demonstrate that one member of this family, CsdA, whose expression is induced by cold shock, interacts physically and functionally with RNase E. Three independent approaches show that after a shift of cultures to 15 degrees C, CsdA co-purifies with RNase E and other components of the RNA degradosome. Moreover, functional assays using reconstituted minimal degradosomes prepared from purified components in vitro show that CsdA can fully replace the resident RNA helicase of the RNA degradosome, RhlB. In addition, under these conditions, CsdA displays RNA-dependent ATPase activity. Taken together, our data are consistent with a model in which CsdA accumulates during the early stages of cold acclimatization and subsequently assembles into degradosomes with RNase E synthesized in cold-adapted cultures. These findings show that the RNA degradosome is a flexible macromolecular machine capable of adapting to altered environmental conditions.

Adaptation, Physiological↗