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PubMed1983

Developmental regulation of Drosophila imaginal disc proteins: synthesis of a heat shock protein under non-heat-shock conditions.

A low-molecular-weight heat-shock protein is reported here to be synthesized in Drosophila imaginal discs under non-heat-shock conditions. This protein has been identified as hsp 23 by its mobility in SDS-gel electrophoresis, by its isoelectric point, and by its partial proteolytic digest pattern. This protein is shown to be synthesized in tissue from late-third-instar larvae using both in vitro and in vivo radiolabeling techniques. Tissues from late-third-instar larvae synthesize hsp 23 at a level much higher than tissues from mid-third-instar larvae. The increased synthesis of this protein at the end of third instar coincides with the rise in ecdysone titer that occurs at this time of development. The developmental regulation of this protein suggests that hsp 23 plays a role in normal development as well as in the heat-shock response.

Animals↗
PubMed1994

Anti-shock effect of pituitary adenylate cyclase activating polypeptide (PACAP) on experimental endotoxin shock in dogs.

Effects of pituitary adenylate cyclase activating polypeptide with 38 amino acid residues (PACAP-38) on both cardiovascular functions and plasma hormone levels during endotoxin shock were studied in anesthetized dogs. When PACAP-38 (a bolus 420 pmol/kg injection or a bolus 420 pmol/kg injection followed by a continuous 30 pmol/kg/min infusion for 60 min) was administered intravenously 5 min after application of endotoxin, both mean arterial pressure and cardiac output were restored at 10 min. The continuous administration of PACAP-38 was more effective in improving the symptoms of shock. Plasma adrenalin and cortisol levels were significantly increased by both regimens. These results clearly indicate that the anti-shock properties of PACAP-38 may be attributed to its abilities to increase plasma cortisol and adrenalin levels and to stimulate cardiac function.

Animals↗
PubMed1983

Venous return in hemorrhagic shock after application of military anti-shock trousers.

UNLABELLED: The effect of Military Anti-Shock Trousers (MAST) on inferior vena cava blood flow was studied during graded hypovolemia using a pump reservoir system and an in-line electromagnetic flowprobe. During hemorrhagic shock MAST inflation increased cardiac output 25.4% ( CONTROL: 0.92 +/- 0.09 l/min) and arterial pressure 50% ( CONTROL: 60 +/- 2 mmHg). The so-called "autotransfusion" effect due to blood displacement from the lower part of the body into the central circulation was found to be only 4.3 +/- 0.6 ml/kg, a volume much less than previously estimated in the literature. We conclude that MAST inflation reliably improves cardiac output and systemic blood pressure above the diaphragm in dogs subjected to hemorrhagic shock. This effect is mainly due to a diversion of the cardiac output to the upper half of the body due to impedance of flow to the abdomen and lower extremities, rather than to a significant volume shift constituting an autotransfusion of blood from the lower part of the body.

Animals↗
PubMed1997

Differential transcript induction of parsley pathogenesis-related proteins and of a small heat shock protein by ozone and heat shock.

Parsley (Petroselinum (crispum L.) is known to respond to pathogen attack by the synthesis of furanocoumarins and to UV irradiation by the synthesis of flavone glycosides whereas ozone treatment results in the induction of both pathways. A cDNA library from parsley plants was differentially screened using labelled reverse-transcribed poly(A)+ RNA isolated from ozone-treated parsley plants. This resulted in the isolation of 13 independent cDNA clones representing ozone-induced genes and of 11 cDNA clones representing ozone-repressed genes. DNA sequencing of several clones resulted in the identification of pathogenesis-related protein 1-3 (PR1-3), of a new member of PR1 cDNAs (PRI-4) and of a small heat shock protein (sHSP). Northern blot analyses showed a transient induction of the three mRNA species after ozone fumigation. In contrast, heat shock treatment of parsley plants resulted in an increase of sHSP mRNA whereas no increase for transcripts of PR1-3 and PR1-4 could be observed. This is the first characterized sHSP cDNA clone for plants induced by heat shock, as well as by oxidative stress caused by ozone.

Amino Acid Sequence↗
PubMed2003

Initial experiences with the Impella device in patients with cardiogenic shock - Impella support for cardiogenic shock.

BACKGROUND: We planned a study to assess the safety, feasibility, and efficacy of the Impella micro-axial blood pump in patients with cardiogenic shock. METHODS: From January 2001 to September 2002 inclusive, 16 patients in cardiogenic shock (maximal inotropic support and with IABP in 11 cases) underwent left ventricle unloading with the Impella pump. 6 were placed via the femoral artery (patients in the coronary care unit) and 10 directly through the aorta (postcardiotomy heart failure). In three patients, the device was used in combination with ECMO. Mean age was 60 years (range 43 - 75), 11 were male. RESULTS: A stable pump flow of 4.24 +/- 0.28 l/min was reached (3.3 +/- 1.9 l/min in patients with ECMO and Impella). Mean blood pressure before Impella) support was 57.4 +/- 13 mmHg, which increased to 74.9 +/- 13 mmHg after 6 hours and 80.6 +/- 17 mmHg (p = 0.003) after 24 hours. Cardiac output increased from 4.1 +/- 1.3 l/min to 5.5 +/- 1.3 (p = 0.003) and 5.9 +/-1.9 l/min (p = 0.01) at 6 and 24 hours. Mean pulmonary wedge pressure decreased from 29 +/- 10 mmHg to 17 +/- 5 mmHg and 18 +/- 7 mmHg at 6 (p = 0.04) and 24 hours. Blood lactate levels decreased significantly after 6 hours of support (from 2.7 +/- 1 to 1.3 +/- 0.5 mmol/l, p = 0.004). Device-related complications included three sensor failures (no clinical action), one pump displacement (replacement) and six incidences of haemolysis (peak free plasma haemoglobin > 100 mg/dl, no clinical action). Eleven patients (68 %) were weaned, six (37 %) survived. CONCLUSIONS: Left ventricular unloading with the Impella pump via the transthoracic or femoral approach is feasible and safe. Support led to a decrease in pulmonary capillary wedge pressure, increase in cardiac output and mean blood pressure, and improved organ perfusion in patients with severe cardiogenic shock.

Adult↗
PubMed1984

Proteins related to the mouse L-cell major heat shock protein are synthesized in the absence of heat shock gene expression.

Heat shock of mouse L cells induces the synthesis of two polypeptides of Mrs 68,000 and 89,000. Using a fragment of a cloned gene encoding the Drosophila melanogaster Mr 70,000 heat shock protein (hsp70), we have shown that this protein has been highly conserved during eukaryotic evolution. We extended this observation by probing at low stringency for the expression in mouse L cells of RNA homologous to the Drosophila hsp70 gene. In addition to the RNA encoding the inducible Mr 68,000 heat shock protein (hsp68), there are mouse mRNAs encoding proteins of Mrs 70,000 and 74,000 that are homologous to the Drosophila hsp70 gene. The Mrs 70,000 and 74,000 proteins and their mRNAs are abundant components of unstressed mouse L cells. These constituitively expressed proteins are unique polypeptides in contrast to the several isoelectric point variants of the inducible hsp68. We do not detect hsp68 or its mRNA in unstressed L cells. In addition to the mRNAs corresponding to hsp68 and the Mrs 74,000 and 70,000 proteins, we detect a fourth RNA homologous to the Drosophila hsp70 gene but whose protein product has not been identified. Our results suggest that the hsp68 gene of mouse L cells is a member of a multigene family and that the individual family members are distinguishable by their degree of similarity but show differences in the regulation of their expression.

Animals↗
PubMed2004

Identification of a new member of the phage shock protein response in Escherichia coli, the phage shock protein G (PspG).

The phage shock protein operon (pspABCDE) of Escherichia coli is strongly up-regulated in response to overexpression of the filamentous phage secretin protein IV (pIV) and by many other stress conditions including defects in protein export. PspA has an established role in maintenance of the proton-motive force of the cell under stress conditions. Here we present evidence for a new member of the phage shock response in E. coli. Using transcriptional profiling, we show that the synthesis of pIV in E. coli leads to a highly restricted response limited to the up-regulation of the psp operon genes and yjbO. The psp operon and yjbO are also up-regulated in response to pIV in Salmonella enterica serovar Typhimurium. yjbO is a highly conserved gene found exclusively in bacteria that contain a psp operon but is physically unlinked to the psp operon. yjbO encodes a putative inner membrane protein that is co-controlled with the psp operon genes and is predicted to be an effector of the psp response in E. coli. We present evidence that yjbO expression is driven by sigma(54)-RNA polymerase, activated by PspF and integration host factor, and negatively regulated by PspA. PspF specifically regulates only members of the PspF regulon: pspABCDE and yjbO. We found that increased expression of YjbO results in decreased motility of bacteria. Because yjbO is co-conserved and co-regulated with the psp operon and is a member of the phage shock protein F regulon, we propose that yjbO be renamed pspG.

Bacterial Proteins↗
PubMed1957

The relationship between the vascular manifestations of shock produced by endotoxin, trauma, and hemorrhage. II. The possible role of the reticulo-endothelial system in resistance to each type of shock.

In studies designed to establish the interrelationship between bacterial endotoxins and the vascular sequelae of hemorrhagic and traumatic shock, the effect of factors known to influence the phagocytic behavior of the reticulo-endothelial system (RES) were investigated. Measures which induced a so called "blockade" of the RES were uniformly associated with an exacerbation of the vascular effects of the endotoxin of E. coli. Such pretreatment also counteracted the cross-tolerance induced by endotoxins against the lethal effects of hemorrhage or drum trauma. The vascular reactions characteristic of irreversible hemorrhagic shock could be simulated by a combination of pretreatment with carbon or proferrin and the infusion of small doses of E. coli endotoxin. An increase in the phagocytic activity of the RES, induced by repeated injections of certain colloids, was associated with an enhanced tolerance of shock. Measurement of carbon clearance values indicated that although an augmented phagocytic capacity was present in rats with induced tolerance to bacterial endotoxins, the development of resistance to trauma was not associated with a comparable change in the phagocytic function of the RES.

Animals↗
PubMed1994

Cloning and expression of cDNA coding for a new allergen from the house dust mite, Dermatophagoides farinae: homology with human heat shock cognate proteins in the heat shock protein 70 family.

An immunoreactive clone, which shares no homology with the major allergens, Der f I and Der f II, was isolated by screening of a Dermatophagoides farinae cDNA library with rabbit antiserum raised against an extract of the house dust mite and sera from patients with mite allergy. The deduced amino acid sequence of the cDNA of the clone is significantly homologous, up to 65.5%, to the carboxyl-terminal region of the heat shock cognate protein (hsc) 71 in the heat shock protein (hsp) 70 family. A pool of the recombinant protein-specific IgE purified from mite-allergic sera recognized a 67 kDa protein on a blot of ATP-binding components partially purified from the mite body extract, while the antibody did not bind to the major allergens. We conclude that the recombinant protein, one of several important allergens, may be a protein in the heat shock protein 70 family from the house dust mite, D. farinae.

Allergens↗
PubMed1999

An open-label dose escalation study of the nitric oxide synthase inhibitor, N(G)-methyl-L-arginine hydrochloride (546C88), in patients with septic shock. Glaxo Wellcome International Septic Shock Study Group.

OBJECTIVE: To assess the effects of the nitric oxide synthase inhibitor, 546C88, in patients with septic shock and to evaluate the range of dose rates that sustain mean arterial pressure (MAP) of > or =70 mmHg. DESIGN: Multicenter, open-label, uncontrolled, dose range finding study. SETTING: Ten intensive care units in Europe and the United States. PATIENTS: Thirty-two patients with septic shock diagnosed within <24 hrs. INTERVENTIONS: Patients received a fixed dose rate of 546C88 at either 1(n = 6), 2.5 (n = 6), 5 (n = 4), 10 (n = 5), or 20 mg/kg/hr (n = 11) by intravenous infusion for up to 8 hrs. Conventional vasoactive therapy was restricted to norepinephrine and/or dobutamine. During 546C88 therapy, MAP was to be maintained between 70 and 90 mm Hg, while attempting to withdraw any concurrent norepinephrine. MEASUREMENTS AND MAIN RESULTS: Systemic and pulmonary hemodynamics, blood gases, and plasma nitrate were assessed. Infusion of 546C88 (1-20 mg/kg/hr) for up to 8 hrs enabled a 60 to 80% reduction of the norepinephrine dose rate in all cohorts, while MAP was sustained at >70 mm Hg. There was an increase in vascular tone and a decrease in cardiac index within the 1st hr of therapy. Systemic vascular resistance returned toward baseline with reduction of concomitant administration of norepinephrine. The decline in oxygen delivery was associated with an increase in extraction and, therefore, the maintenance of oxygen consumption. There was a sustained reduction of venous admixture within the 1st hr of therapy. 546C88 was not associated with any major or dose-dependent adverse effect on pulmonary, hepatic, or renal function. CONCLUSIONS: Treatment with the nitric oxide synthase inhibitor, 546C88, can restore the balance of vasomotor tone, thereby, maintaining blood pressure and reducing or eliminating the requirement for norepinephrine therapy in patients with septic shock. Infusion of 546C88 (1-20 mg/kg/hr) appears to have a satisfactory overall safety profile.

Adult↗
PubMed1992

The human heat shock protein hsp70 interacts with HSF, the transcription factor that regulates heat shock gene expression.

Transcriptional regulation of the human hsp70 gene in response to heat shock and other forms of physiological stress occurs through the activation of heat shock transcription factor (HSF). Exposure of cells to a heat shock temperature of 42 degrees C results in transient activation of HSF; its DNA-binding activity increases rapidly, plateaus, and attenuates, during which the intracellular levels of hsp70 increase. In an effort to understand whether HSF is regulated negatively by hsp70, we have examined whether HSF associates with hsp70. We show that activated HSF associates with hsp70 and that the interaction is detected as the levels of hsp70 increase in the cell. Addition of ATP and other hydrolyzable nucleotides results in the dissociation of hsp70 from HSF while nonhydrolyzable nucleotide analogs do not disrupt the complex. We demonstrate that exogenous recombinant wild-type hsp70 can associate with activated HSF, whereas no association is observed with an amino-terminal or a carboxy-terminal deletion mutant of hsp70. We also show that hsp70 blocks the in vitro activation of HSF from its cryptic non-DNA-binding state to a DNA-binding form; this inhibitory effect of hsp70 is abolished by ATP. We suggest that hsp70 may negatively regulate the activation of HSF.

Adenosine Triphosphate↗
PubMed1999

The informed consent process and the use of the exception to informed consent in the clinical trial of diaspirin cross-linked hemoglobin (DCLHb) in severe traumatic hemorrhagic shock. DCLHb Traumatic Hemorrhagic Shock study group.

UNLABELLED: In the clinical trial of diaspirin cross-linked hemoglobin (DCLHb), optimal therapy required the immediate enrollment of patients with severe, uncompensated, traumatic hemorrhagic shock. When it was not feasible to obtain prospective consent, an exception to informed consent was used according to FDA regulation 21 CFR 50.24. OBJECTIVES: To examine the informed consent process and the use of the consent exception and consent to continue (CTC), and to describe the patients for whom this process was used. METHODS: This was a multicenter, randomized, controlled, single-blinded efficacy trial of DCLHb as an adjunct to standard therapy in the treatment of severe, traumatic hemorrhagic shock. Patients with unstable vital signs or a critical base deficit were treated, with a primary study endpoint of 28-day mortality. RESULTS: During the 11-month study period, 112 patients were randomized in 18 U.S. trauma centers, and data from 98 of the infused patients were analyzed. Prospective consent was obtained from two patients, three family members, and one legally authorized representative (LAR) (6%). Consent to continue was requested for 89 patients (89%), and full participation was granted for 87 of these patients (98%). Consent to continue was provided by 54 (98%) of the 55 patients approached. The mean number of days for family/LAR CTC was 1.1 +/-3.8 days, and 50% of the time it was obtained on the day of study enrollment. Patient CTC was obtained in an average of 13 +/- 23 days, with a median of four days. Patients treated in this protocol were more likely to have sustained penetrating trauma than the overall trauma patient population treated in these trauma centers (44% vs 21%, p = 0.002). CONCLUSIONS: Informed consent in this study of an emergent therapy most often involved the use of the consent exception and consent to continue, the latter of which occurred in a timely manner. Nearly all of those who were approached for CTC approved full participation in the study, suggesting acceptance of the process outlined in the new regulations. Patients treated in a hemorrhagic shock clinical trial may differ from the general trauma patient population.

Adult↗
PubMed1964

ELECTROCONVULSIVE SHOCK, RETROACTIVE AMNESIA, AND THE SINGLE-SHOCK METHOD.

If electroconvulsive shock is given immediately after a learning session, retroactive amnesia for that response occurs. Such results may be due to production of aversive responses or to interference with consolidation of the neural engram, or to both. Aversive responses or competing responses are not adequate explanations for retroactive amnesia. Consolidation theory provides the most plausible explanation. The single-shock method is an appropriate approach for studying the relationships between electroconvulsive shock and retroactive amnesia.

Amnesia↗
PubMed1997

Characterization of cspB, a cold-shock-inducible gene from Lactococcus lactis, and evidence for a family of genes homologous to the Escherichia coli cspA major cold shock gene.

Upon temperature downshift, the major cold shock protein CspA is highly induced in Escherichia coli. This protein being conserved in other bacteria, we used a PCR-based approach with a pair of degenerate primers derived from highly conserved regions of the CspA-related proteins to evidence the presence of at least three related genes in Lactococcus lactis. One of them, cspB, was cloned and sequenced. It encodes a 66-residue protein which possesses 60% sequence identity with E. coli CspA. Following a cold shock from 30 to 15 degrees C, the level of the cspB mRNA transcript increased, as shown by Northern blot hybridization. In addition, induction of cspB-directed beta-galactosidase activity was observed. These results indicate that the L. lactis cspB gene is cold shock inducible.

Amino Acid Sequence↗
PubMed1988

A developmentally regulated membrane protein gene in Dictyostelium discoideum is also induced by heat shock and cold shock.

We have analyzed the expression of the Dictyostelium gene P8A7 which had been isolated as a cDNA clone from an early developmentally regulated gene. The single genomic copy generated two mRNAs which were subject to different control mechanisms: while one mRNA (P8A7S) was regulated like the cell-type-nonspecific late genes, the other one (P8A7L) was induced during development, when cells were allowed to attach to a substrate, and when cells were subjected to stress, such as heat shock and cadmium. Interestingly the same induction was also observed with cold shock. RNA processing was inhibited by heat and cold shock, leading to nuclear accumulation of a precursor. The translated region of the cDNA was common to both mRNAs and encoded an unusually hydrophobic peptide with the characteristics of a membrane protein.

Amino Acid Sequence↗
PubMed1982

Intracellular translocation of cellular and heat shock induced proteins upon heat shock in Drosophila Kc cells.

The intracellular distribution of cellular and heat shock induced proteins (hsp) was studied during a heat shock to Drosophila Kc cells. The different hsp's are unequally distributed between the intracellular organelles; while hsp 84 shows an exclusive cytoplasmic location, hsp 70 is equally distributed between the nucleus and the cytoplasm. The low molecular weight (MW) hsp's 22--26 are mainly concentrated in the nuclear fraction. Hsp 34 also shows a preferential nuclear localization but differs from the 22-26 hsp group with regard to its solubility in salt. During the heat shock (HS) treatment, a major preexisting microsomal polypeptide of relative mass (Mr) 45 000 with some properties similar to cytoskeletal proteins is translocated to the nuclear pellet. This translocation does not occur during arsenite treatment which also induces the synthesis of some hsp's. Furthermore, the hsp's synthesized in response to this arsenite treatment do not become associated with the nucleus as during the HS. Consequently the nuclear translocation of the 45 000 Mr protein does not seem to be involved in the induction of the high MW group of hsp's. Furthermore, it suggests that the hsp's which are found in the nuclear pellet upon HS do not have a nuclear localization per se. It rather reflects a temperature-dependent translocation of certain cellular proteins and hsp to the nucleus during a HS.

Animals↗
PubMed1981

Irreversible thermic shock in rats: methods and results of a standardized shock model.

A standardized model for thermic shock in rats is described: 30% of the body surface, i.e. an oval-shaped area from neck to tail and limited by the connecting line between front and back limb, is exposed to 70 degrees C water for 180 seconds. The mean survival time was 2.63 +/- 1.22 hours. Immediately after burn injury, thermic shock developed with decline of respiratory and heart frequency and there was a decrease of arterial blood pressure in the first hour after shock had been induced. Severe decline in pO2 in arterial blood and in ATP occurred 30 minutes after injury and a similar increase in blood glucose, lactate, pCO2 and arterial pH was noted. Pathological changes were demonstrable in liver, kidneys, spleen, heart, lung, small intestine and pancreas: disseminated intravascular coagulation and capillary stasis were predominant in all organs; in addition different changes in organs are described (cell injury, oedema etc. in lung, liver, kidney and pancreas).

Animals↗
PubMed1993

Do heat shock proteins play a role in Graves' disease? Heat shock protein-specific T-cells from Graves' disease thyroids do not recognize thyroid epithelial cells.

Thyroid-derived T-cells from patients with Graves' disease were analyzed for their reactivity to recombinant heat shock proteins (hsp) and autologous thyroid epithelial cells (TEC). Five of six uncloned T-cell lines responded to stimulation with recombinant mycobacterial 71-kilodalton (kDa) hsp and cross-reacted with the corresponding amoebial and human proteins. Only one line reacted with recombinant 65-kDa hsp. Thyroid-derived T-cell lines also showed a proliferative response to TEC, which could be increased in four of the lines, when hsp expression was induced in thyroid cells by heat stress before the initiation of coculture. Clonal specificity analysis of thyroid-derived T-cell clones, however, demonstrated that distinct T-cells were responsible for the recognition of recombinant hsp and TEC. None of the clones responsive to recombinant hsp recognized TEC, whereas TEC-responsive clones did not react with recombinant hsp. Interestingly, the response of the majority of TEC-reactive clones could be dramatically increased when heat-shocked TEC were used as stimulator cells. These results suggest that T-cells specific for hsp of the 70- or 60-kDa families do not recognize TEC in the autoimmune thyroid gland. Heat shock-inducible proteins may, however, still play a role in the autoimmune process by facilitating the presentation of thyroid-specific autoantigen(s) to autoreactive T-cells.

Adult↗