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PubMed1986

Side effects of extracorporeal shock-wave exposure in patients treated by extracorporeal shock-wave lithotripsy for upper urinary tract stone.

The side effects of shock-wave exposure on patients treated by extracorporeal shock-wave lithotripsy were analyzed by measuring chemical substances including cell-escaped enzymes in the blood and urine. Free hemoglobin, glutamic oxaloacetic transaminase (GOT) and lactate dehydrogenase (LDH) increased as a function of shock-wave count. Total bilirubin, GOT and LDH reached a peak on the 1st postoperative day and decreased to pretreatment values by the 4th day. Creatine phosphokinase and myoglobin also significantly increased on the 1st postoperative day but returned to pretreatment levels by the 4th day. The urinary ratio of N-acetyl-beta-d-glucosaminase to creatinine significantly increased after treatment and was still high on the 4th day. These results suggest that significant hemolysis and myolysis developed owing to shock-wave exposure, and that the kidney was damaged to some extent. Therefore, these side effects must be taken into account in determining the dose and frequency of treatment.

Adult↗

PubMed2000

Multicenter, randomized, controlled trial of 150-J biphasic shocks compared with 200- to 360-J monophasic shocks in the resuscitation of out-of-hospital cardiac arrest victims. Optimized Response to Cardiac Arrest (ORCA) Investigators.

BACKGROUND: In the present study, we compared an automatic external defibrillator (AED) that delivers 150-J biphasic shocks with traditional high-energy (200- to 360-J) monophasic AEDs. METHODS AND RESULTS: AEDs were prospectively randomized according to defibrillation waveform on a daily basis in 4 emergency medical services systems. Defibrillation efficacy, survival to hospital admission and discharge, return of spontaneous circulation, and neurological status at discharge (cerebral performance category) were compared. Of 338 patients with out-of-hospital cardiac arrest, 115 had a cardiac etiology, presented with ventricular fibrillation, and were shocked with an AED. The time from the emergency call to the first shock was 8.9+/-3.0 (mean+/-SD) minutes. CONCLUSIONS: The 150-J biphasic waveform defibrillated at higher rates, resulting in more patients who achieved a return of spontaneous circulation. Although survival rates to hospital admission and discharge did not differ, discharged patients who had been resuscitated with biphasic shocks were more likely to have good cerebral performance.

Adult↗

PubMed1981

Effects of ratio contingencies on responding maintained by schedules of electric-shock presentation (response-produced shock).

Squirrel monkeys' lever pressing was established under fixed-interval schedules of electric-shock presentation (response-produced shock). After appropriate temporal patterns of lever pressing were engendered, either fixed-ratio schedules of shock presentation were added to the fixed interval, or yoked variable-ratio schedules were substituted for the fixed-interval schedules. When fixed-ratio schedules were added, there was an initial rise in response rate and schedule-appropriate patterns of responding developed. After many sessions, however, responding ceased abruptly, in some cases with remarkable quickness. When variable-ratio schedules were substituted, responded declined gradually and eventually was poorly maintained. Ratio contingencies may not support responding as well as interval contingencies when electric shock is the maintaining event.

Journal Article↗

PubMed2000

Escape from shock versus escape from shock accompanied by a visual stimulus in rats.

Two groups of 15 rats each were trained in a shuttle box to escape foot-shock either unsignalled or presented in compound with a visual cue: darkness. The visual cue presented in shock compartment amplifies the behavioral tendency actually prevailing in the response repertory of the rat. During the 1st session the compound enhanced the species-specific flight resulting in shortening of the rat's escape latency. Thereafter, during subsequent sessions, darkness exaggerated resistance to enter the other compartment; thus escape latencies were longer under compounded than under unsignalled procedure. The darkness cue reduces the intertrial response rate relative to the unsignalled group. This latter finding supports the discrimination model of the effect, since the compound helps the animals to discriminate the illuminated "safe" period between trials from the aversive shock period. Our data seem to suggest that the darkness presented synchronously with escapable grid-shock acquires aversive properties.

Animals↗

PubMed1991

[Extracorporeal shock wave lithotripsy and biological effects of underwater shock waves].

The recent development in the treatment of the urinary stones has much to do with underwater shock waves. And urologists have become more aggressive in using this modality in the treatment of the complicated stone patient. However, controversy persists regarding the extent to which the applied voltage and shock wave number interact to induce both cellular injury and stone fragmentation and also the appropriate timing of repeat lithotripsy treatments. It is very short time since underwater shock wave has been initially applied to human body. The effects of the shock wave on the microstructure of the tissues are poorly understood. The questions, what happens at the F2 focus and what happens to the energy after arriving at the F2, remain unclear. The bioeffects of ESWL should be more and more scrutinized.

Animals↗

PubMed1991

[Extracorporeal shock wave lithotripsy for renal and ureteral calculi with MPL-9000. Correlation between stone burden and shock wave energy].

Clinical results of ESWL for renal and ureteral stone with MPL-9000 were presented. We also reviewed correlation between stone burden and shock wave energy. We studied 210 cases (295 sessions) of renal stone and 109 cases (154 sessions) of ureteral stone that were treated from November 1988 till January 1989 and from November 1989 till May 1990. Of those sessions, 76 sessions of renal stone cases and 53 of ureteral stone cases were carried out ambulatorily. Successful disintegration (within 4 mm) rate was 86% of renal stones, 84% of ureteral stones, and stone free rate after 6 months was 72% of renal stones and 84% of ureteral stones. As for the complications, brain infarction occurred in one case, subcapsular hematoma of the kidney in one, and arythmia in 5. No other severe side effects were observed. Between shock wave energy (the number of shock wave shots x voltage) and stone burden (long axis x short axis of the stone), a significant correlation was found in renal stone cases, but not in ureteral stone cases. E/B (shock wave energy/stone burden) was 33,100 (kv.shots/cm2) for the renal stone and 56,000 (kv.shots/cm2) for the ureteral stone. These results suggest that there is still another unknown factor, which is not related with renal stone, for successful disintegration of ureteral stone. We also confirmed that more energy is necessary for destruction of ureteral stone than for that of renal stone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Synergistic effect of heat-shock and UV-irradiation on mitosis and protein synthesis in G2-phase plasmodia of Physarum polycephalum Schw--reduction in UV-induced mitotic delay in a preheat-shocked system.

The synergistic effect of UV irradiation and heat-shock during the last 3 hr of G2 phase of the cell cycle in the plasmodia of P. polycephalum, in terms of mitotic delay and inhibition of protein synthesis, has been evaluated. The mitotic delay due to both perturbers coordinately increased closer to mitosis. Maximum mitotic delay was obtained in plasmodia heat-shocked after UV irradiation, indicating the presence in this system of either a heat-labile mitogenic substance which is comparatively less susceptible to UV or a substance which is made more susceptible to hyperthermia by UV. A protective role for heat-shock applied before irradiation has been observed in that, radiation-induced mitotic delay is significantly reduced in this combination. There was severe inhibition of translation in all the perturbed classes. Organelle level effects which are independent of major protein synthetic activities or different levels of heat-shock protein production could be the reason for the lack of correlation between percentage inhibition of general protein synthesis and the extent of mitotic delay with respect to the two double-perturbed systems.

Fungal Proteins↗

PubMed1991

Extra corporeal shock wave lithotripsy of bile duct stones: absence of short term complications with the use of very high number of shock waves.

Extracorporeal shock wave lithotripsy (ESWL), generated by the Siemens lithotripter (Lithostar), was used in six patients (two males, four females, aged 28 to 70 years) with large bile duct stones (diameter 16 mm to 30 mm; single in five, multiple in one) in whom routine endoscopic measures had failed. Disintegration of stones was achieved in four patients. The mean number of shocks delivered per patient, at energy levels generated by 19 kv, was 18,267 (range 4200-39,000) over 1 to 8 sessions, with a maximum of 6000 shocks per session. Exacerbation of cholangitis occurred in one patient after stone disintegration. Cutaneous petechiae were noted in four patients. Our report describes the use of a very high number of shock waves in the treatment of bile duct stones, with no appreciable short term complications noted in this small experience. Our initial experience of treating large bile duct stones with ESWL appears encouraging and safe.

Adult↗

PubMedDate not supplied

Enhancement of chemotherapeutic effects with focused shock waves: extracorporeal shock wave chemotherapy (ESWC).

The effects of shock waves in combination with various anti-cancer agents i.e. Bleomycin (BLM), Cisplatin (CDDP) and 5-fluorouracil (5-FU) on tumor cells suspended in media containing these agents were examined. GCIY cells derived from human gastric cancer and LS 174T and SW480 cells derived from human colon cancers were used for in vitro experiments; GCIY and SW480 cells were also transplanted into nude mice for in vivo study. It was only with BLM that enhancement was evident in all three cell lines, with a degree of chemotherapeutic enhancement proportional to the amount of shock wave energy applied. Ladder formation of DNA in GCIY cells was observed only when treated with both BLM and shock waves in combination. When SW480 and GCIY cells transplanted into the backs of nude mice were treated with a combination of intravenously (i.v.) injected BLM and regional exposure to shock waves, a significant enhancement of chemotherapeutic effects was observed in terms of the tumor growth curve.

Animals↗

PubMed2006

Heat shock transcription factor (Hsf)-4b recruits Brg1 during the G1 phase of the cell cycle and regulates the expression of heat shock proteins.

Human brahma-related gene 1(Brg1) is a subunit of the switching/sucrose non-fermenting (SWI/SNF) chromatin-remodeling complex and regulates transcription during cell growth and differentiation and has been found to be mutated in many types of human cancers. Mammalian heat shock factor 1 (Hsf1), which binds conserved sequences on the promoter of the hsp70 gene when cells are exposed to various stress stimuli, utilizes Brg1-SWI/SNF complexes and stimulates transcription in vitro at the level of initiation and elongation. In contrast to the stress-inducibility of Hsf1, in vitro transcribed/translated Hsf4b binds to the heat shock element (HSE) constitutively and loses its ability to bind HSEs following stress. The regulation of Hsf4b transcriptional activity in vivo remains unclear. Here, we present evidence that Hsf4b recruits Brg1 complexes to the promoters of heat shock proteins (HSPs) under physiological growth conditions. Furthermore, in an asynchronous cell population, the association of Hsf4b with Brg1 complexes is regulated in response to activation/inactivation of the extracellular signal regulated protein kinase 1/2 (ERK1/2) signaling pathway. Since Brg1 is also the target of mitogen-activated protein (MAP) kinases and other protein kinases and it is hyperphosphorylated and inactivated during the G2/M phase of the cell cycle, we tested whether the association of Hsf4b with Brg1 complexes is altered during the cell cycle. The results indicate that association of Hsf4b with Brg1 complexes is undetectable during G2/M; however, an Hsf4b interaction with Brg1 complexes is evident at 1-3 h after progression of cells into G1, where chromatin structure is presumed to be more accessible to transcriptional regulatory proteins. At this time, Hsf4b exhibits increased DNA-binding activity and is detectable on promoters of multiple Hsps. To determine the unique role of Hsf4b in stimulating the expression of Hsps during the cell cycle, experiments were conducted with mouse embryo fibroblasts (MEFs) deficient in individual Hsfs. The results indicate that in the absence of Hsf1 and Hsf2, Hsf4b expression in cells leads to increased ability of Hsf4b to bind HSE during G1, leading to enhanced synthesis of inducible Hsp70.

Animals↗

PubMed1996

The transcriptional regulation of heat shock genes: a plethora of heat shock factors and regulatory conditions.

The inducible regulation of heat shock gene transcription is mediated by a family of heat shock factors (HSF) that respond to diverse forms of physiological and environmental stress including elevated temperature, amino acid analogs, heavy metals, oxidative stress, anti-inflammatory drugs, arachidonic acid, and a number of pathophysiological disease states. The vertebrate genome encodes a family of HSFs which are expressed ubiquitously, yet the DNA binding properties of each factor are negatively regulated and activated in response to specific conditions. This chapter will discuss the regulation of the HSF multi-gene family and the role of these transcriptional activators in the inducible expression of genes encoding heat shock proteins and molecular chaperones.

DNA-Binding Proteins↗

PubMed2004

The gene for the heat-shock protein HSP100 is induced by blue light and heat-shock in the fungus Phycomyces blakesleeanus.

We cloned and sequenced the Phycomyces hspA gene. The hspA gene product is a 901-amino-acid protein member of the clpB/HSP100 family. HSP100 proteins are ATPases involved in high-temperature tolerance, proteolysis, and protein disaggregation. Phycomyces HSP100 is composed of a domain presumably involved in protein-protein interactions and two ATP-binding domains. The hspA promoter contains three heat-shock elements that are presumably involved in the activation of hspA after heat-shock. In addition, four short sequences are present in the hspA promoter and in the promoter of the photoinducible genes carB and carRA; and these are candidates as binding sites for light-regulated transcription factors. Blue light can increase transcription of the hspA gene 10-fold, with a threshold of 1 J/m2. The threshold for hspA photoactivation is 10(4) times higher than the thresholds for blue-light regulation of sporangiophore development and photocarotenogenesis, which suggests that there are differences in the photosensory systems for gene photoactivation and mycelial photoresponses. A heat-shock of 30 min at 34 degrees C or 42 degrees C increased hspA gene activity 160-fold. The differences in maximum hspA gene transcription by blue light and heatshock suggest the presence of different regulatory mechanisms.

Adenosine Triphosphatases↗

PubMed1995

Derepression of the activity of genetically engineered heat shock factor causes constitutive synthesis of heat shock proteins and increased thermotolerance in transgenic Arabidopsis.

ATHSF1 is a heat shock transcription factor (HSF) of Arabidopsis that is constitutively expressed but its activity for DNA binding, trimer formation and transcriptional activation of heat shock (hs) genes is repressed at normal temperatures. In this study the functional properties of chimeric HSF-glucuronidase (GUS) fusion proteins were tested. Ectopic expression of HSF-GUS or GUS-HSF in transgenic Arabidopsis plants resulted in a derepression of HSF functions as shown by trimer formation, specific DNA binding, and the constitutive expression of heat shock proteins (HSPs) at normal temperature. A novel GUS activity-staining protocol was used to show the specific binding of trimeric HSF fusion proteins to DNA and following hs, an interaction between chimeric HSF-GUS and authentic HSF proteins. The chimeric HSFs were insensitive to the negative regulation that counteracts activation of the authentic HSF at normal temperature. Heterotrimer complexes were reconstituted in vitro from recombinant ATHSF1 and HSF-GUS proteins expressed in Escherichia coli and using this protocol, the temperature-dependent activation of wt HSF was monitored in vivo and in vitro. Transgenic plants expressing constitutively active HSF-GUS fusion proteins are also constitutive for HSPs. Approximately 20% of the maximum heat-inducible levels of HSP18 were already present at normal temperature. The level of basic thermotolerance was significantly enhanced in these plants. The results indicate that genetic engineering using protein fusion is a very effective means to derepress the activity of an important regulatory protein in plants, that consequently activates a constitutive hs response in the absence of heat stress and eventually alters the thermotolerance phenotype.

Acclimatization↗

PubMed2000

Heat and chemical shock potentiation of glucocorticoid receptor transactivation requires heat shock factor (HSF) activity. Modulation of HSF by vanadate and wortmannin.

Heat shock and other forms of stress increase glucocorticoid receptor (GR) activity in cells, suggesting cross-talk between the heat shock and GR signal pathways. An unresolved question concerning this cross-talk is whether heat shock factor (HSF1) activity is required for this response. We addressed this issue by modulating HSF1 activity with compounds acting by distinct mechanisms: sodium vanadate (SV), an inhibitor of protein phosphatases; and wortmannin, an inhibitor of DNA-dependent protein kinase. Using HSF1- and GR-responsive CAT reporters, we demonstrate that SV inhibits both HSF1 activity and the stress potentiation of GR, while having no effect on the hormone-free GR or HSF1. Paradoxically, SV increased hormone-induced GR activity in the absence of stress. In contrast, wortmannin increased HSF1 activity in stressed cells and had no effect on HSF1 in the absence of stress. Using the pMMTV-CAT reporter containing the negative regulatory element 1 site for DNA-dependent protein kinase, wortmannin was found to increase the GR response. However, in cells expressing a minimal promoter lacking negative regulatory element 1 sites, wortmannin had no effect on the GR in the absence of stress but increased the stress potentiation of GR. Our results show that the mechanism by which GR activity is increased in stressed cells requires intrinsic HSF1 activity.

3T3 Cells↗

PubMed2006

Genome-wide analysis reveals new roles for the activation domains of the Saccharomyces cerevisiae heat shock transcription factor (Hsf1) during the transient heat shock response.

In response to elevated temperatures, cells from many organisms rapidly transcribe a number of mRNAs. In Saccharomyces cerevisiae, this protective response involves two regulatory systems: the heat shock transcription factor (Hsf1) and the Msn2 and Msn4 (Msn2/4) transcription factors. Both systems modulate the induction of specific heat shock genes. However, the contribution of Hsf1, independent of Msn2/4, is only beginning to emerge. To address this question, we constructed an msn2/4 double mutant and used microarrays to elucidate the genome-wide expression program of Hsf1. The data showed that 7.6% of the genome was heat-induced. The up-regulated genes belong to a wide range of functional categories, with a significant increase in the chaperone and metabolism genes. We then focused on the contribution of the activation domains of Hsf1 to the expression profile and extended our analysis to include msn2/4Delta strains deleted for the N-terminal or C-terminal activation domain of Hsf1. Cluster analysis of the heat-induced genes revealed activation domain-specific patterns of expression, with each cluster also showing distinct preferences for functional categories. Computational analysis of the promoters of the induced genes affected by the loss of an activation domain showed a distinct preference for positioning and topology of the Hsf1 binding site. This study provides insight into the important role that both activation domains play for the Hsf1 regulatory system to rapidly and effectively transcribe its regulon in response to heat shock.

DNA-Binding Proteins↗

PubMed2006

Emergency revascularization in patients with cardiogenic shock on admission: a report from the SHOCK trial and registry.

AIMS: To determine clinical correlates and optimal treatment strategy in patients with cardiogenic shock (CS) on admission. METHODS AND RESULTS: In SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? (SHOCK) trial and registry patients with left ventricular (LV) dysfunction (n=1053), CS on admission occurred in 26% of directly admitted patients (n=166/627). Time from myocardial infarction to CS was shorter, initial haemodynamic profile poorer, and aggressive treatment less frequent in CS on admission than in delayed CS patients. CS on admission patients constituted a smaller relative proportion (11%) of the transferred (n=48/426) when compared with the directly admitted cohort (P<0.001). In-hospital mortality was higher (75 vs. 56%; P<0.001) with more rapid death (24-h mortality 40 vs. 17%; P<0.001) in CS on admission than in delayed CS patients. Emergency revascularization reduced in-hospital mortality in CS on admission (60 vs. 82%; P=0.001) and in delayed CS patients similarly (46 vs. 62%; P<0.001; interaction P=0.25). After adjustment for clinical differences, CS on admission was an independent predictor of in-hospital mortality (P=0.008). CONCLUSION: CS on admission patients have a worse outcome but benefit equally from emergency revascularization as delayed CS patients, emphasizing the need for rapid and direct access of CS on admission patients to facilities providing this care.

Aged↗

PubMed1994

Fine structure analyses of the Drosophila and Saccharomyces heat shock factor--heat shock element interactions.

Heat shock genes are activated by the binding of the heat shock transcription factor (HSF) to heat shock elements (HSEs), consisting of arrays of the 5-bp unit NGAAN arranged as inverted repeats. Here, we have investigated the interaction of the 5-bp unit with HSFs of Drosophila and Saccharomyces. Mutations within the conserved, central trinucleotide GAA reduce the relative binding affinity of both HSFs. In addition, the base at position 1 (N1) also influences binding, with a strong preference for an A at this position. Methylation interference initially indicated that HSF contacts A1 in the minor groove, but interacts with the immediately adjacent base G2 in the major groove. Further characterization of this apparently abrupt minor to major groove transition by substitution of A1 with an inosine, shows that HSF contacts A1 in the major groove. We offer an explanation for this apparent contradiction and propose that HSF recognizes the HSE primarily through contacts within the major groove of the DNA helix. Finally, based on these observations and a re-evaluation of the base frequencies and criteria for consensus sequence assignment, we propose that the sequence AGAAN more accurately represents the consensus HSE motif.

Animals↗

PubMed2000

Recombinant humanized monoclonal antibody against CD18 (rhuMAb CD18) in traumatic hemorrhagic shock: results of a phase II clinical trial. Traumatic Shock Group.

BACKGROUND: Activated neutrophils have been shown to play a pivotal role in resuscitation injury after traumatic hemorrhagic shock. Blocking the adhesion of neutrophils with a recombinant humanized monoclonal antibody against CD18 (rhuMAb CD18) may reduce resuscitation injury but increase the risk of infection. This was a dose-finding phase II study to determine safety, pharmacokinetics, pharmacodynamics, and clinical outcome parameters for additional studies. METHODS: This was a prospective, placebo-controlled, randomized (3:1), double-blind phase II trial enrolling 116 blunt and penetrating trauma patients from 14 trauma centers over a 9-month period. Patients with hypotension (blood pressure < or =90 mm Hg) from hemorrhagic shock were given a single intravenous dose of rhuMAb CD18 or placebo. The three doses tested were 0.5, 1, and 2 mg/kg. The drug was administered within 4 hours of the hypotensive episode and no later than 6 hours from time of injury. Exclusion criteria included head injury resulting in Glasgow Coma Scale score less than 8 or a history of cardiopulmonary resuscitation in the trauma center. An independent Drug Safety and Monitoring Review Board periodically reviewed unblinded data for safety issues and to give approval for dose escalation. RESULTS: Minor and major infection rates in rhuMAb CD18 groups were comparable to placebo. There was no evidence of antibody formation against rhuMAb CD18. Linear PK was observed within the dose range studied. Duration of neutrophil binding was dose-dependent, with 2 mg/kg resulting in greater than 90% neutrophil CD18 receptor saturation for approximately 48 hours. The mortality was 6.7% (2 of 30) in the placebo group, 4.8% (1 of 21) in the 0.5-mg/kg group, 8.5% (4 of 47) in the 1-mg/kg group, and 0% (0 of 18) in the 2-mg/kg group. The study was not powered for efficacy, and none of the efficacy variables demonstrated statistical significance. Favorable trends were seen in the 2-mg/kg group as compared with placebo in median intensive care unit length of stay (5 vs. 9 days) and median time on ventilator (34 vs. 72 hours). CONCLUSIONS: A single 2-mg/kg dose of rhuMAb CD18 maintains greater than 90% saturation of neutrophil CD18 receptors for approximately 48 hours in patients with traumatic hemorrhagic shock undergoing resuscitation. There was no trend toward increased infection. A larger trial is needed to demonstrate the clinical efficacy of rhuMAb CD18, perhaps using more reliable endpoints.

Adult↗