ライフサイエンスコーパス: shock

1 argely resistant to endotoxin-induced septic shock.

2 ced microbial fitness after exposure to heat shock.

3 s a very rare cause of recurrent hypovolemic shock.

4 y-four patients (25.0%) progressed to septic shock.

5 ic neutrophil subset in patients with septic shock.

6 ion plus infection, severe sepsis, or septic shock.

7 echanical circulatory support in cardiogenic shock.

8 l immune collapse syndrome similar to septic shock.

9 rs are involved in the development of septic shock.

10 ng an unexpected negative stimulus, electric shock.

11 a may not be the only factor inducing septic shock.

12 ty in patients with severe sepsis and septic shock.

13 t causes widespread tissue damage and septic shock.

14 as not performed due to risk of anaphylactic shock.

15 of suspected infection and suspected septic shock.

16 ocytes facilitate the pathobiology of septic shock.

17 hed mortality of IL-15 KO mice during septic shock.

18 ssociation with and relevance to cardiogenic shock.

19 eline mortality risk in children with septic shock.

20 s ongoing at the time of death due to septic shock.

21 , and 1.8% (95% CI, 0.8-3.0%; P = 0.001) for shock.

22 ar permeability that may lead to hypovolemic shock.

23 C57Black 6 mice, adult patients with septic shock.

24 use of at least 60% for patients with septic shock.

25 s such as shear stress, DNA damage, and heat shock.

26 alpha1-adrenoceptor expression in endotoxic shock.

27 dification codes for severe sepsis or septic shock.

28 ns is probably critical to outcome in septic shock.

29 for fluid-refractory severe sepsis or septic shock.

30 for absorption and dissipation of mechanical shock.

31 H3 to the stability observed without osmotic shock.

32 with progression of severe sepsis to septic shock.

33 18 hours after induction of murine endotoxic shock.

34 l ligation and puncture or endotoxin-induced shock.

35 host resistance to endotoxin-induced septic shock.

36 key roles in P. euphratica response to salt shock.

37 l ICU patients with severe sepsis and septic shock.

38 eters for risk stratification in cardiogenic shock.

39 eral strategy in cancer patients with septic shock.

40 amic support of newborn and pediatric septic shock.

41 ch as DNA damage, oxidative stress, and heat shock.

42 at determine the endogenous amplification of shocks.

43 reasing association between CSs and electric shocks.

44 propriate shocks, which comprised 38% of all shocks.

45 ge were also associated with appropriate ICD shocks.

46 nterventional study in a rat model of septic shock (128 adult males) to assess the effects of ELA and

47 rapid identification of patients with septic shock, 2) a "resuscitation and stabilization bundle" to

48 Maternal complications included cardiogenic shock (24%), mechanical support (28%), urgent percutaneo

49 The Septic Shock 3.0 definition would have decreased sample size by

50 eived starch, and among patients with septic shock, 68.3% had lactate measured and 64% received norep

51 This is reflected in rates of shock (7 [30.4%] vs 19 [61.3%]; P = .03), need for mecha

52 CRC tissue exposed to hypoxia, induced heat-shock 70-kDa protein-1-like (HSPA1L) expression stabiliz

53 a (038.x), severe sepsis (995.92), or septic shock (785.52), as well as all subsequent hospitalizatio

54 lay, which combines an initial Collisionless Shock Acceleration (CSA) to a boost procured by a TNSA-l

55 these conditions a Low Density Collisionless Shock Acceleration (LDCSA) mechanism is at play, which c

56 observed the signature of the Collisionless Shock Acceleration mechanism, namely quasi-monoenergetic

57 ed by the pSOFA score, and sepsis and septic shock according to the Sepsis-3 definitions.

58 itically ill patients with sepsis and septic shock, acute respiratory distress syndrome, and major tr

59 ion of suckling mice from endotoxin-mediated shock, an outcome that is dependent on the host IFN resp

60 ity rate of 12.1%, and 347 (4.0%) had septic shock and a mortality rate of 32.3%.

61 ning variants motivated aversively with foot shock and appetitively with food.

62 ng fear conditioning and to both the CS with shock and CS without shock during fear recall.

63 Alarm, shock and disbelief were frequently expressed initial re

64 Before, at the end of shock and every 12 hours of resuscitation, datasets comp

65 appear independent of the well-studied heat shock and insulin signaling pathways, indicating that th

66 zed that SAED would reduce the time to first shock and lead to higher rates of cardioversion and surv

67 acute coronary syndrome-related cardiogenic shock and may help therapeutic decision making in these

68 ibiotics and enhance survival following heat shock and membrane stress.

69 n transplant patients, complicated by septic shock and multiple organ failure, including acute renal

70 how alcohol intoxication impacts hemorrhagic shock and resuscitation-induced microvascular leakage us

71 put in an adult porcine model of hemorrhagic shock and resuscitation.

72 She lost consciousness in shock and sustained life-threatening injuries.

73 in a mouse model of resuscitated hemorrhagic shock and tissue trauma (HS/T).

74 dy we selected patients admitted with septic shock and treated for more than 4 days from a prospectiv

75 authors analyzed the long-term incidence of shocks and complications.

76 bility of quasicrystals during high-pressure shocks and for the interpretation of the phase assemblag

77 rporeal membrane oxygenation for cardiogenic shock, and 3) extracorporeal cardiopulmonary resuscitati

78 elevation myocardial infarction, cardiogenic shock, and multivessel disease, and were associated with

79 sisting of an auditory CS paired with a foot shock, and the auditory CS was re-presented during subse

80 ation of neutrophils in patients with septic shock, and those with a high percentage of olfactomedin-

81 ient to dampen the mismatches, which we call shocks, and they may remain and grow.

82 T and amygdala may regulate responses during shock anticipation and actual shock confrontation.

83 we show that in each sample when going from shock anticipation to the moment of shock confrontation

84 amygdala, but not BNST, hyperactivity during shock anticipation.

85 rate of successful cardioversion after first shock (AOR, 0.73; 95% CI, 0.51-1.06; P=0.10).

86 Sepsis and septic shock are common and, at times, fatal in pediatrics.

87 ardia (heart rate, < 80 beats/min) in septic shock are unknown.

88 However, these shocks are essentially eliminated by the assimilation of

89 o study the properties of smallest exogenous shocks as a function of the parameters that determine th

90 t interfere with the proper encoding of tone-shock associations that eventually lead to enhanced cue-

91 More patients in the control group had shock at enrollment (14 vs 3 patients).

92 5 vs 44-year-old; p = 0.01), had more severe shock (base deficit, -9.2 vs -5.5; p = 0.005), greater o

93 ess response resembling the response to heat shock, but the transcriptional basis of this response re

94 sepsis but enables the development of septic shock by maintaining NK cell numbers and integrity.

95 flammatory cytokine production during septic shock caused by cecal ligation and puncture or endotoxin

96 IL-15 SA treatment also exacerbated septic shock caused by cecal ligation and puncture when given a

97 xosomes harvested after T/HS, but not before shock, caused recruitment of inflammatory cells in the l

98 s suggests that in patients with cardiogenic shock complicating ST-segment-elevation myocardial infar

99 y recently been applied to plasticity during shock compression and have yet to provide detailed insig

100 In this Article, the shock compression of analogue precursor chondrite materi

101 ntalum is also a material for which previous shock compression simulations and experiments have provi

102 hitlockite transformation into merrillite by shock-compression levels relevant to meteorites, includi

103 ed with GroEL(SR) under both normal and heat-shock conditions.

104 ing from shock anticipation to the moment of shock confrontation neural activity shifted from a regio

105 sponses during shock anticipation and actual shock confrontation.

106 continued to display accurate memory of the shock-context association.

107 Strategies to reduce shocks could result in cost savings.

108 outcomes of patients meeting Sepsis-3 septic shock criteria versus patients meeting the "old" (1991)

109 Mortality in cardiogenic shock (CS) remains high.

110 infarction (AMI) complicated by cardiogenic shock (CS) remains high.

111 We find that hyperosmotic shock decreases SH3 stability in cells, consistent with

112 shock event was defined as >/=1 spontaneous shocks delivered by an implanted device.

113 massively transfused patients in hemorrhagic shock demonstrated SD physiology on admission.

114 refractory arrhythmic storm and cardiogenic shock despite optimal medical therapy were implanted wit

115 The foot-shock-driven excitation within the LHb requires glutamat

116 skin conductance responses to the CS without shock during fear conditioning and to both the CS with s

117 and to both the CS with shock and CS without shock during fear recall.

118 talization, 149 (65.0%) had sepsis or septic shock during their course.

119 A shock event was defined as >/=1 spontaneous shocks deliv

120 ental claims databases linked to adjudicated shock events from remote monitoring data.

121 Shock events were adjudicated and classified as inapprop

122 bserve that aversive stimuli, including foot-shocks, excite LHb neurons and promote escape behaviors

123 eralization of SCRs and explicit measures of shock expectancy.

124 nse pathways, such as those mediated by heat shock factor 1 (HSF1) and nuclear factor-erythroid 2 p45

125 we demonstrated that the modulation of heat-shock factor-1 by knockdown in nCPCs or overexpression i

126 One leading candidate pathway is heat-shock factor-1, potentially affecting 8 identified pathw

127 ary bodies, interpreting the significance of shock features in minerals and for using them as diagnos

128 ment initiative for severe sepsis and septic shock focused on the resuscitation bundle on 90-day mort

129 ents presenting with severe sepsis or septic shock from 2011 to 2013.

130 rate of successful cardioversion after first shock (from 12.3% to 13.8%; P=0.13).

131 e oxygenation, if available, when refractory shock has a significant cardiogenic component (2D), and

132 , the prognosis of patients with cardiogenic shock has remained poor.

133 tilization (HCU) and expenditures related to shocks have not been quantified.

134 rended toward a lower risk of an appropriate shock (hazard ratio, 0.61; 95% CI, 0.33-1.12; P=0.108).

135 g effective signals, including hypoxia, cold shock, heat shock, oxidative stress, exercise-induced ad

136 no benefit from EGDT for patients with worse shock (higher serum lactate level, combined hypotension

137 can lead to rapid reversal of hypoxemia and shock; however, it can also result in varying degrees of

138 jury was 2.212 (95% CI: 1.334-3.667), septic shock (HR = 1.895, 95% CI: 1.081-3.323) and model for en

139 and dysfunction associated with hemorrhagic shock (HS) in the rat.

140 g a transgenic fish model that exhibits heat-shock (HS) inducible impaired heart regeneration.

141 Remarkably, heat shock (HS)-induced RCD, but not reproductive or vascular

142 de(LPS)-induced shock (LPSS) and hemorrhagic shock (HS).

143 pria TH2 cells, mast cells, and eosinophils, shock (hypothermia), mast cell degranulation (increased

144 y in patients with CS, derived from the IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock)

145 Validation in the IABP-SHOCK II registry population showed good discrimination

146 The IABP-SHOCK II risk score can be easily calculated in daily cl

147 plasma leakage that results in hypovolaemic shock in a small proportion of individuals.

148 sublethal doses of LPS induced hypoglycemic shock in mice within 1-2 h.

149 eroxia during resuscitation from hemorrhagic shock in swine with preexisting coronary artery disease

150 otects from excessive inflammation and acute shock in vivo.

151 implantable cardioverter-defibrillator (ICD) shocks in small series of patients with structural heart

152 patients (8.7%) experienced 37 inappropriate shocks (incidence rate 0.9 per 100 person-years).

153 In human plasma, osmotic shock increased cBIN1 detection by enzyme-linked immunos

154 or HSF1 in the induction of a subset of heat shock-induced readthrough transcripts.

155 After shocks, inpatient cardiovascular procedures were common,

156 Cardiogenic shock is a high-acuity, potentially complex, and hemodyn

157 Fluid resuscitation following hemorrhagic shock is often problematic, with development of prolonge

158 Plasma from an acute attack induced a shock-like syndrome when injected into rats.

159 ng how rock-forming minerals transform under shock loading is critical for modeling collisions betwee

160 ull mutant, chromatin decondensation at heat shock loci is unaffected in the absence of JIL-1 as well

161 dels of both lipopolysaccharide(LPS)-induced shock (LPSS) and hemorrhagic shock (HS).

162 rol were older, with a greater prevalence of shock, major organ dysfunction, bacteremia, inflammatory

163 ictors of in-hospital death were cardiogenic shock (odds ratio, 6.01; 95% confidence interval, 4.19-8

164 A sub-lethal hydrostatic pressure (HP) shock of approximately 100 MPa elicits a RecA-dependent

165 her research should examine whether repeated shocks of this kind lead to substantial increases in the

166 meeting the "old" (1991) criteria of septic shock only.

167 Patients with cardiogenic shock or cardiac arrest on presentation were excluded.

168 ongevity of animals exposed to hormetic heat shock or HSF-1 overexpression.

169 lantation profile of 1 (critical cardiogenic shock) or 2 (progressive decline) were assessed with the

170 en cardiac arrest, appropriate defibrillator shock, or death in either group.

171 signals, including hypoxia, cold shock, heat shock, oxidative stress, exercise-induced adaptation, ca

172 reatment group (p = 0.02) and independent of shock (p = 0.04).

173 utive sample of all severe sepsis and septic shock patients (defined: infection, >/= 2 systemic infla

174 resuscitation provided to sepsis and septic shock patients at initial presentation and 2) determine

175 Adult sepsis and septic shock patients captured in a prospective quality improve

176 the distribution of extreme states within a shocked powder mixture, and represents the first mesosco

177 hrough an action, and yoked extinction, with shock presentation matched to the active condition, but

178 tic indicators of impact conditions, such as shock pressure.

179 l changes in microcrystals of ZIF-8 at lower shock pressures ( approximately 2.5 GPa), and amorphizat

180 fluorescence microscopy to investigate Heat Shock Protein (HSP) gene conformation and 3D nuclear org

181 The 90-kDa heat shock protein (Hsp90) chaperone system affects the accum

182 The 90-kDa heat shock protein (Hsp90) is a widely conserved and ubiquito

183 displayed improved binding to the small heat shock protein (HspB8) in ischemic skeletal muscle cells

184 Clustered class-I small heat-shock protein (sHSP) chaperone genes, SlHSP17.6, SlHSP20

185 a transient increase of phosphorylated heat shock protein 27, p38 mitogen-activated protein kinase,

186 se (mtUPR) as measured by expression of heat shock protein 60, Clp protease, and Lon peptidase 1.

187 P. aeruginosa GroEL, a homolog of heat shock protein 60, was identified as one of the factors r

188 he pharmacochaperone noribogaine or the heat shock protein 70 (HSP70) inhibitor pifithrin-mu such tha

189 Stress-inducible heat shock protein 70 (hsp70) interacts with superoxide dismu

190 ith ATP-dependent chaperones, including heat shock protein 70 (Hsp70).

191 RNAs, including Cdg7_FLc_0990, involved heat-shock protein 70-mediated nuclear importing mechanism.

192 ntrol DCs, covalently bind to chaperone heat shock protein 70.

193 f the auxin co-receptor TIR1, involving HEAT SHOCK PROTEIN 90 (HSP90) [9].

194 ress this need, we explored the role of heat-shock protein 90 (Hsp90) in opioid-induced MOR signaling

195 We found that inhibitors of heat shock protein 90 (HSP90) induced apoptosis in BL cells i

196 Heat shock protein 90 (HSP90) inhibition is an attractive str

197 Heat shock protein 90 (Hsp90) is an essential eukaryotic mole

198 and/or K(+) flux and the activation of heat shock protein 90 (HSP90), a protein required for the act

199 e, we chose to focus on an inhibitor of heat shock protein 90 beta (HSP90beta).

200 rogenase, alpha-enolase, filamin-A, and heat shock protein 90, were identified in samples of apical p

201 Although well-studied cold-shock protein A (CspA) family members are induced and fu

202 The heat shock protein also seems to regulate the cross-talk betw

203 tory use of an evolutionarily conserved heat shock protein and present a distinctive mechanism for ho

204 erotonin N-acetyltransferase and 14-3-3:heat shock protein beta-6 complexes revealed similarities in

205 romosome 19 that fuses part of the DnaJ heat shock protein family (Hsp40) member B1 gene (DNAJB1) to

206 Mutations in the small heat shock protein Hsp27, encoded by the HSPB1 gene, have bee

207 Furthermore, mRNA for the major heat shock protein Hsp70 is transcribed at robust levels in b

208 ued with therapeutic application of the heat shock protein in vivo.

209 rotein, fibrin degradation product, and heat shock protein-70 improved risk reclassification.

210 ions promoting protein unfolding, small heat shock proteins (sHsps) prevent the irreversible aggregat

211 The interaction between the Heat Shock Proteins 70 and 40 is at the core of the ATPase re

212 Cellular protein homeostasis depends on heat shock proteins 70 kDa (Hsp70s), a class of ubiquitous an

213 the mechanisms by which mRNAs encoding cold shock proteins escape cooling-induced translational repr

214 Astrocytic exosomes carry heat shock proteins that can reduce the cellular toxicity of

215 n of mitochondrial matrix proteases and heat shock proteins was initially described.

216 transcription factors, chaperones, and heat shock proteins) were highly expressed in Namikonga.

217 A strong thermal shock, provided by convection at 60 degrees followed by

218 y evaluating complications and inappropriate shock rate.

219 In this study, we report a new shock recovery experiment aimed at synthesizing decagona

220 sed to analyze variables associated with ICD shock recurrence and mortality after CSD.

221 nd was randomized on subsequently developing shock-refractory VF/VT.

222 k = 1.09 [1.00-1.18]; p = 0.04), presence of shock (relative risk = 1.007 [1.002-1.013]; p = 0.006),

223 Mortality from cardiogenic shock remains unacceptably high despite early coronary r

224 Surprisingly, we found that heat shock represses multiple immune genes in the abdomen and

225 pment of severe IgE-mediated hypovolemia and shock required VE-restricted ABL1 expression.

226 traint blocks have significant effect on the shock-resistibility.

227 and evaluated their ability to suppress heat shock response (HSR) in MM cells.

228 The heat shock response (HSR) is a mechanism to cope with proteot

229 IHSF115 was employed to probe the human heat shock response at the transcriptome level.

230 ssion of molecular chaperones and other heat shock response genes.

231 D simulations discussed here investigate the shock response of Al microstructures comprising of grain

232 similar stress responses, including the heat shock response.

233 Outcomes included mortality, frequency of shock reversal, acquisition of nosocomial infections, an

234 siology, causes, and outcomes of cardiogenic shock; reviews contemporary best medical, surgical, mech

235 hallenges, possibly at the cost of endotoxic shock risk.

236 sheet of paper, and demonstrate its use as a shock sensor for bioactive compounds (e.g. formaldehyde)

237 arly Management Bundle, Severe Sepsis/Septic Shock (SEP-1) performance measure to the Hospital Inpati

238 Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria in the emergency department se

239 Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) uses the Sequential Organ Failure Asses

240 Advancing age, shock severity, and persistent organ dysfunction are pre

241 cipients by mechanism of injury, prehospital shock, severity of limb amputation, head injury, and tor

242 the early management of severe sepsis/septic shock (SS/SS) in Emergency Department (ED) has yet to be

243 ents within 12 hours of severe sepsis/septic shock (SS/SS), and at set intervals out to 28 days, and

244 During sepsis and shock states, mitochondrial dysfunction occurs.

245 statement of cocaine seeking induced by foot-shock stress, but in the absence of continued global ele

246 Applying powerful laser-driven shocks (stresses of up to one-third million atmospheres,

247 the SAED implementation on the time to first shock, successful cardioversion, and patient outcomes wa

248 This scientific statement on cardiogenic shock summarizes the epidemiology, pathophysiology, caus

249 erase II occupancy in DoG regions after heat shock, supporting our findings.

250 ng dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) occur.

251 patients within 24 hours of onset of dengue shock syndrome (DSS), and from healthy controls.

252 ses dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS).

253 Toxic shock syndrome (TSS) is caused by staphylococcal and str

254 sometimes administered for presumptive toxic shock syndrome (TSS), but its frequency of use and effic

255 fever, dengue hemorrhagic fever, and dengue shock syndrome and is endemic to tropical and subtropica

256 -Valentine Leukocidin toxin (PVL), and toxic shock syndrome toxin-1 (tst) genes.

257 phases and discuss the implications of this shock synthesis for the stability of quasicrystals durin

258 s, secreted into ML after trauma/hemorrhagic shock (T/HS) have the potential to activate immune cells

259 3 days at full dose in patients with septic shock that is not responsive to fluid and moderate- to h

260 n to find the scenario of smallest exogenous shock that, should it occur, would lead to a given final

261 treatment of patients with sepsis and septic shock, that is, moxifloxacin, meropenem, and piperacilli

262 acute myocardial infarction with cardiogenic shock, the 30-day risk of a composite of death or severe

263 When combined with NO2(-) shock, this prolonged the duration over which insufficie

264 therapy (EGDT) reduced mortality from septic shock, three multicenter trials (ProCESS, ARISE, and Pro

265 nce, in which participants could prevent the shock through an action, and yoked extinction, with shoc

266 th fragile couplings that amplify even small shocks, thus preventing functionality.

267 mammary cells at different times after serum shock to study how time of day shifts drug metabolism in

268 ons drastically impaired the ability of foot shock to suppress operant responding for food.

269 Graded shocks to the solitary tract (ST) always (93%) triggered

270 n folding and pro-survival machinery by heat shock transcription factor 1 (HSF1) ameliorates biochemi

271 We investigated the role that the heat shock transcription factor HSF-1 played in determining a

272 nal response is mediated by a family of heat-shock transcription factors.

273 d 90-day mortality in Vasopressin and Septic Shock Trial in lactate subgroups.

274 II (Intraaortic Balloon Pump in Cardiogenic Shock) trial.

275 d by the formation of an ion pair created by shock-triggered proton transfer from phenol to PVP.

276 ate, and HCU and expenditures, stratified by shock type, were quantified.

277 t patients with NF and vasopressor-dependent shock undergoing surgical debridement from 2010 to 2014

278 gressively increased risk of appropriate ICD shocks until >/=98% RVP.

279 group (the most common being sepsis, septic shock, viral sepsis, and pneumonia).

280 Refractory hypotensive shock was fatal in 55 of 115 patients treated with angio

281 Hemorrhagic shock was induced in rats by withdrawing 60% of the bloo

282 plications as energy absorbing materials for shock wave energy mitigation due to their nanoporosity.

283 MOFs may prove useful in the dissipation of shock wave energy through large structural changes (free

284 Pressure-driven shock waves in solid materials can cause extreme damage

285 owever, the biomolecular mechanisms by which shock waves interact with diseased and healthy cellular

286 The 1- and 5-year rates of appropriate shock were 5.8% and 13.5%, respectively.

287 ents from 5 days to 18 years old with septic shock were enrolled.

288 ation myocardial infarction, and cardiogenic shock were included.

289 after conditioning and responsivity to foot shock were unaffected by optogenetic silencing.

290 res related to appropriate and inappropriate shocks were not significantly different.

291 IL-15 SA treatment amplified endotoxin shock, which was prevented by NK cell or IFN-gamma deple

292 es was substantial, even after inappropriate shocks, which comprised 38% of all shocks.

293 ure to the threat of unpredictable, aversive shocks while undergoing magnetoencephalography.

294 eriods of safety and threat of unpredictable shocks while we recorded brain activity with fMRI.

295 edical and surgical ICU patients with septic shock who received vasopressin infusion added to at leas

296 meeting criteria for severe sepsis or septic shock who were admitted to the ICU from the emergency de

297 Patients diagnosed for septic shock within the first 48 hours of ICU admission were in

298 Although the proportion of patients shocked within 2 minutes of arrival increased during the

299 ear memory by receiving mild footshocks in a shock zone on a track, we analyzed place cells when the

300 memory retrieval behavior: avoidance of the shock zone.