ライフサイエンスコーパス: shock

1 outcomes (eg, stroke, bleeding, cardiogenic shock).

2 tential to cause fatal hemorrhagic fever and shock.

3 believe, represents the true onset of septic shock.

4 ment abolished the protective effect of heat shock.

5 ity in children with severe sepsis or septic shock.

6 6, 24, 48, 72, and 96 hours in patients with shock.

7 btained from three large databases of septic shock.

8 e hypoxic respiratory failure and vasoplegic shock.

9 e-threatening conditions such as hemorrhagic shock.

10 identified as a potential therapy for septic shock.

11 re more susceptible to LPS-induced endotoxic shock.

12 28% of children with severe sepsis or septic shock.

13 ne vs placebo for adult patients with septic shock.

14 on for refractory postcardiotomy cardiogenic shock.

15 ldren encountering community-acquired septic shock.

16 to external stimuli including odor and body shock.

17 vere abdominal pain, cardiac dysfunction and shock.

18 wed for the development of sepsis and septic shock.

19 otic administration for patients with septic shock.

20 culatory support in cardiogenic and/or mixed shock.

21 factors and post-traumatic sepsis and septic shock.

22 e 2: 54 +/- 20), 53 (54%) experienced septic shock.

23 g to acute respiratory distress syndrome and shock.

24 phagocytic lymphohistiocytosis, and cytokine shock.

25 l clearance in the juvenile host with septic shock.

26 g risk of transition from sepsis into septic shock.

27 at closing the CO2 gap improves mortality in shock.

28 cue signaled when a lever press would avoid shock.

29 rction, multivessel disease, and cardiogenic shock.

30 O) is increasingly used to treat cardiogenic shock.

31 adverse outcomes including sepsis and septic shock.

32 ry end points included death and appropriate shocks.

33 aine exclusively, or repeatedly self-inflict shocks.

34 s the radiation models invoking relativistic shocks.

35 vice-related complications and inappropriate shocks.

36 llin and Outcome in Severe Sepsis and Septic Shock-1) enrolled 583 septic patients.

37 2.53 (2.49-2.56); and severe sepsis without shock, 2.48 (2.45-2.51).

38 dration (45.4%), sepsis (41.1%), cardiogenic shock (20.9%), and diabetic ketoacidosis (16%).

39 odification code for severe sepsis or septic shock; 3,021 of these patients (28%) had an immunocompro

40 te kidney injury (63%), transaminitis (31%), shock (31%), acute respiratory distress syndrome (25%),

41 Three months following septic shock, 346 of 389 subjects (88.9%) were alive and 43 of

42 stly complications were postoperative septic shock (4.0-fold, 95% CI 3.58-4.43) renal insufficiency/f

43 t the characteristic) are as follows: septic shock, 7.27 (7.19-7.35); metastatic cancer and acute leu

44 e signaling that requires extracellular heat shock 70-kDa protein (HSP70).

45 alosin-containing protein/p97 (VCP) and heat shock 70-kDa protein 8 (HSPA8).

46 ere end of the KD spectrum, with cardiogenic shock a common presentation together with other features

47 fear learning, the association of a cue and shock across an empty trace interval of several seconds

48 otein C and Corticosteroids for Human Septic Shock, adjunctive hydrocortisone therapy showed a 90-day

49 In patients with shock after acute myocardial infarction (AMI), the optim

50 nalysis of post-cardiac arrest patients with shock after AMI randomized in the Neuroprotect (Neuropro

51 s of acute myocardial infarction-cardiogenic shock (AMI-CS) in young adults.

52 e of acute myocardial infarction-cardiogenic shock (AMI-CS).

53 tment in Critically Ill Patients with Septic Shock and Activated Protein C and Corticosteroids for Hu

54 n of DMF protects against lipopolysaccharide shock and alleviates familial Mediterranean fever and ex

55 achycardia (VT) in patients with cardiogenic shock and concomitant VT refractory to antiarrhythmic dr

56 hen analyze plasma from patients with septic shock and find that increasing levels of IL-6 and bla(TE

57 tment in Critically Ill Patients with Septic Shock and hydrocortisone at a 50 mg IV bolus every 6 hr

58 activation in vivo under ART.IMPORTANCE The "shock and kill" HIV cure strategy attempts to reverse an

59 hose that reactivate the latent virus (e.g., shock and kill) would be detrimental to astrocyte functi

60 equently occurs in patients with cardiogenic shock and may aggravate shock severity and organ failure

61 d flow is rapidly altered during circulatory shock and may remain altered despite apparent systemic h

62 regulation hypersensitizes parasites to heat shock and PI3K inhibitors.

63 e durvalumab plus tremelimumab group (septic shock and pneumonitis), and one (<1%) patient in the che

64 in one patient in the placebo group (septic shock and pulmonary oedema) and one patient in the ripre

65 Patients with septic shock and S. aureus bacteremia admitted directly from th

66 r support among critically ill patients with shock and to determine whether such relative hypotension

67 ngers-Lactate over 30 min) for management of shock and/or hypoperfusion within 12h of cardiac surgery

68 imination between a context paired with foot shocks and a different context never paired with foot sh

69 ons are involved in the response to 'genomic shock' and environmental adaptation during polyploid for

70 tment in Critically Ill Patients with Septic Shock) and $30,911 (Activated Protein C and Corticostero

71 n (88%) (nine cardiac arrest; 13 cardiogenic shock) and three had venovenous extracorporeal membrane

72 31% received mechanical ventilation, 19% had shock, and 588 (3.1%) died during their hospitalization.

73 y score 33); 33% developed sepsis, 6% septic shock, and in-hospital mortality was 14%.

74 LPS can cause death as a result of septic shock, and its lipid A core is the target of polymyxin a

75 agocytic lymphohistiocytosis, sepsis, septic shock, and other conditions were distinctly different, w

76 ials were performed in the setting of septic shock, and the most frequent comparator was a combinatio

77 RAs that enhance the activities of multiple "shock-and-kill" agents, which in turn may inform ongoing

78 The "shock-and-kill" human immunodeficiency virus type 1 (HIV

79 The "shock-and-kill" pharmacological ap-proach aims to reacti

80 oided cost was multiplied by expected septic shock annual incidence.

81 ritically ill patients with sepsis or septic shock are at an increased risk of death.

82 nclusions: Vasopressor-treated patients with shock are often exposed to a significant degree and dura

83 ) were defined as a composite of cardiogenic shock, arrest, complete heart block, and cardiac death.

84 es in patients with severe sepsis and septic shock as a result of the full implementation of the Affo

85 hole responded similarly for both reward and shock, as well as for cues that predicted their occurren

86 known mechanisms of Hippo regulation by heat shock, as well as physiological functions of YAP, in the

87 ntilated, and 42% in severe sepsis or septic shock at infection onset.

88 ence interval] were IEAT (2.41 [1.19-4.91]), shock at onset (4.62 [2.49-8.56]), and pneumonia (3.01 [

89 of HAT therapy among U.S. adults with septic shock before and after study publication and to compare

90 g intensive care and/or patients with septic shock), blending together mortality estimates from patie

91 . coli proliferation was exacerbated by heat shock but was nearly eliminated in a ClpB-deficient E. c

92 % CI, 1.30-3.82; p = 0.004) in patients with shock, but only those from medical and surgical ICUs.

93 Cardiogenic shock can occur due to acute ischaemic or non-ischaemic

94 entially limiting use of TRI (renal failure, shock, cardiac arrest, and mechanical circulatory suppor

95 ost common cardiovascular complications were shock, cardiac arrhythmias, pericardial effusion, and co

96 contrast, glucose starvation or hyperosmotic shock causes cell shrinking, which results in membrane s

97 owed significantly altered responses to heat shock challenge.

98 was associated with up-regulation of 24 heat shock chaperones involved in protein folding and with th

99 of long-term balancing selection in the heat-shock co-chaperone sacsin We conducted a genome-wide ass

100 tive identification of HSP70 and 71 kDa heat shock cognate (HSC70) clients using a ubiquitin-mediated

101 HSCB (heat shock cognate B), which encodes a mitochondrial cochaper

102 drial cochaperone, also known as HSC20 (heat shock cognate protein 20), is the partner of mitochondri

103 mperature) or dynamically by laser-generated shock compression (up to 130 GPa and 6,000 K along the M

104 s of a tone coterminating with a periorbital shock (conditioning) or trials in which these stimuli we

105 lying disease, the management of cardiogenic shock consists of vasopressors and inotropes; however, t

106 Based on SCR, both groups generalized the shock contingency to the reinforced conceptual category,

107 en excited onset, daily repetition of lesser shocks could also bring on insanity.

108 g the management and outcomes of cardiogenic shock (CS).

109 esicle size distribution testifies to a post-shock decompression that induced melting and extensive v

110 Frequency of inappropriate shocks decreased over follow-up, likely reflecting stand

111 cell ensemble stability, demonstrating that shock delivery induces several days of high fear and low

112 ly PCI Versus Multivessel PCI in Cardiogenic Shock) demonstrated superior outcome for culprit-lesion-

113 (3%), and 1 (1%) patients in the fixed-dose, shock-dependent, and no hydrocortisone groups, respectiv

114 s' most recent presidential voting (plus new shocks); earlier history does not matter.

115 In this article, we use shock electrodialysis to selectively, continuously, and

116 Factor 1 (HSF1) that activates HSR, and heat shock elements (HSEs), the binding sites for HSF1 - betw

117 ur resuscitation in 688 patients with septic shock enrolled in the ProCESS trial.

118 ransformation from graphite during an impact shock event characterized by peak pressures possibly as

119 Lungs from mice undergoing hemorrhagic shock exhibited a significant increase in miR-19b and a

120 ed transcriptional program regulated by heat shock factor 1 (Hsf1) in eukaryotic cells.

121 ted in vitro that active RhoC increased heat shock factor 1 (HSF1) phosphorylation, which induced the

122 tegrity of two crucial HSR regulators - Heat Shock Factor 1 (HSF1) that activates HSR, and heat shock

123 The severity of cardiogenic shock following asystolic cardiac arrest is dependent on

124 Cardiogenic shock following cardiopulmonary resuscitation for sudden

125 aquatic organisms such as zebrafish, osmotic shock following injury is believed to be an early and po

126 rrest, and aborted SCD, that is, appropriate shock following primary prevention implantable cardiover

127 taken before ICD implantation to prevent ICD shocks for VT) and deferred ablation after 3 ICD shocks

128 ks for VT) and deferred ablation after 3 ICD shocks for VT.

129 The 18-month all-cause shock-free rate was 90.6% (lower confidence limit, 89.0%

130 The initial diagnosis was characterized by shock, grief, and "devastation" for most parents.

131 their occurrence (i.e., reward > neutral and shock > neutral; attention).

132 The combination of shock heating and nonintrusive laser detection provides

133 kthroughs in typhoid control nor any chaotic shocks, history suggests that we should expect typhoid e

134 reflected outcome identity (i.e., reward or shock); however, the population of neurons as a whole re

135 scriptional activation occurring during heat shock (HS) induction is associated with the generation o

136 ncluding major trauma, burns, or hemorrhagic shock (HS).

137 dysfunction, and received more inappropriate shocks (IAS) than in typical transvenous ICD trials.

138 e that metabolic derangement due to advanced shock in critically injured patients leads to the pulmon

139 activation of a single glomerulus with foot shock in mice induces freezing to light stimulation alon

140 alpha and IFN-gamma caused a lethal cytokine shock in mice that mirrors the tissue damage and inflamm

141 d the role of caspase-11 in mediating septic shock in response to lethal doses of lipopolysaccharide

142 2 (P2) is critical for LPS-induced endotoxic shock in wild-type mice.

143 Inappropriate ICD shocks in 39 patients occurred most commonly <5 years af

144 1 ICD complication, including inappropriate shocks in 42 (25.5%) patients and lead dysfunction in 36

145 We present a study on the shock-induced collapse of spherical cavities in a solid

146 e endothelial cell phenotype (s) that causes Shock-Induced Endotheliopathy in trauma.

147 A minimum of 4 shock-induced endotheliopathy phenotypes were identified

148 II is rapidly released from pausing at heat shock-induced genes, while most genes are paused and tra

149 targeting signaling pathways of the osmotic shock inducer sorbitol, we could largely rule out the st

150 Heat shock induces a conserved transcriptional program regula

151 Septicemia with septic shock is the most common cause of death, with mortality

152 The pathophysiology of this shock is unclear, and effective therapies for improving

153 targeted or global attacks; extinctions; or shocks is vital to the survival of the network itself, a

154 HIV infection, diarrhea, pneumonia, shock, lack of appetite, and lower WHZ are independent p

155 eutron stars or black holes) or relativistic shocks launched from such objects have been much debated

156 ive care units in 14 centers for cardiogenic shock, left ventricular dysfunction, and severe inflamma

157 volunteers and 70 patients with circulatory shock (< 12 hr duration), defined as the need for vasopr

158 d prognosis of acute ischemic stroke, septic shock, lung injuries, insulin resistance in diabetic pat

159 cardiac function, reduced myocardial damage, shock, lung injury and improved survival independent of

160 We, therefore, hypothesized that, heat shock may also be especially toxic to myeloma cells by c

161 Weather shocks may exacerbate vulnerabilities among women in sub

162 ilicates in NWA 7983 record a high degree of shock metamorphism.

163 e and vasopressor duration for patients with shock.Methods: We performed a retrospective cohort study

164 rambucil plus obinutuzumab group (n=1 septic shock, n=1 metastatic skin squamous carcinoma).

165 outcomes among critically ill patients with shock.Objectives: To investigate the magnitude of relati

166 io, 1.23; 95% CI, 0.89 to 1.70); appropriate shocks occurred in 83 and 57 patients, respectively (haz

167 Postcardiotomy cardiogenic shock occurs in 2-6% of patients undergoing cardiac surg

168 e also characterize the long-term effects of shock on place cell ensemble stability, demonstrating th

169 The effect of heat shock on YAP is dominant to other signals known to modul

170 terval [CI], 2.3-202.8; P = .008) and septic shock (OR, 11.9; 95% CI, 4.2-34.1; P < .001) were indepe

171 age admitted for heart failure, cardiogenic shock, or LVAD implantation from 2012 to 2015.

172 avlovian task that predicted whether reward, shock, or nothing would be delivered to the rat being re

173 ioning, despite an equivalent number of tone-shock pairings.

174 les from 10 healthy volunteers and 20 septic shock patients stratified using human leukocyte antigen-

175 lthy volunteers, intermediate mHLA-DR septic shock patients, and low mHLA-DR septic shock patients.

176 eptic shock patients, and low mHLA-DR septic shock patients.

177 ly PCI Versus Multivessel PCI in Cardiogenic Shock), patients with CS complicating acute myocardial i

178 otein C and Corticosteroids for Human Septic Shock) per patient.

179 tale of privilege, hardship, discrimination, shocking perseverance, and grand adventure.

180 9 with nonanterior STEMI without cardiogenic shock, PPCI offered a 0.4% absolute mortality benefit ov

181 s with presumptive COVID-19 with cardiogenic shock, PPCI offered substantial mortality benefit to pat

182 The heat-inducible activity of heat-shock promoters from several SfHsp genes was tested in S

183 have a differential sensitivity to hypotonic shock proportional to their size.

184 Here, we show that the heat-shock protease FtsH is generally required for growth arr

185 nd overlaps functionally with the other heat-shock protease-encoding genes hslVU, lon, and clpXP to p

186 Systematic deletion of the heat-shock protease-encoding genes reveals that the proteases

187 uting to PIC assembly and expression of Heat Shock Protein (HSP) genes.

188 The molecular chaperone 90-kDa heat-shock protein (Hsp90) assists the late-stage folding and

189 ing the surface presented LAP receptor, heat shock protein 60 and ameliorates the Lm-induced intestin

190 nes, such as those that are part of the heat shock protein 70 (Hsp70) family of proteins that bind an

191 after pre-fusion the HyT degrader with heat shock protein 70 (HSP70).

192 Here, we identified Leishmania donovani heat shock protein 78 (LdHSP78), a putative caseinolytic prot

193 Ganetespib, a highly potent heat shock protein 90 inhibitor, blocks multiple oncogenic pa

194 SF1) phosphorylation, which induced the heat shock protein 90alpha (HSP90alpha) expression, leading t

195 in 20), is the partner of mitochondrial heat shock protein A9 (HSPA9).

196 human molecular chaperone protein, DnaJ heat shock protein family (Hsp40) member B6 (DNAJB6), efficie

197 with differential upregulation of three heat-shock protein genes, allowed aphids to occupy higher and

198 unfolding of its structure convert the heat shock protein Hsp33 into a highly active chaperone holda

199 ntary target-engagement method, HIPStA (Heat Shock Protein Inhibition Protein Stability Assay), a hig

200 UIMs function by interacting with the heat shock protein, Hsc70-4, whose reduction diminishes ataxi

201 STIP1 is a co-chaperone for the heat-shock protein, HSP90, and has been shown to have diverse

202 Induction of heat shock proteins (HSPs) confers protection against aminogl

203 Heat shock proteins (HSPs), through regulation of extracellul

204 Small heat shock proteins (sHSPs) are an ubiquitous protein family

205 Small heat shock proteins (sHsps) are conserved, ubiquitous members

206 Small heat-shock proteins (sHsps) are molecular chaperones that fac

207 Small heat-shock proteins (sHSPs) are ubiquitously expressed molecu

208 Small heat-shock proteins (sHsps) compose the most widespread famil

209 , homologs of the respective eukaryotic heat shock proteins Hsp104 and Hsp70, are essential in the re

210 Heat shock proteins of 70 kDa (Hsp70s) are ubiquitous and hig

211 known to underlie thermal stress (i.e., heat shock proteins) even at low temperatures that reflected

212 ith neuroprotective molecules including heat shock proteins, synapsin 1, unique microRNAs, and glutam

213 The inappropriate shock rate (3.1% at 1 year) is the lowest reported for t

214 Among patients with early septic shock, receipt of HAT was not associated with mortality

215 Here we present U-Pb ages for impact-driven shock-recrystallised accessory minerals.

216 Shock-recrystallised monazite yields a precise impact ag

217 ECMO) support for sepsis-induced cardiogenic shock refractory to conventional treatments.

218 al after out-of-hospital cardiac arrest from shock-refractory ventricular fibrillation/pulseless vent

219 tis related to atezolizumab [n=1] and septic shock related to nab-paclitaxel [n=1]) and one (<1%) pat

220 tus" tiers from 3 to 6 and added cardiogenic shock requirements for some heart transplant candidates

221 ise impact age of 2229 +/- 5 Ma, coeval with shock-reset zircon.

222 sults were observed for the association with shock resolution.

223 ased capacity to mount responses by the heat shock response (HSR) and other proteostatic network path

224 lar Hsp90, which results in a prolonged heat shock response despite concomitant degradation of the co

225 rate that acidification is required for heat shock response induction in translationally inhibited ce

226 t, and that coordinated activity of the heat-shock response is required to ensure ongoing protein qua

227 Activation of this heat shock response is triggered by heat-induced misfolding o

228 shock transcriptional response, but the heat shock response pathway is not yet fully understood.

229 king Mgat4d generally mounted a similar heat shock response to control germ cells, but could not main

230 During the heat shock response, RNA Pol II is rapidly released from paus

231 monocytes exhibited an altered in vitro heat shock response.

232 of AFFL-2 is necessary for its role in heat shock response.

233 ed networks was disrupted by inhibiting vCA1 shock responses during memory encoding.

234 immunosuppressive phenotype and altered heat shock responses.

235 ern in monocytes and altered immune and heat shock responsiveness after 30 days.

236 emporary circulatory support for cardiogenic shock, reviews the evidence informing indications and co

237 maladaptive attractions, even to the painful shock-rod, recruit mesocorticolimbic incentive-related c

238 Multiple organ failure and early cardiogenic shock seem to markedly impact the prognosis, suggesting

239 nts with cardiogenic shock and may aggravate shock severity and organ failure.

240 model the change in mobility as an exogenous shock similar to a natural disaster.

241 stages A through D (all P<0.01) but not SCAI shock stage E.

242 SIRS and mortality was evaluated across SCAI shock stage using logistic regression and Cox proportion

243 and 1-year mortality among patients in SCAI shock stages A through D (all P<0.01) but not SCAI shock

244 ascular Angiography and Interventions (SCAI) shock stages using admission data.

245 id polymethyl methacrylate medium, driven to shock states between 0.49 and 16.60 GPa.

246 thod to assess tissue perfusion to determine shock status.

247 ection risk based on presence of cardiogenic shock, suspected coronary territory, and presence of kno

248 1132), KD shock syndrome (n = 45), and toxic shock syndrome (n = 37) who had been admitted to hospita

249 ts with Kawasaki disease (KD) (n = 1132), KD shock syndrome (n = 45), and toxic shock syndrome (n = 3

250 but distinct from Kawasaki disease and toxic shock syndrome admitted to a New York City hospital in l

251 hat can have manifestations similar to toxic shock syndrome or Kawasaki disease.

252 The comparison with patients with KD and KD shock syndrome provides insights into this syndrome, and

253 ion of symptoms that strongly resemble toxic shock syndrome, an escalation of the cytotoxic adaptive

254 reported cases of Kawasaki's disease, toxic shock syndrome, myocarditis, and potential MIS-C in hosp

255 necrotizing fasciitis or streptococcal toxic shock syndrome.

256 lized skin abscess to life-threatening toxic shock syndrome.

257 of death, limb loss, and streptococcal toxic shock syndrome.

258 to severe dengue hemorrhagic fever or dengue shock syndrome; however, the complexities of DENV immuno

259 going PCI for AMI complicated by cardiogenic shock, the mean (SD) age was 65.0 (12.6) years, 67.0% we

260 .98).Conclusions: Among children with septic shock, the PERSEVERE biomarkers predict severe D(3) SA-A

261 vice-related complications and inappropriate shocks; the noninferiority margin for the upper boundary

262 CA1 neurons did not respond to tone and foot shock throughout the training and recall cycles.

263 pective cohort study of adults admitted with shock to Calgary ICUs (June 2012-December 2018).

264 icipants could administer painful electrical shocks to a 'victim' in exchange for money, either by th

265 an welfare both directly and indirectly, via shocks to ecosystems and the services they provide.

266 to gamble, subjecting themselves to electric shocks to satisfy their curiosity for trivial knowledge

267 In multivariate Cox-regression, duration of shock-to-first device (hours, hazard ratio, 1.05 [95% CI

268 l system, we targeted the gene encoding Heat Shock Transcription Factor 1 (HSF1) and obtained larvae

269 Heat shock transcription factor 1 (HSF1) orchestrates cellula

270 Furthermore, we demonstrated that the heat shock transcription factor HSFA6a directly binds the AtP

271 es, HSF1 is the master regulator of the heat shock transcriptional response, but the heat shock respo

272 up of patients with severe sepsis and septic shock treated with hydrocortisone, high-dose ascorbic ac

273 ients with severe sepsis-induced cardiogenic shock treated with VA-ECMO had a large and significant i

274 om 686 consecutive patients with cardiogenic shock treated with VA-ECMO with or without left ventricu

275 lower mortality in patients with cardiogenic shock treated with VA-ECMO, despite higher complication

276 The CULPRIT-SHOCK trial (Culprit Lesion Only PCI Versus Multivessel

277 In the CULPRIT-SHOCK trial (The Culprit Lesion Only PCI Versus Multives

278 We analyzed patients from the CULPRIT-SHOCK trial with respect to the time of hospital admissi

279 otein C and Corticosteroids for Human Septic Shock trials.

280 ncRNA using this approach revealed that heat shock, unlike the unfolded protein response, leads to re

281 alline diamonds and nanodiamonds in a highly shocked ureilite can be explained by catalyzed transform

282 Isolated exosomes from heat-shocked utricles were sufficient to improve survival of

283 etrospectively for cardiac and liver injury, shock, ventilation, mortality, and viral clearance.

284 iating therapy, whereas patients with septic shock warrant emergent broad-spectrum antibiotics.

285 d a different context never paired with foot shock was retained normally for 15 d.

286 Septic shock was the main reason for admission mostly of pulmon

287 to a large extent the extreme excitation and shock wave propagation inside the colloidal crystal.

288 minal boosts," yielding defects analogous to shock waves.

289 imaging through laser-spark plasma-generated shock-waves and to enable three-dimensional tracking of

290 sis through the application of laser-induced shock-waves to a prototypical organic carbon-rich liquid

291 roup (two from pneumonia and one from septic shock) were considered treatment-related; no deaths in t

292 rs of vasopressor support for nonhemorrhagic shock, were prospectively enrolled.

293 at neurons in ACC are modulated by reward or shock when delivered to a conspecific and when experienc

294 h with different probabilities of generating shocks, while also seeing the image of a social partner.

295 of 82 patients (aged >=18 years) with septic shock who received VA-ECMO at five academic ECMO centres

296 He was in a septic shock with multiple organ failure up on presentation to

297 t mortality and rate of recovery from septic shock with over 90% accuracy.

298 5% CI, 1.03-1.46; p = 0.025) and cardiogenic shock within 48 hours post-ICU admission (odds ratio, 9.

299 ause previous studies do not vary reward and shock within the same experiment, it has been unclear wh

300 channels modify the general equilibrium, as shocks would do in general equilibrium macroeconomic mod