ライフサイエンスコーパス: septic

1 The prevalence of septic acute kidney injury and impact on functional stat

2 hologic changes found in modern experimental septic acute kidney injury models.

3 te functional outcomes of children suffering septic acute kidney injury.

4 retic therapy on mortality in critically ill septic adults.

5 on after pulmonary vein ablation, leading to septic air emboli and requiring urgent cardiac surgery.

6 anged over time, the only difference between septic and nonseptic animals was mesangial expansion on

7 n interference ratings were compared between septic and nonseptic patients and healthy controls.

8 expression is increased on CD4(+) T cells in septic animals and human patients at early time points.

9 ex vivo experiments at 24 hours to identify septic animals with good prognosis.

10 more likely to develop meningoencephalitis, septic arthritis, and spinal infection.

11 enous implant-related infection comprised of septic arthritis, osteomyelitis, and biofilm formation o

12 ated at the host-pathogen interface during a septic bacterial infection.

13 Septic bi-transgenic animals had decreased crypt apoptos

14 The mechanism(s) for septic cardiomyopathy in humans is not known.

15 , the alterations in messenger RNA levels in septic cardiomyopathy were both distinct from and more p

16 ification of genes with altered abundance in septic cardiomyopathy, ischemic heart disease, or dilate

17 used NK cell depletion if given 4 d prior to septic challenge and conferred protection.

18 of alphaMbeta2, increased survival against a septic challenge with lipopolysaccharide (LPS) by 2-fold

19 If given immediately prior to septic challenge, IL-15-neutralizing IgG M96 failed to p

20 Based on our finding that septic children with this SNP had longer pediatric inten

21 were increased in septic WT mice, but not in septic CIRP KO mice.

22 iary obstruction are at high risk to develop septic complications after endoscopic retrograde cholang

23 associated with increased susceptibility to septic complications after trauma, which is indicated by

24 ich reflects severe bacterial infections and septic condition but has not been studied in urinary tra

25 opulation and compare them to a nonobstetric septic control group.

26 102 patients with confirmed first-ever, non-septic CVT.

27 ific marker of NETosis, were elevated during septic episodes.

28 Septic fabpi-TAg mice had an unexpected increase in vill

29 l increase in villus apoptosis compared with septic fabpi-TAg mice, associated with decreased prolife

30 villus and crypt apoptosis were increased in septic fabpi-TAg mice.

31 traction coupling decreased by 43% +/- 4% in septic hearts.

32 In genome-wide analyses of blood mRNA from septic human neonates, expression of the IL-17 receptor

33 duction, and lead to more severe LPS-induced septic hypothermia when reconstituted into mast cell-def

34 Hemolysis is a complication in septic infections with Staphylococcus aureus, which util

35 inflammation and survival in the setting of septic insult by targeting MyD88- and Toll/IL-1R domain-

36 Additionally, septic MDSCs had suppressed HLA gene expression and up-r

37 intestinal MFG-E8 expression in LPS-induced septic mice and attenuated LPS inhibitory effects on int

38 Adoptive transfer of B-1a cells into septic mice significantly attenuated systemic inflammati

39 Importantly, surviving septic mice with conditionally deficient NFI-A myeloid c

40 ed neutrophil infiltration into the lungs of septic mice.

41 as well as the MPO activity in the lungs of septic mice.

42 de were delivered by tail vein injections to septic mice.

43 vascular coagulation and end-organ damage in septic mice.

44 high) cells isolated from the bone marrow of septic mice.

45 e, bacterial proliferation, and mortality of septic newborn mice.

46 In septic, nontransplanted mice at 24 hours, Ppara mice had

47 one obstetric-based and four general) in the septic obstetric population and compare them to a nonobs

48 es individually, successful treatment of the septic patient with chronic critical illness and persist

49 , its clinical course, and how we manage the septic patient.

50 ood discriminatory power for the identifying septic patients (AUROC = 0.915, 95% CI [0.827, 1.000]).

51 Septic patients are especially prone to IIT-induced hypo

52 Septic patients as identified by International Classific

53 Platelets in septic patients demonstrated increased levels of surface

54 ting characteristic curve for discriminating septic patients from patients with noninfectious inflamm

55 eters (NEUT-Y and NEUT-RI) demonstrated that septic patients had significantly higher levels of neutr

56 Septic patients had significantly more CD19 B cells expr

57 Our results raise the possibility that septic patients have impaired insulin clearance, which c

58 arly initiation of effective antibiotics for septic patients is essential for patient survival.

59 2632 patients, of whom 794 had sepsis (30.2 septic patients per 100 ICU beds, 95% CI 28.4-31.9).

60 on profile of messenger RNAs in the heart of septic patients reveals striking decreases in expression

61 alue of fever in the emergency department in septic patients subsequently admitted to the ICU.

62 A total of 146 septic patients were found for the obstetric cohort and

63 esuscitation bundles, mortality was lower in septic patients who underwent source control than in tho

64 sis and primary intestinal pathology than in septic patients without primary intestinal pathology.

65 We investigated interphysician variation in septic patients' door-to-antimicrobial time.

66 tion, GLUT1 expression, and glucose entry in septic patients' T lymphocytes, leading to their enhance

67 were observational or randomized studies of septic patients, evaluation of antipyretic treatment, mo

68 urrent guidelines for care of critically ill septic patients, increased body temperature in the emerg

69 s using human vascular cells and plasma from septic patients.

70 nted in human cells treated with plasma from septic patients.

71 kappaB inhibitor BAY 11-7082, or plasma from septic patients.

72 scriminatory power for the identification of septic patients.

73 del to closely mirror the treatment of human septic patients.

74 gnetic resonance spectroscopy was altered in septic patients.

75 21, with nadir values significantly lower in septic patients.

76 the omental neutrophil response exacerbates septic progression of peritonitis.

77 n-approved serotonin agonist (lorcaserin) to septic rats greatly improved repetitive firing and motor

78 mic voltage clamp of spinal motor neurons in septic rats were employed to explore potential mechanism

79 art from bacterial proliferation, triggers a septic response and contributes to mortality in this mod

80 RATIONALE: Heterogeneity in the septic response has hindered efforts to understand patho

81 lar and molecular mechanisms involved in the septic response is questionable.

82 and BTK regulate thermal homeostasis during septic response through mast cell function in mice.

83 Septic Sharpin-deficient mice displayed enrichment in ma

84 Interventional study in a rat model of septic shock (128 adult males) to assess the effects of

85 .01-1.10), P = 0.02), and presence of sepsis/septic shock (2.70 (1.17-6.28), P = 0.02).

86 pticemia (038.x), severe sepsis (995.92), or septic shock (785.52), as well as all subsequent hospita

87 from the emergency department with sepsis or septic shock (defined: infection, >/= 2 systemic inflamm

88 dney injury was 2.212 (95% CI: 1.334-3.667), septic shock (HR = 1.895, 95% CI: 1.081-3.323) and model

89 d the Early Management Bundle, Severe Sepsis/Septic Shock (SEP-1) performance measure to the Hospital

90 ational Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria for objective and consi

91 ational Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) criteria in the emergency depart

92 ational Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) present clinical criteria for th

93 ational Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) uses the Sequential Organ Failur

94 ted to the early management of severe sepsis/septic shock (SS/SS) in Emergency Department (ED) has ye

95 74 patients within 12 hours of severe sepsis/septic shock (SS/SS), and at set intervals out to 28 day

96 ects of plasma samples from 13 patients with septic shock (with or without severe acute kidney injury

97 arison and 28-day mortality of patients with Septic Shock 3.0 definition (lactate > 2 mmol/L) differ

98 The Septic Shock 3.0 definition and our findings have import

99 The Septic Shock 3.0 definition could alter treatment compar

100 The Septic Shock 3.0 definition decreased sample size by hal

101 The Septic Shock 3.0 definition would have decreased sample

102 day], ventricular fibrillation [120 mg/day], septic shock [80 mg/day], and neutropenia [120 mg/day]).

103 onia [n=2], interstitial lung disease [n=1], septic shock [n=1], and unknown [n=1]) and two (<1%) of

104 uses in the combination group (sepsis [n=2], septic shock [n=1], congestive cardiac failure [n=1], an

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

106 Consecutive adult patients with septic shock admitted between November 2009 and Septembe

107 The cohort included adults with septic shock admitted to study hospitals between July 1,

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

109 with septic shock, plasma from patients with septic shock and acute kidney injury inhibited neutrophi

110 an important role in acute injury, including septic shock and acute lung injury.

111 al to 18 years old with severe sepsis and/or septic shock and antimicrobial administration within 24

112 role in many inflammatory diseases including septic shock and atherosclerosis.

113 tcomes in the overall group of patients with septic shock and elevated lactate.

114 are frequently elevated in severe sepsis or septic shock and have relevant prognostic value, which m

115 element in the management of severe sepsis, septic shock and in sports performance evaluation.

116 th increased progression of severe sepsis to septic shock and increased mortality.

117 ical criteria currently reported to identify septic shock and inform the Delphi process; (2) a Delphi

118 reatment by the investigator (pneumonia, and septic shock and multiorgan failure).

119 GITB in transplant patients, complicated by septic shock and multiple organ failure, including acute

120 development of secondary conditions such as septic shock and multiple-organ failure.

121 lying immune status impacts on the course of septic shock and on the susceptibility to ICU-acquired c

122 rched for terms related to severe sepsis and septic shock and terms related to polymyxin B hemoperfus

123 s us to reevaluate the current management of septic shock and to assess whether we are inadvertently

124 his study we selected patients admitted with septic shock and treated for more than 4 days from a pro

125 Sepsis and septic shock are common and, at times, fatal in pediatri

126 mmon in septic shock, but many patients with septic shock are relatively bradycardic.

127 model for end stage liver disease (MELD) and septic shock are the independent predictors of 50 days i

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

129 All adults treated with severe sepsis or septic shock between 2005 and 2014, using administrative

130 ce of acute decompensation, 20 patients with septic shock but no cirrhosis or liver disease, and 20 h

131 Furthermore, niacin rescued mice from septic shock by diminishing inflammatory symptoms and th

132 sis of sepsis but enables the development of septic shock by maintaining NK cell numbers and integrit

133 s proinflammatory cytokine production during septic shock caused by cecal ligation and puncture or en

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

135 ne the outcomes of patients meeting Sepsis-3 septic shock criteria versus patients meeting the "old"

136 defined as suspected infection and suspected septic shock decreased significantly after the intervent

137 As mortality of septic shock decreases, new therapies focus on improving

138 cohort studies to achieve consensus on a new septic shock definition and clinical criteria; and (3) c

139 e (19 participants) to revise current sepsis/septic shock definitions.

140 , 57% of patients meeting old definition for septic shock did not meet Sepsis-3 criteria.

141 study included adult patients with sepsis or septic shock due to bloodstream infections caused by GNB

142 Compared with hospital admission with septic shock during quarters of normal use, hospital adm

143 12 of whom 58,045 received a vasopressor for septic shock during the first 2 days of hospitalization.

144 r hospitalization, 149 (65.0%) had sepsis or septic shock during their course.

145 nrolled 3,663 patients with severe sepsis or septic shock during three 4-month periods between 2011 a

146 improvement initiative for severe sepsis and septic shock focused on the resuscitation bundle on 90-d

147 ve patients presenting with severe sepsis or septic shock from 2011 to 2013.

148 ions, but can also lead to sepsis and lethal septic shock if overactivated.

149 atients were further categorized as Sepsis-3 septic shock if they demonstrated hypotension, received

150 d consecutive patients with severe sepsis or septic shock in 2 intensive care units in the Netherland

151 rtile range, 57-79 years]; 47.0% women) with septic shock in 26 hospitals that demonstrated at least

152 mortality in patients with severe sepsis and septic shock in specific disease severity subgroups.

153 Adult cancer patients with septic shock in the first 6 hours of ICU admission.

154 Among patients with septic shock in US hospitals affected by the 2011 norepi

155 Septic shock is a major cause of death worldwide and a c

156 Relative bradycardia in patients with septic shock is associated with lower mortality, even af

157 tematic review, surveys, and cohort studies, septic shock is defined as a subset of sepsis in which u

158 ng of sepsis, neutrophils from patients with septic shock likewise exhibited a significantly increase

159 alance, this candidate pathway might benefit septic shock management.

160 not affect mouse survival in an LPS-induced septic shock model.

161 the Surviving Sepsis Campaign in refractory septic shock only.

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

163 n or equal to two organ failures at day 7 of septic shock or 28-day mortality, had a higher percentag

164 ce of two or more organ failures at day 7 of septic shock or 28-day mortality.

165 matic review identified 44 studies reporting septic shock outcomes (total of 166,479 patients) from a

166 Consecutive sample of all severe sepsis and septic shock patients (defined: infection, >/= 2 systemi

167 talloid resuscitation provided to sepsis and septic shock patients at initial presentation and 2) det

168 Adult sepsis and septic shock patients captured in a prospective quality

169 Inadequate stratification of septic shock patients may result in inappropriate treatm

170 outcome of 6-hour mean arterial pressure in septic shock patients receiving vasopressin who were on

171 To compare the hemodynamic response in septic shock patients receiving vasopressin who were on

172 Samples from septic shock patients were obtained at day 3 and compare

173 study evaluates whether emergency department septic shock patients without a fever (reported or measu

174 irus reactivations were documented in 68% of septic shock patients without prior immunodeficiency and

175 to one bundle element for severe sepsis and septic shock patients.

176 Among patients with severe sepsis or septic shock receiving antimicrobials in the emergency d

177 ity improvement initiatives to improve early septic shock recognition and first-hour compliance to th

178 d May 2015, enrolling adult patients who had septic shock requiring vasopressors despite fluid resusc

179 Adult patients with septic shock requiring vasopressors.

180 er might therefore occur in the absence of a septic shock response because of the inhibiting effect o

181 ary analysis of two clinical trials of early septic shock resuscitation.

182 One infant had septic shock shortly after transplantation, resulting in

183 Septic shock should be defined as a subset of sepsis in

184 /critical illness myopathy and severe sepsis/septic shock studies.

185 ital stays in patients with severe sepsis or septic shock subsequently admitted to the ICU.

186 for >/= 3 days at full dose in patients with septic shock that is not responsive to fluid and moderat

187 e studied data from patients with sepsis and septic shock that were reported to the New York State De

188 Retrospective study of patients admitted for septic shock to study ICUs during 2005-2013.

189 in plasma cytokine levels in Vasopressin and Septic Shock Trial for lactate less than or equal to 2 v

190 The Protocol-based Care for Early Septic Shock trial found no differences across alternati

191 28- and 90-day mortality in Vasopressin and Septic Shock Trial in lactate subgroups.

192 2 % higher than the original Vasopressin and Septic Shock Trial mortality.

193 epinephrine and mortality in Vasopressin and Septic Shock Trial.

194 in regulating the pathogenesis of sepsis and septic shock via their effects on neutrophil survival an

195 The incidence of severe sepsis and septic shock was 9.7%.

196 Patients from 5 days to 18 years old with septic shock were enrolled.

197 arrival with a diagnosis of severe sepsis or septic shock were included.

198 similar sensitivity toward endotoxin-induced septic shock when compared to control mice.

199 iberal transfusion strategy in patients with septic shock when compared with the restrictive strategy

200 Medical and surgical ICU patients with septic shock who received vasopressin infusion added to

201 tients meeting criteria for severe sepsis or septic shock who were admitted to the ICU from the emerg

202 Patients with septic shock with lactate greater than 2 mmol/L or less

203 nderlying immune conditions on the course of septic shock with respect to both mortality and the deve

204 Patients diagnosed for septic shock within the first 48 hours of ICU admission

205 its spectrum of diseases (severe sepsis and septic shock), which are leading causes of death in inte

206 ol for rapid identification of patients with septic shock, 2) a "resuscitation and stabilization bund

207 linical Modification codes for severe sepsis/septic shock, 2) Martin approach, and 3) Angus approach.

208 Among 378 patients with septic shock, 207 of 378 (55%; 50-60%) were febrile by h

209 .9% received starch, and among patients with septic shock, 68.3% had lactate measured and 64% receive

210 s in critically ill patients with sepsis and septic shock, acute respiratory distress syndrome, and m

211 In emergency department patients with septic shock, afebrile patients received lower rates of

212 In patients with septic shock, alterations in inflammation, coagulation,

213 ubpopulation of neutrophils in patients with septic shock, and those with a high percentage of olfact

214 Tachycardia is common in septic shock, but many patients with septic shock are re

215 s associated with improved outcomes in adult septic shock, but pediatric guidelines do not endorse it

216 expressed gene in nonsurvivors of pediatric septic shock, compared with survivors.

217 A subset of patients with sepsis progress to septic shock, defined by profound circulatory, cellular,

218 and one each of acute myocardial infarction, septic shock, encephalopathy, general deterioration in p

219 rian using the keywords: sepsis, septicemia, septic shock, endotoxemia, persistent pulmonary hyperten

220 ional normalized ratio, acute kidney injury, septic shock, hepatic encephalopathy and model for end s

221 orepinephrine, the cornerstone treatment for septic shock, in sepsis-induced immunoparalysis.

222 Secondary outcomes were time until septic shock, mortality in the intensive care unit or ho

223 e blood culture Staphylococcus haemolyticus, septic shock, multiple organ failure including acute res

224 We identified 1,554 patients with septic shock, of whom 686 (44%) met criteria for relativ

225 Within severe sepsis/septic shock, patients with bloodstream infection could

226 Compared with plasma from patients with septic shock, plasma from patients with septic shock and

227 in patients with sepsis, severe sepsis, and septic shock, respectively.

228 irical treatment of patients with sepsis and septic shock, that is, moxifloxacin, meropenem, and pipe

229 Among survivors of sepsis and septic shock, the use of a primary care-focused team-bas

230 rected therapy (EGDT) reduced mortality from septic shock, three multicenter trials (ProCESS, ARISE,

231 olysaccharide (LPS), resulting in sepsis and septic shock, two major causes of death worldwide, signi

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

233 rial of mesenchymal stromal cells (MSCs) for septic shock, we applied systematic review methodology t

234 surgical ICU patients with severe sepsis and septic shock.

235 stratification according to the presence of septic shock.

236 ir, and metabolism in the pathophysiology of septic shock.

237 he current study is limited to patients with septic shock.

238 nt survival, particularly in the presence of septic shock.

239 ents who are relatively bradycardic while in septic shock.

240 or hRetn in lipopolysaccharide (LPS)-induced septic shock.

241 mponent of G(-) bacterial cell wall) induced septic shock.

242 causes of death were respiratory failure and septic shock.

243 Patients with severe sepsis and/or septic shock.

244 e important implications for trial design in septic shock.

245 coid receptors in murine endotoxic and human septic shock.

246 on of antibiotics to patients with sepsis or septic shock.

247 ative bradycardia will benefit patients with septic shock.

248 and nonobese patients with severe sepsis or septic shock.

249 treatment in patients with severe sepsis and septic shock.

250 information regarding the pathophysiology of septic shock.

251 increased odds of mortality were greatest in septic shock.

252 h a liberal strategy in cancer patients with septic shock.

253 repinephrine, the first-line vasopressor for septic shock.

254 hemodynamic support of newborn and pediatric septic shock.

255 Six hundred twenty-eight patients with septic shock.

256 ance to endotoxin- and polymicrobial-induced septic shock.

257 mparisons in randomized controlled trials in septic shock.

258 were largely resistant to endotoxin-induced septic shock.

259 utralizing IgG M96 failed to protect against septic shock.

260 th and without hydrocortisone, in a model of septic shock.

261 onditions, including immune paralysis during septic shock.

262 th severe sepsis prevents the development of septic shock.

263 negative bacteria can be a potent inducer of septic shock.

264 ion/cardiogenic shock, injury, and infection/septic shock.

265 lactate level, and base deficit to identify septic shock.

266 ry, mortality, and plasma cytokines in human septic shock.

267 uirements, organ dysfunction, and death from septic shock.

268 timate baseline mortality risk for pediatric septic shock.

269 d eighty-four patients (25.0%) progressed to septic shock.

270 athogenic neutrophil subset in patients with septic shock.

271 ysfunction plus infection, severe sepsis, or septic shock.

272 y lethal immune collapse syndrome similar to septic shock.

273 l factors are involved in the development of septic shock.

274 bacteria may not be the only factor inducing septic shock.

275 mortality in patients with severe sepsis and septic shock.

276 ion that causes widespread tissue damage and septic shock.

277 pisodes of suspected infection and suspected septic shock.

278 T lymphocytes facilitate the pathobiology of septic shock.

279 stablished mortality of IL-15 KO mice during septic shock.

280 ate baseline mortality risk in children with septic shock.

281 that was ongoing at the time of death due to septic shock.

282 lt male C57Black 6 mice, adult patients with septic shock.

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

284 ical Modification codes for severe sepsis or septic shock.

285 pathogens is probably critical to outcome in septic shock.

286 hway in host resistance to endotoxin-induced septic shock.

287 d 2015 for fluid-refractory severe sepsis or septic shock.

288 ociated with progression of severe sepsis to septic shock.

289 iated with a 8.0% increase in progression to septic shock.

290 olfactomedin-4+ neutrophils in patients with septic shock.

291 ze neutrophil heterogeneity in children with septic shock.

292 ynamic Support of Neonates and Children with Septic Shock." Society of Critical Care Medicine members

293 ace water can indicate the overall extent of septic system impact, while the presence of well-removed

294 oncentrations, consistent with recharge from septic systems (high delta(15)N, low delta(18)O), variab

295 Onsite wastewater treatment systems, such as septic systems, serve 20% of U.S. households and are com

296 treated wastewater from failing or outdated septic systems.

297 The lifetime of the NZB, septic tank aeration, and use of solar energy have been

298 yclin D2 were decreased in jejunal tissue in septic transgenic mice.

299 Wild-type mice made septic via cecal ligation and puncture had decreased cry

300 CHOP, cleaved caspase-12) were increased in septic WT mice, but not in septic CIRP KO mice.