ライフサイエンスコーパス: SIRS

1 SIRS and organ system dysfunctions were defined using 20

2 SIRS and the decision rule may be helpful in identifying

3 SIRS can have a sterile cause or can be initiated by an

4 SIRS developed in 112 patients (27%).

5 SIRS had lower net benefit than qSOFA and CRB, significa

6 SIRS occurs in 27% of patients admitted for gastrointest

7 SIRS patients developing sepsis were compared with those

8 SIRS presented the worst discrimination, followed by qSO

9 SIRS resembles sepsis, triggered by exogenous macromolec

10 SIRS, qSOFA, the Confusion, Respiratory Rate and Blood P

11 atients] to 18.3% [2037 of 11,119], P<0.001; SIRS-negative group: from 27.7% [100 of 361] to 9.3% [12

12 Most patients met >/=2 SIRS criteria 17 hours before the combined outcome compa

13 the highest non-ICU score of patients, >/=2 SIRS had a sensitivity of 91% and specificity of 13% for

14 Infected patients more often developed a SIRS and one of greater magnitude.

15 .8%) patients who did not become infected, a SIRS on admission was associated with a more critical il

16 Overall, 504 (56.8%) patients manifested a SIRS during their illness, with a maximum of 1, 2, and 3

17 In this study, we report that a SIRS-like response can be induced in mice by administrat

18 For patients with a SIRS, the proportions of infected and noninfected patien

19 lity increased linearly with each additional SIRS criterion (odds ratio for each additional criterion

20 eas of aseptic necrosis in the RV 24 h after SIRS induction.

21 ROC = 0.79; 95% CI, 0.78-0.80; P < .001) and SIRS (AUROC = 0.76; 95% CI, 0.75-0.77; P < .001).

22 mples were drawn on days 0, 1, 3, and 7, and SIRS was scored during 48 hours after surgery.

23 ), qSOFA (AUC, 0.69; 95% CI, 0.67-0.70), and SIRS (AUC, 0.65; 95% CI, 0.63-0.66) (P < 0.01 for all pa

24 a key link between trauma, inflammation and SIRS.

25 SOFA, qSOFA, and SIRS criteria applied to data collected within 24 hours

26 nd phagocytic cells that underlie sepsis and SIRS and consider how these might be targeted for therap

27 take place within the CNS during sepsis and SIRS and the development of new therapies for these seri

28 re neutrophils circulating during sepsis and SIRS.

29 SOFA was statistically greater than SOFA and SIRS, supporting its use as a prompt to consider possibl

30 Measurement of qSOFA, SOFA, and SIRS.

31 ol the dermal inflammatory source, attenuate SIRS, and reduce acute lung injury.

32 (but not specific) predictors of bacteremia (SIRS, negative LR, 0.09 [95% CI, 0.03-0.26]; decision ru

33 4-0.85) vs 0.65 (95% CI, 0.59-0.70) for both SIRS and severe sepsis (P < .001; incremental AUROC, 0.1

34 The qSOFA performed better than both SIRS and severe sepsis in predicting in-hospital mortali

35 ciated with a loss of the redox balance, but SIRS can also develop in noninfectious states.

36 ve been established for patients affected by SIRS.

37 innate immunities are greatly influenced by SIRS levels.

38 tients meeting the exclusive day 3 category, SIRS resolved.

39 es while also studying their role in causing SIRS.

40 ss, with a maximum of 1, 2, and 3 concurrent SIRS components in 166, 238, and 100 patients, respectiv

41 ients with 0, 1, 2, and 3 maximum concurrent SIRS components, respectively.

42 vere sepsis) or less than two SIRS criteria (SIRS-negative severe sepsis).

43 had signs meeting two or more SIRS criteria (SIRS-positive severe sepsis) or less than two SIRS crite

44 nt in 12 patients who subsequently developed SIRS (postoperative day 6) compared with 27 who did not,

45 patients hospitalized on the wards developed SIRS at least once during their ward stay.

46 ted and overactive in patients who developed SIRS (P < 0.0001).

47 her preoperatively in patients who developed SIRS.

48 to identify serum markers that differentiate SIRS with and without infection.

49 We propose that parenchymal cells direct SIRS in response to LPS.

50 similar phenotypic expression, these diverse SIRS etiologies may induce divergent genotypic expressio

51 During SIRS, the expression of several genes, such as chemokine

52 n is one of the first organs affected during SIRS, and sepsis and the consequent neurological complic

53 le modulating the brain transcriptome during SIRS.

54 of overall mitotic timing ensures efficient SIRS.

55 cy for in-hospital mortality than did either SIRS or severe sepsis.

56 ise and multitarget therapeutic approach for SIRS and sepsis.

57 eting predetermined physiologic criteria for SIRS (considered criteria-based sepsis).

58 hen 82% of the patients met the criteria for SIRS.

59 dity for in-hospital mortality was lower for SIRS (AUROC = 0.64; 95% CI, 0.62-0.66) and qSOFA (AUROC

60 he proinflammatory cytokines responsible for SIRS initiation.

61 ar correlations with mortality were seen for SIRS associated with fungal infection, bacteremia, and b

62 presents a potential therapeutic target for SIRS and ALI induced after HS.

63 sting future mediator-directed therapies for SIRS/MOF before clinical trials, and it may provide insi

64 s (95% CI 7.8-8.7) per 1000 person-years for SIRS, 5.8 events (5.4-6.1) per 1000 person-years for SOF

65 care unit (ICU) patients meeting two of four SIRS criteria at an academic medical center for whom pla

66 the exaggerated production of IFN-gamma from SIRS splenocytes.

67 ole of tissue injury in the progression from SIRS to shock is incompletely understood.

68 al infection and differentiating sepsis from SIRS.

69 terial infection, while 75 (46.3%) fulfilled SIRS criteria; 58 patients (35.8%) developed MOF during

70 ositive severe sepsis and 13,278 (12.1%) had SIRS-negative severe sepsis.

71 tients, 103 had definite sepsis, and 159 had SIRS.

72 Among these, 96,385 patients (87.9%) had SIRS-positive severe sepsis and 13,278 (12.1%) had SIRS-

73 ship between cytokines and their blockers in SIRS.

74 es are novel targets for drug development in SIRS and sepsis.

75 e (odds ratio [OR]=1.9 per point increase in SIRS, 95% confidence interval [CI]=1.3-2.9), inflammator

76 we identify MMP8 as an essential mediator in SIRS and, hence, a potential drug target.

77 NAs (n = 116) were generally up-regulated in SIRS compared to no-SIRS patients.

78 KIP may be a potential therapeutic target in SIRS by curbing effector cytokine production from CD8(+)

79 NAs appeared less abundant in sepsis than in SIRS.

80 ty of heparan sulfate and elastase to induce SIRS depends on functional Toll-like receptor 4, because

81 In the presence or absence of infections, SIRS is a major determinant of MOF and mortality in AH,

82 QR: 1.15-1.92) fold higher for non-infective SIRS and sepsis respectively (p < 0.0001), hence CIR-miR

83 cally ill patients, sepsis and non-infective SIRS are associated with substantial, differential chang

84 lly affected during sepsis and non-infective SIRS.

85 n = 23) or non-severe (n = 21) non-infective SIRS; or no SIRS (n = 16) were studied.

86 on drives LPS-induced systemic inflammation; SIRS does not develop in mice lacking TLR4 expression on

87 INTERPRETATION: SIRS, SOFA, and qSOFA classifications identified differe

88 When evaluating only patients not meeting SIRS criteria, 68% of patients with ASB received antibio

89 Of 2593 first infection events, 1526 met SIRS criteria, 1080 met SOFA criteria, and 378 met qSOFA

90 (125 [13%] of 960 patients died) or who met SIRS criteria (128 [9%] of 1392 patients died).

91 26.6] per 100 person-years) or those who met SIRS criteria (14.7 deaths [12.5-17.2] per 100 person-ye

92 PMphi from mild SIRS mice exhibited typical properties for classically a

93 CIDbgMN mice inoculated with PMphi from mild SIRS mice survived after the same infection.

94 and CLP-induced sepsis, are induced in mild SIRS mice.

95 her hand, as compared with normal mice, mild SIRS mice were resistant to these infections.

96 e SIRS mice were compared with those of mild SIRS mice after infection with Enterococcus faecalis or

97 h progressive encephalopathy manifested more SIRS components than other infected patients.

98 o whether they had signs meeting two or more SIRS criteria (SIRS-positive severe sepsis) or less than

99 compared among patients meeting two or more SIRS criteria and by the presence or absence of organ sy

100 41) of the included patients met two or more SIRS criteria at least once during their ward stay.

101 The need for two or more SIRS criteria to define severe sepsis excluded one in ei

102 points in 90.1%; 86.7% manifested 2 or more SIRS criteria, and 54.4% had a qSOFA score of 2 or more

103 ion, 39,105 (14.5%) patients met two or more SIRS criteria, and patients presenting with SIRS had hig

104 in SOFA score by 2 or more points, 2 or more SIRS criteria, or a qSOFA score of 2 or more points for

105 ar characteristics and changes in mortality (SIRS-positive group: from 36.1% [829 of 2296 patients] t

106 on-severe (n = 21) non-infective SIRS; or no SIRS (n = 16) were studied.

107 enerally up-regulated in SIRS compared to no-SIRS patients.

108 e sepsis (4.87 ng/ml), 44 with noninfectious SIRS (2.33 ng/ml), and eight without SIRS (1.97 ng/ml).

109 Sepsis was the cause of SIRS in 63% of patients (70/112).

110 However, when the cause of SIRS is not infection, for example, in burn patients, is

111 ngth of hospital stay, presence and cause of SIRS, presence of organ failure, and in-hospital mortali

112 ng patients with clinical characteristics of SIRS, as defined by criteria based on physician diagnosi

113 c cultures, a higher number of components of SIRS at admission was associated with more frequent wors

114 5% vs. 50% for 0, 1, and >or=2 components of SIRS, P < 0.05).

115 okine that contributes to the development of SIRS and ALI.

116 ores are risk factors for the development of SIRS in patients hospitalized for gastrointestinal bleed

117 eptic humans and rodents, the development of SIRS is associated with a loss of the redox balance, but

118 he mechanisms involved in the development of SIRS should be investigated; procalcitonin serum levels

119 icle postulates a three-stage development of SIRS, in which stage 1 is a local production of cytokine

120 rapeutic implications for the development of SIRS, sepsis, and shock in humans exposed to a wide arra

121 001) were associated with the development of SIRS.

122 of cytokine production to the development of SIRS.

123 Clinical diagnosis of SIRS is strongly associated with increased total plasma

124 ation without having a clinical diagnosis of SIRS.

125 The effects of SIRS on the body are myriad and have been defined and il

126 27 who did not, when no clinical evidence of SIRS was apparent (preoperatively or days 1 and 2).

127 NA DAMPs is associated with the evolution of SIRS, MODS, and mortality in severely injured human subj

128 The CNS regulates many features of SIRS such as fever, cardiovascular, and neuroendocrine r

129 eding NCSz onset, and the negative impact of SIRS on functional outcome at 3 months was mediated in p

130 molecular explanation for the initiation of SIRS.

131 Central and systemic manifestations of SIRS can be induced by LPS or IL-1beta administration.

132 By testing a T cell-dependent mouse model of SIRS that utilizes staphylococcal enterotoxin A specific

133 The presence of SIRS and infections was assessed in all patients, and mu

134 We hypothesize that the presence of SIRS may predispose to MOF and death.

135 The presence of SIRS was a major predictor of MOF (odds ratio = 2.69, P

136 eutic strategy to prevent the progression of SIRS to shock.

137 ify markers that predict patients at risk of SIRS 5 days before the onset of clinical signs.

138 ions of the IIR and its disordered states of SIRS/MOF.

139 espite the TCR-dependent defects seen in our SIRS model.

140 qSOFA and CRB outperformed SIRS and presented better clinical usefulness as prompt

141 ce (MR) imaging at 3 T with a whole-brain PC-SIRS imaging sequence with alternating SL-on and SL-off

142 Including PC-SIRS as prior information improved the evidence of the s

143 The topography of PC-SIRS effects was compared with the seizure onset zone at

144 tatistics were used to test whether prior PC-SIRS information could improve IED source reconstruction

145 ycled stimulus-induced rotary saturation (PC-SIRS) approach with spin-lock (SL) preparation and wheth

146 ctable during interictal periods with the PC-SIRS approach in patients with epilepsy.

147 nce interval: 0.40, 0.94) by means of the PC-SIRS technique.

148 f gene expression exist across the pediatric SIRS, sepsis, and septic shock spectrum, septic shock is

149 uction in patients who develop postoperative SIRS and identify markers that predict patients at risk

150 CD14CD16 monocytes, on day 1 or 2 predicted SIRS with accuracy 0.89 to 1.0 (areas under receiver ope

151 with in-hospital NCSz had a more pronounced SIRS response (odds ratio [OR]=1.9 per point increase in

152 tory signaling appears effective in reducing SIRS and subsequent systemic complications after burn in

153 thy with the systemic inflammatory response (SIRS) and infection.

154 eveloped the Social Impairment Rating Scale (SIRS), rated by a clinician after a structured interview

155 ttempt to demonstrate the effects of sepsis (SIRS plus infection) on whole body metabolism, outline t

156 evelopment of complications including sepsis/SIRS.

157 on at greatly increased risk of later sepsis/SIRS.

158 later (minimum 4 days) development of sepsis/SIRS (odds ratio, 12.9; 95% confidence interval, 3.4-47.

159 dent predictor for the development of sepsis/SIRS after correction for age, bypass time, complexity o

160 ion and the subsequent development of sepsis/SIRS in children undergoing cardiopulmonary bypass.

161 Severe SIRS mice were greatly susceptible to E. faecalis, MRSA,

162 discrimination of severe sepsis from severe SIRS (0.742-0.917 AUC of ROC curves).

163 h peritoneal macrophages (PMphi) from severe SIRS mice died after infection with E. faecalis or MRSA,

164 rophages (CAMphi), whereas those from severe SIRS mice exhibited typical properties for alternatively

165 Morbidity and mortality rates of severe SIRS mice were compared with those of mild SIRS mice aft

166 uted with effector cells from mild or severe SIRS mice and exposed to various infections.

167 Induction of CAMphi may protect severe SIRS patients against infections.

168 h sepsis and those from patients with severe SIRS.

169 pabilities are generated in mice with severe SIRS.

170 th physician-diagnosed sepsis, septic shock, SIRS, or sepsis syndrome documented in the medical recor

171 anism termed Separation-Into-Recent-Sisters (SIRS).

172 be used with the APACHE-IV score to stratify SIRS patients at high mortality risk.

173 In this study, SIRS components were recorded on admission and during ep

174 The Steroids In caRdiac Surgery (SIRS) study is a double-blind, randomised, controlled tr

175 usceptible-infectious-recovered-susceptible (SIRS) model and weekly estimates of influenza incidence.

176 usceptible-infectious-recovered-susceptible (SIRS) transmission model to age- and type-specific HPV p

177 usceptible-infectious-recovered-susceptible (SIRS)-like phenomenology of infection and immunity to Bo

178 the systemic response inflammatory syndrome (SIRS) and the presence of myocarditis with focal areas o

179 re, systemic inflammatory response syndrome (SIRS score), multiple organ dysfunction syndrome (MODS)

180 the systemic inflammatory response syndrome (SIRS) and a multivariable decision rule with major and m

181 the systemic inflammatory response syndrome (SIRS) and confirm the hypothesis that cytokine storm occ

182 ers systemic inflammatory response syndrome (SIRS) and dengue shock syndrome (DSS), with subsequent m

183 ith systemic inflammatory response syndrome (SIRS) and sepsis at low risk for organ dysfunction and d

184 ing systemic inflammatory response syndrome (SIRS) and sepsis.

185 the systemic inflammatory response syndrome (SIRS) and subsequent systemic complications.

186 ing systemic inflammatory response syndrome (SIRS) and the events that lead to multiorgan failure and

187 and systemic inflammatory response syndrome (SIRS) are major causes of morbidity and mortality after

188 of systemic inflammatory response syndrome (SIRS) associated with a procoagulant state.

189 the systemic inflammatory response syndrome (SIRS) criteria and organ dysfunctions, but most studies

190 the systemic inflammatory response syndrome (SIRS) criteria from the sepsis definition.

191 of systemic inflammatory response syndrome (SIRS) criteria to identify patients at high risk of mort

192 and systemic inflammatory response syndrome (SIRS) criteria, elevated sepsis-related organ failure as

193 re, systemic inflammatory response syndrome (SIRS) criteria, Logistic Organ Dysfunction System (LODS)

194 the systemic inflammatory response syndrome (SIRS) criteria.

195 for systemic inflammatory response syndrome (SIRS) criteria.

196 of systemic inflammatory response syndrome (SIRS) even in the absence of an infection.

197 the systemic inflammatory response syndrome (SIRS) followed for development of ALI, duration of mecha

198 The systemic inflammatory response syndrome (SIRS) in acute liver failure (ALF), in which infection i

199 to systemic inflammatory response syndrome (SIRS) induced by TNFalpha, which can be suppressed by RI

200 Systemic inflammatory response syndrome (SIRS) is a highly mortal inflammatory disease, associate

201 The systemic inflammatory response syndrome (SIRS) is a life-threatening medical condition characteri

202 Systemic inflammatory response syndrome (SIRS) is a potentially lethal condition, as it can progr

203 Systemic inflammatory response syndrome (SIRS) is associated with the development of severe medic

204 The systemic inflammatory response syndrome (SIRS) is the massive inflammatory reaction resulting fro

205 ere systemic inflammatory response syndrome (SIRS) is the massive recruitment of immature neutrophils

206 Systemic inflammatory response syndrome (SIRS) is typically associated with trauma, surgery, or a

207 The systemic inflammatory response syndrome (SIRS) is typified by the presence of fever, hemodynamic

208 ced Systemic Inflammatory Response Syndrome (SIRS) more rapidly than wild type mice while Ripk3-/- mi

209 The systemic inflammatory response syndrome (SIRS) occurs frequently in critically ill patients and p

210 Systemic inflammatory response syndrome (SIRS) occurs in a range of infectious and non-infectious

211 ult systemic inflammatory response syndrome (SIRS) patients enrolled at the emergency department.

212 s a systemic inflammatory response syndrome (SIRS) that is clinically much like sepsis.

213 the systemic inflammatory response syndrome (SIRS) were assessed in 137 patients undergoing major abd

214 is, systemic inflammatory response syndrome (SIRS), documented infections, and response to antimicrob

215 the systemic inflammatory response syndrome (SIRS), includes changes in heart rate, respiratory rate,

216 of systemic inflammatory response syndrome (SIRS), including acute lung injury (ALI), through activa

217 FA, Systemic Inflammatory Response Syndrome (SIRS), Modified Early Warning Score (MEWS), and the Nati

218 of systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), and m

219 the systemic inflammatory response syndrome (SIRS), or sepsis.

220 of systemic inflammatory response syndrome (SIRS).

221 of systemic inflammatory response syndrome (SIRS).

222 ive systemic inflammatory response syndrome (SIRS).

223 ith systemic inflammatory response syndrome (SIRS).

224 the systemic inflammatory response syndrome (SIRS).

225 ial systemic inflammatory response syndrome (SIRS; excessive pro-, but no/low anti-inflammatory plasm

226 is (systemic inflammatory response syndrome [SIRS] in the presence of significant infection).

227 al (systemic inflammatory response syndrome [SIRS]) and laboratory (tumor necrosis factor receptor 1

228 lt (systemic inflammatory response syndrome; SIRS) in the absence of infection.

229 ude AUROC, 0.753 [99% CI, 0.750-0.757]) than SIRS criteria (crude AUROC, 0.589 [99% CI, 0.585-0.593])

230 plex LODS but was statistically greater than SIRS and qSOFA, supporting its use in clinical criteria

231 stic accuracy for in-hospital mortality than SIRS criteria or the qSOFA score.

232 These findings suggest that SIRS criteria and qSOFA may have limited utility for pre

233 The SIRS trial does not support the routine use of methylpre

234 lyses based on direct comparisons across the SIRS, sepsis, and septic shock spectrum, and all availab

235 In ALF, the SIRS, whether or not precipitated by infection, appears

236 ogression of the individuals is given by the SIRS model, with an individual becoming infected on cont

237 terval [CI], 0.96 to 0.97; odds ratio in the SIRS-negative group, 0.96; 95% CI, 0.94 to 0.98; P=0.12

238 baseline characteristics (odds ratio in the SIRS-positive group, 0.96; 95% confidence interval [CI],

239 , these findings support the validity of the SIRS as an instrument to measure the social symptoms of

240 The magnitude of the SIRS in 273 patients with bacterial infection correlated

241 In 20 FTD patients, we used the SIRS to study the anatomic basis of social impairments.

242 Results suggest that when using the SIRS model the ensemble filters and the basic PF are mor

243 stinct social impairments measured using the SIRS.

244 8-0.64 mum) were higher in patients with the SIRS and high-grade HE, and MPs in the 0.36-0.64-mum siz

245 specific size ranges are associated with the SIRS, systemic complications, and adverse outcome of ALI

246 an MDL-1-specific agonist antibody leads to SIRS, shock, and death.

247 size range increased in direct proportion to SIRS severity (P < 0.001) and grade of HE (P < 0.002).

248 What triggers SIRS in the absence of infection, however, is unknown.

249 ional increase in risk at a threshold of two SIRS criteria.

250 e in the risk of death at a threshold of two SIRS criteria.

251 IRS-positive severe sepsis) or less than two SIRS criteria (SIRS-negative severe sepsis).

252 Finally, by blocking RKIP in wild-type SIRS splenocytes, the IFN-gamma response by CD8(+) Vbeta

253 es are present between sepsis and uninfected SIRS prior to the clinical appearance of sepsis.

254 Critically ill uninfected SIRS patients were followed longitudinally for the devel

255 s suggest that screening ward patients using SIRS criteria for identifying those with sepsis would be

256 .5-85.5 ng/mL), critically ill children with SIRS (median 107.5 ng/mL, IQR 89-178.5 ng/mL), and criti

257 ave some effect on survival in patients with SIRS and gram-negative sepsis; however, additional studi

258 serum levels identified those patients with SIRS and infection.

259 Here, 275 patients with SIRS and plasma levels of von Willebrand factor (VWF), t

260 ay mortality in critically ill patients with SIRS and sepsis.

261 Patients with SIRS had significantly increased mtDNA DAMP levels in al

262 4%; p < .0001) were higher in patients with SIRS than in those without SIRS.

263 Importantly, the course of patients with SIRS with and without infection was similar in terms of

264 ot predictive for mortality in patients with SIRS, opposite of the processing of VWF after release.

265 er-based model that identifies patients with SIRS/sepsis at low risk for death and organ dysfunction.

266 SIRS criteria, and patients presenting with SIRS had higher in-hospital mortality than those without

267 Among Caucasian subjects with SIRS (n = 750), we identified a nominal association betw

268 atients with definite sepsis than those with SIRS (P = .023).

269 er disease between patients with and without SIRS.

270 ectious SIRS (2.33 ng/ml), and eight without SIRS (1.97 ng/ml).

271 her in-hospital mortality than those without SIRS (4.3% vs. 1.2%; P < 0.001).

272 in patients with SIRS than in those without SIRS.