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 was present in 33.9% of patients upon CICU admissio

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

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

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

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

15 Patients with >=2/4 SIRS criteria based on admission laboratory and vital si

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

17 .8%) patients who did not become infected, a SIRS on admission was associated with a more critical il

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

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

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

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

22 After multivariable adjustment, SIRS was associated with higher hospital and 1-year mort

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

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

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

26 ), 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

27 a key link between trauma, inflammation and SIRS.

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

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

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

31 re neutrophils circulating during sepsis and SIRS.

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

33 Measurement of qSOFA, SOFA, and SIRS.

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

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

36 The association between SIRS and mortality was evaluated across SCAI shock stage

37 4-0.85) vs 0.65 (95% CI, 0.59-0.70) for both SIRS and severe sepsis (P < .001; incremental AUROC, 0.1

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

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

40 ve been established for patients affected by SIRS.

41 innate immunities are greatly influenced by SIRS levels.

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

43 es while also studying their role in causing SIRS.

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

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

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

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

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

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

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

51 her preoperatively in patients who developed SIRS.

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

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

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

55 e whether systemic inflammation truly drives SIRS in this population and whether patients with SIRS r

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

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

58 ted with secondary hyporesponsiveness during SIRS.

59 le modulating the brain transcriptome during SIRS.

60 of overall mitotic timing ensures efficient SIRS.

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

62 ise and multitarget therapeutic approach for SIRS and sepsis.

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

64 of CICU patients meet clinical criteria for SIRS at the time of admission, and these patients have h

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

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

67 he proinflammatory cytokines responsible for SIRS initiation.

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

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

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

71 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

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

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

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

75 al infection and differentiating sepsis from SIRS.

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

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

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

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

80 and vital sign data were considered to have SIRS.

81 ship between cytokines and their blockers in SIRS.

82 An upper temperature of 37.5 degrees C in SIRS criteria improved BSI screening in transplant recip

83 that while the HSC reservoir was depleted in SIRS, HSCs were spared in CHRFAM7A-transgenic mice and t

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

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

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

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

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

89 NAs appeared less abundant in sepsis than in SIRS.

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

91 nd they explain how some snake venoms induce SIRS-like conditions.

92 esponse syndrome [SIRS] or snakebite-induced SIRS-like conditions), we employed the C-type lectin-rel

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

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

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

96 lly affected during sepsis and non-infective SIRS.

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

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

99 pared these results to those for the initial SIRS criteria obtained in triage.

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

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

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

103 (125 [13%] of 960 patients died) or who met SIRS criteria (128 [9%] of 1392 patients died).

104 26.6] per 100 person-years) or those who met SIRS criteria (14.7 deaths [12.5-17.2] per 100 person-ye

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

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

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

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

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

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

111 via the emergency department with 2 or more SIRS criteria (1 269 998 male patients [81.4%]; median [

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

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

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

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

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

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

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

119 Among critically ill patients with 2 or more SIRS criteria, treatment with a low-normal Pao2 target c

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

121 model of human inflammatory disease, namely SIRS, the systemic inflammatory response syndrome that a

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

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

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

125 We sought to determine the association of SIRS with illness severity and survival across the spect

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

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

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

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

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

131 5% vs. 50% for 0, 1, and >or=2 components of SIRS, P < 0.05).

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

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

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

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

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

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

138 001) were associated with the development of SIRS.

139 of cytokine production to the development of SIRS.

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

141 ation without having a clinical diagnosis of SIRS.

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

143 27 who did not, when no clinical evidence of SIRS was apparent (preoperatively or days 1 and 2).

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

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

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

147 molecular explanation for the initiation of SIRS.

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

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

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

151 The presence of SIRS identified CICU patients at increased risk of short

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

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

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

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

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

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

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

159 Among these patients, SIRS was present in 59.2% of patients, while sepsis was

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 evelopment of complications including sepsis/SIRS.

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

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

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

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

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

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

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

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

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

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

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

187 h sepsis and those from patients with severe SIRS.

188 pabilities are generated in mice with severe SIRS.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 of systemic inflammatory response syndrome (SIRS) criteria as a screening tool; however, its role in

210 ify systemic inflammatory response syndrome (SIRS) criteria for transplant recipients.

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

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

213 on systemic inflammatory response syndrome (SIRS) criteria, and Blantyre census population data, we

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

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

216 for systemic inflammatory response syndrome (SIRS) criteria.

217 the systemic inflammatory response syndrome (SIRS) criteria.

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

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

220 The systemic inflammatory response syndrome (SIRS) frequently occurs in patients with cardiogenic sho

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

243 R: systemic inflammatory response syndrome (SIRS), spontaneous bacteria peritonitis (SBP), and pneum

244 ith systemic inflammatory response syndrome (SIRS).

245 the systemic inflammatory response syndrome (SIRS).

246 of systemic inflammatory response syndrome (SIRS).

247 of systemic inflammatory response syndrome (SIRS).

248 ive systemic inflammatory response syndrome (SIRS).

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

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

251 g., systemic inflammatory response syndrome [SIRS] or snakebite-induced SIRS-like conditions), we emp

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

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

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

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

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

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

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

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

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

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

262 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

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

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

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

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

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

268 stinct social impairments measured using the SIRS.

269 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

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

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

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

273 For comparison, the triage SIRS criteria and the initial lactate > 3 mmol/L had sen

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

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

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

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

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

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

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

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

282 .5-85.5 ng/mL), critically ill children with SIRS (median 107.5 ng/mL, IQR 89-178.5 ng/mL), and criti

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

284 serum levels identified those patients with SIRS and infection.

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

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

287 Patients with SIRS had higher illness severity, worse shock, and more

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

289 in this population and whether patients with SIRS respond differently to supportive therapies for sho

290 4%; p < .0001) were higher in patients with SIRS than in those without SIRS.

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

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

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

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

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

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

297 er disease between patients with and without SIRS.

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

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

300 in patients with SIRS than in those without SIRS.