ライフサイエンスコーパス: sepsis

1 ective against mortality during experimental sepsis.

2 and improve infectious outcomes in neonatal sepsis.

3 y play a central role in the pathogenesis of sepsis.

4 the clinical symptoms that usually accompany sepsis.

5 potential protective agent against neonatal sepsis.

6 ity in clinical cohorts and animal models of sepsis.

7 ayed cord separation, failure to thrive, and sepsis.

8 n is a key determinant of gene expression in sepsis.

9 ors as a therapeutic strategy in adults with sepsis.

10 vailable in patients with trauma who develop sepsis.

11 ruses, fungi or parasites could also lead to sepsis.

12 costs of care for patients hospitalized with sepsis.

13 have coincided with increasing awareness of sepsis.

14 o more severe infection during Gram-negative sepsis.

15 ntibiotic treatment or episodes of suspected sepsis.

16 cells are attractive therapeutic targets in sepsis.

17 a sign of the body's host immune response to sepsis.

18 the bedside of critically ill patients with sepsis.

19 distress syndrome, acute chest syndrome, and sepsis.

20 mplicate adaptive immunity in post-traumatic sepsis.

21 of which had not been previously reported in sepsis.

22 cquired infections, all of which can lead to sepsis.

23 rtality from bloodstream infection (BSI) and sepsis.

24 (Bell stage II or more), and culture-proven sepsis.

25 factor in reducing mortality associated with sepsis.

26 of severe systemic inflammatory syndrome and sepsis.

27 were more susceptible K. pneumoniae-induced sepsis.

28 Ps, and improves outcome in murine models of sepsis.

29 ore traditional ELISpot assay using PBMCs in sepsis.

30 natural competence during pneumonia-derived sepsis.

31 will augment the treatment and prevention of sepsis.

32 ciation between HMOs and late-onset neonatal sepsis.

33 Improving Pediatric Sepsis Outcomes Critical Sepsis.

34 of evidence to guide antibiotic duration in sepsis.

35 nged and persistent during pneumonia-derived sepsis.

36 ry and improved survival after polymicrobial sepsis.

37 tidis causes life-threatening meningitis and sepsis.

38 , particularly in the more chronic phases of sepsis.

39 opment in a mouse model of pneumonia-derived sepsis.

40 nts in an ICU are particularly vulnerable to sepsis.

41 ossible mechanism for Tie2 downregulation in sepsis.

42 standard approach in certain cases, such as sepsis.

43 the cost of hospitalization with and without sepsis.

44 There were 35,244 first episodes of sepsis (17,886, 51%, female; median age 71 years, interq

45 Condition Category 8), 6.76 (6.71-6.82); all sepsis, 2.63 (2.62-2.65); respiratory arrest (Hierarchic

46 Combining the variables in Sepsis-2 and Sepsis-3 improved the discrimination (C-sta

47 We found that Sepsis-2 and Sepsis-3-based sepsis diagnoses represent s

48 among 1,460 patients with suspected sepsis (sepsis-2 definition), BC and PCR/ESI-MS on whole blood w

49 180 stillbirths) and congenital infection or sepsis (27 [15%]).

50 Combining the variables in Sepsis-2 and Sepsis-3 improved the discrimination (C-statistic = 0.74

51 ce area with regard to infection and sepsis (Sepsis-3) over a 14-day time course.

52 We found that Sepsis-2 and Sepsis-3-based sepsis diagnoses represent separate pheno

53 sociated variously with dehydration (45.4%), sepsis (41.1%), cardiogenic shock (20.9%), and diabetic

54 Of the 19,113 pediatric admissions with sepsis (6,300 [33%] previously healthy and 12,813 [67%]

55 ian injury severity score 33); 33% developed sepsis, 6% septic shock, and in-hospital mortality was 1

56 ere arrhythmias (19%), cardiac arrest (10%), sepsis (7%), and acute renal failure requiring dialysis

57 pies have been proposed for the treatment of sepsis, a syndrome resulting from a dysregulated immune

58 Describe the epidemiology of sepsis across the transition from the International Clas

59 ority hospitals on outcomes in patients with sepsis across the United States.

60 en for inclusion based on their relevance to sepsis, acute inflammation, sepsis-related immune suppre

61 More rigor is needed in tracking sepsis after trauma and evaluating the effectiveness of

62 d interest in RAGE for its potential role in sepsis, along with a host of other inflammatory diseases

63 th records to calculate mortality related to sepsis among each of the 282 underlying causes of death

64 2 critically ill patients, including 53 with sepsis and 59 with intracerebral hemorrhage, along with

65 2 critically ill patients, including 53 with sepsis and 59 with intracerebral hemorrhage.

66 riers and fulminant disease characterized by sepsis and acute respiratory failure.

67 hronic lung disease, can cause pneumonia and sepsis and can trigger exacerbations of lung diseases.

68 In some mice, acute pneumonia quickly led to sepsis and death, accompanied by increasing intensity of

69 t and prognosis strategies in the setting of sepsis and discuss future challenges.

70 enetic modifiers can mitigate the effects of sepsis and improve survival as well as reverse sepsis-as

71 hat might help distinguish between pediatric sepsis and infection-negative systemic inflammation and

72 infection (bacterial and viral), and between sepsis and infection.

73 Many hemodynamically stable patients with sepsis and low acuity of illness may benefit from furthe

74 s study can be useful to distinguish between sepsis and noninfectious systemic inflammation.

75 fecal samples associated with development of sepsis and obesity by age 2 years.

76 ge of antibiotics for pneumonia and neonatal sepsis and of oral rehydration solution for diarrhoea wo

77 death in the gemcitabine alone group due to sepsis and one treatment-related death in the gemcitabin

78 susceptibility to adverse outcomes including sepsis and septic shock.

79 dence rate of emergency department-attending sepsis and severe sepsis in adults was 1772 per 100 000

80 y be a source of circulating histones during sepsis and should be further explored.

81 the ability to immunophenotype patients with sepsis and to guide potential new immunotherapies.

82 ted and become dysfunctional during clinical sepsis, and contribute to tissue-specific cytokine respo

83 hospitalization, intubation, prolonged stay, sepsis, and death.

84 us nosocomial infections such as bacteremia, sepsis, and endocarditis.

85 which can arise in response to nephrotoxins, sepsis, and ischemia/reperfusion, and in chronic kidney

86 f cardiovascular nature, respiratory origin, sepsis, and multiorgan failure were significantly lower

87 i-inflammatory properties, protect mice from sepsis, and prevent IL-1beta secretion by monocytes from

88 driven by dysregulated inflammation, such as sepsis, and raise the possibility that CB(1)R-signaling

89 driver for many diseases, including cancer, sepsis, and stroke.

90 MAIT cells during clinical and experimental sepsis, and their contribution to host responses.

91 olesterol (HDL-C) decline drastically during sepsis, and this phenomenon is explained, in part, by th

92 alth loss, but data for the global burden of sepsis are limited.

93 rgeting patients with clinical indicators of sepsis are needed to guide measures to safely reduce ant

94 ng the benefits of specific interventions in sepsis, argues for an individualized and titrated approa

95 nhibited in blood monocytes of patients with sepsis as compared with nonseptic patients.

96 view, we discuss the metabolic signatures of sepsis as they relate to the loss of glycocalyx integrit

97 trum of presentation and disease severity in sepsis, as well as the complexity surrounding the benefi

98 transplantation may be a treatment option in sepsis associated with immunosuppression.

99 uction was 2.55% (p = 0.32) in patients with sepsis-associated coagulopathy.

100 Sepsis-associated encephalopathy (SAE) is an acutely pro

101 Known sepsis-associated genes included complement component 3;

102 demonstrated that pericyte miR-145a mediates sepsis-associated microvascular dysfunction, potentially

103 e-blood gene-expression studies have defined sepsis-associated molecular signatures, but have not res

104 psis and improve survival as well as reverse sepsis-associated organ injury.

105 essing patients with suspected infection and sepsis at hospital admission.

106 Unfortunately, the heterogeneity of sepsis at the individual patient level has hindered adva

107 ysis syndrome (in three [18%] patients); and sepsis, atrial flutter, indirect hyperbilirubinaemia, ce

108 ed features, to identify a patient's risk of sepsis based on physiologic data streams.

109 In doing so, a sepsis biomarker could be used for earlier identificatio

110 ve emerged as a better platform for neonatal sepsis biomarkers detection.

111 eview one of the most common clinically used sepsis biomarkers, procalcitonin, and its roles in sepsi

112 cant research has been conducted to identify sepsis biomarkers.

113 Worldwide sepsis burden is likely to be underestimated, and data f

114 as highly expressed during pneumonia-derived sepsis but failed to turn off the competent state in mic

115 sociated with improved outcomes in pediatric sepsis, but minimal data exist to guide empiric therapy.

116 flammatory cytokine response during neonatal sepsis by directly compromising control of bacteria that

117 FMT) reverses the course of otherwise lethal sepsis by enhancing pathogen clearance via the restorati

118 es (C-statistic = 0.84, 95% CI 0.81-0.86) or sepsis (C-statistic = 0.80, 95% CI 0.78-0.82).

119 he Cre-loxP system protects mice from lethal sepsis (caecal ligation and puncture or infection by Esc

120 ften associated with hemodynamic compromise, sepsis, cardiac surgery, or exposure to nephrotoxins.

121 The aggregate costs of sepsis care for Medicare beneficiaries will continue to

122 of hospital mandates and policies to improve sepsis care in patients after trauma.

123 Mandated protocolized sepsis care was not associated with significant changes

124 e contributed to significant improvements in sepsis care.

125 tiation of septicemic melioidosis from other sepsis cases had a sensitivity of 82%, specificity of 93

126 improves animal survival in three models of sepsis (cecal ligation and puncture or bacteremia with E

127 tly reduce 28-day all-cause mortality in the Sepsis Coagulopathy Asahi Recombinant LE Thrombomodulin

128 d for an inpatient hospital admission with a sepsis code are nearly indistinguishable by other diagno

129 ent hospital admission including an explicit sepsis code for those beneficiaries in those calendar ye

130 gests that an inpatient stay that included a sepsis code not only identifies beneficiaries who were l

131 spital admission associated with an explicit sepsis code rose from 811,644 to 1,136,889.

132 from those whose admissions will not have a sepsis code, their healthcare trajectories following the

133 inpatient hospital admission, those who had sepsis coded during the index admission were more likely

134 and correlates of EBV-positivity in a large sepsis cohort.

135 likely to have comorbid pneumonia and severe sepsis.Conclusions: Noninvasive ventilation use during a

136 been remarkable over the last 2 decades, but sepsis continues to be a major cause of death in this po

137 l regression to predict Medicare beneficiary sepsis costs.

138 The clinical evidence for sepsis could typically attribute to bacterial infection

139 Blocking or deleting TNFR2 during sepsis decreased the susceptibility to secondary infecti

140 The Improving Pediatric Sepsis Outcomes Sepsis definitions demonstrated strengths in content val

141 We found that Sepsis-2 and Sepsis-3-based sepsis diagnoses represent separate phenotypes with poor

142 5%; odds ratio, 4.31; 95% CI, 2.01-10.28) of sepsis diagnosis compared with IV piggyback.

143 teria from whole blood as demanded for rapid sepsis diagnosis where minimal numbers of bacteria need

144 ntensive care, 2% (95% CI, 1%-3%) included a sepsis diagnosis, and <1% (95% CI, 0%-1%) resulted in re

145 ractory CRS concurrent with culture-positive sepsis died, and 3 achieved CR.

146 detects acidosis in regions associated with sepsis-driven proinflammatory responses.

147 eeks and a higher proportion developed fatal sepsis during the neonatal period.

148 epartment staff participated in a designated sepsis education before the model was introduced.

149 ment, duration of coma, delirium, hypoxemia, sepsis, education level, hospital type, insurance status

150 Accordingly, the Life After Pediatric Sepsis Evaluation investigation was conducted to describ

151 ability (95% uncertainty intervals [UIs]) of sepsis following an infection consultation.

152 Checkpoint inhibitors have been proposed for sepsis following reports of increased checkpoint molecul

153 source algorithms for the early detection of sepsis from clinical data.

154 y Challenge 2019 on the "Early Prediction of Sepsis from Clinical Data." It consisted of ICU patient

155 The creation of dedicated sepsis guidelines and their broad dissemination over the

156 In fact, the term "viral sepsis" has been recently coined to describe the clinica

157 Identification and outcomes in patients with sepsis have improved over the years, but little data are

158 ith sepsis, we identified that patients with sepsis have increased amounts of platelet-associated his

159 raction of patients initially diagnosed with sepsis have noninfectious conditions.

160 from mortality during SARS-CoV-2 infection, sepsis, hemophagocytic lymphohistiocytosis, and cytokine

161 all-cause pediatric hospitalizations, severe sepsis hospitalizations were eight-fold more likely to i

162 Among 18,210 pediatric severe sepsis hospitalizations, 1,024 (5.6%) underwent device p

163 colostrum with a reduced risk of late-onset sepsis (HR: 0.63; 95% CI: 0.41, 0.97).

164 resulted in earlier electronic health record sepsis identification in greater than 50% of patients.

165 nhance timely electronic health record-based sepsis identification.

166 ly ill oncology and hematology patients with sepsis improved significantly over time.

167 ockout (KO) mice were greatly protected from sepsis in a clinically relevant version of the cecal lig

168 evaluate the immune status of patients with sepsis in a rapid and quantifiable manner has undoubtedl

169 gency department-attending sepsis and severe sepsis in adults was 1772 per 100 000 person-years (95%

170 ovides an update on the current knowledge of sepsis in immunocompromised patients without human immun

171 ment of multidrug-resistant bacteria-induced sepsis in mice with immunosuppression.

172 xperimental autoimmune encephalomyelitis and sepsis in mice.

173 from disseminating systemically and causing sepsis in neonatal mice.

174 hospital costs in patients hospitalized with sepsis in New York State.

175 or GBS) is a common cause of bacteremia and sepsis in newborns, pregnant women, and immunocompromise

176 Identifying sepsis in pediatric patients is difficult and can lead t

177 e potentially treatment related (one case of sepsis in the 2.5 mg/kg cohort and one case of haemophag

178 milk oligosaccharides (HMOs) and late-onset sepsis in very-low-birth-weight infants, and to describe

179 Age-standardised sepsis incidence fell by 37.0% (95% UI 11.8-54.5) and mo

180 llenges to shorter antimicrobial duration in sepsis include inadequate source control, treatment of m

181 fy major biomarkers associated with neonatal sepsis including Serum Amyloid A (SAA), C - reactive pro

182 cases of Improving Pediatric Sepsis Outcomes Sepsis, including 8,565 with Improving Pediatric Sepsis

183 l membrane oxygenation (VA-ECMO) support for sepsis-induced cardiogenic shock refractory to conventio

184 Patients with severe sepsis-induced cardiogenic shock treated with VA-ECMO ha

185 we identified FOSL1 as a novel regulator of sepsis-induced deviant angiogenic signaling in mouse lun

186 dentify novel signaling pathways programming sepsis-induced deviant lung angiogenesis.

187 es, including autoantigens, is a hallmark of sepsis-induced immunoparalysis.

188 dings describe in vivo mechanisms underlying sepsis-induced immunosuppression and identify TNFR2pos T

189 cific miR-145a-knockout mouse and determined sepsis-induced organ injury, lung and renal vascular lea

190 owledge, the potential roles of microRNAs in sepsis-induced pericyte dysfunction have not been explor

191 ivation of Treg during Staphylococcus aureus sepsis induces CD4+ T-cell impairment and increases susc

192 cross the world are occurred due to neonatal sepsis infections.

193 Sepsis initiates simultaneous pro- and anti-inflammatory

194 method for computing risk of transition from sepsis into septic shock.

195 Sepsis is a complex process defined as life-threatening

196 th the hypothesis that viral reactivation in sepsis is a consequence of immune compromise and is asso

197 Sepsis is a heterogeneous disease state that is both com

198 Systemic sepsis is a known risk factor for bronchopulmonary dyspl

199 Critical illness such as sepsis is a life-threatening syndrome defined as a dysre

200 Sepsis is a series of clinical syndromes caused by the i

201 The efficacy of NT therapies in murine sepsis is both time-dependent and charge-dependent.

202 Sepsis is characterized by a dysregulated immune respons

203 Sepsis is commonly present with high lethality in the se

204 fication and validation for the treatment of sepsis is of the utmost importance.

205 guidance regarding antimicrobial duration in sepsis is surprisingly limited.

206 Sepsis is the most common cause of death for patients in

207 ics and mortality for patients with possible sepsis is therefore critical to finding the best balance

208 Sepsis is typically triggered by an overwhelming systemi

209 idney injury (AKI), a common complication of sepsis, is associated with substantial morbidity and mor

210 morbidity among children initially surviving sepsis, is unknown.

211 The inclusion of ferritin into the sepsis laboratory panel is warranted.

212 eased risk for the development of late-onset sepsis (LOS).

213 biomarkers, procalcitonin, and its roles in sepsis management in these three areas.

214 0th Edition, coding strategy for identifying sepsis may capture a larger patient population within ad

215 r than or equal to 2 as a screening tool for sepsis may miss patients who ultimately die.

216 We hypothesized that sepsis may represent the first manifestation of underlyi

217 o cause infection in both a subcutaneous and sepsis model of infection.

218 In-hospital pediatric sepsis mortality has decreased substantially, but long-t

219 Sepsis mortality has improved following advancements in

220 was associated with significantly decreased sepsis mortality in the UK Biobank (hazard ratio, 0.77 [

221 quencing to profile the blood of people with sepsis (n = 29) across three clinical cohorts with corre

222 ted malaria (n = 91), or suspected bacterial sepsis (n = 56), as well as healthy participants (n = 50

223 cellulitis (n=3 [3%]), fall (n=3 [3%]), and sepsis (n=3 [3%]).

224 tropenia) and four in the intravenous group (sepsis [n=2], hepatitis B reactivation [n=1], and Pneumo

225 Critically ill patients with sepsis or septic shock are at an increased risk of death

226 ds of PICU mortality in children with severe sepsis or septic shock.

227 s are present in 28% of children with severe sepsis or septic shock.

228 ision, Clinical Modification code for severe sepsis or septic shock; 3,021 of these patients (28%) ha

229 th baseline hypofibrinolysis associated with sepsis, organ failure, and short-term mortality.

230 is, including 8,565 with Improving Pediatric Sepsis Outcomes Critical Sepsis.

231 loss-of-function is associated with improved sepsis outcomes in the adult host through increased hepa

232 The Improving Pediatric Sepsis Outcomes Sepsis definitions demonstrated strength

233 Among Improving Pediatric Sepsis Outcomes Sepsis patients, 60.8% were admitted to

234 Improving Pediatric Sepsis Outcomes Sepsis was defined by electronic health

235 ere were 23,976 cases of Improving Pediatric Sepsis Outcomes Sepsis, including 8,565 with Improving P

236 sitivity and specificity of the diagnosis of sepsis over current clinical criteria approaches.

237 Also, we found that during a murine model of sepsis, P2X7 receptor activity is important for maintain

238 within the stromal compartment to exacerbate sepsis pathogenesis via differential impacts on IL-6-rel

239 were indicative of complicated course in all sepsis patients (all area under the receiver operating c

240 prospective observational study included 239 sepsis patients admitted and enrolled between January 20

241 llowing initial fluid resuscitation identify sepsis patients with differing risk for progression of A

242 longitudinal measurements were compared for sepsis patients with versus without acute respiratory di

243 Among Improving Pediatric Sepsis Outcomes Sepsis patients, 60.8% were admitted to intensive care,

244 In human sepsis patients, multiple epigenetic modifying enzymes s

245 del more closely approximated human surgical sepsis patients, particularly in the more chronic phases

246 Among critically ill surgical sepsis patients, persistent AKI and the absence of renal

247 f adverse events, mortality, and costs among sepsis patients.

248 001) and cellular ATP content (p < 0.001) in sepsis patients.

249 he gold standard to inform novel pathways of sepsis physiology and its therapeutic direction.

250 to identify acute AF precipitants (surgery, sepsis, pneumonia, pneumothorax, respiratory failure, my

251 Machine learning augments burn sepsis prediction.

252 unosuppressive medication, in the context of sepsis, rapamycin has the opposite effect.

253 l plasma collected within 3 days (time 1) of sepsis recognition and at 3-6 days (time 2) and 7-14 day

254 have proposed new clinical criteria that aid sepsis recognition, the fundamental need for early detec

255 Patients with sepsis regardless of race who were treated in disproport

256 uated the effects of the 2013 New York State sepsis regulations on the costs of care for patients hos

257 The percentage of sepsis-related deaths by underlying GBD cause in each lo

258 eir relevance to sepsis, acute inflammation, sepsis-related immune suppression, and sepsis-related or

259 Sepsis-related mortality for each age group, sex, locati

260 tion, sepsis-related immune suppression, and sepsis-related organ failure.

261 Neutrophils play a crucial role in sepsis, releasing neutrophil extracellular traps (NETs)

262 Sepsis remains among the most common complications from

263 Sepsis remains medically challenging, with high morbidit

264 The model has been the mainstay of sepsis research for decades and continues to be consider

265 sorely lacking and should be a priority for sepsis researchers.

266 ere inflammation (n = 104, 35.6%) related to sepsis, respiratory failure, acute respiratory distress

267 ing leukocytes, specifically patients with a Sepsis Response Signature endotype (SRS1) that we have p

268 y such patients we aimed to use knowledge of sepsis response subphenotypes based on transcriptomic st

269 Moreover, overall sepsis risk was low and did not change significantly as

270 could be used for earlier identification of sepsis, risk stratification/prognostication, and/or guid

271 Second, among 1,460 patients with suspected sepsis (sepsis-2 definition), BC and PCR/ESI-MS on whole

272 dy surface area with regard to infection and sepsis (Sepsis-3) over a 14-day time course.

273 nts with hemophagocytic lymphohistiocytosis, sepsis, septic shock, and other conditions were distinct

274 munology, as well as a small number of human sepsis studies, suggest that epigenetic regulation may p

275 critical next step is to develop a consensus sepsis subclassification system, which includes transcri

276 nzymes show differential expression in early sepsis, suggesting a role for epigenetics in coordinatin

277 discuss the interactions between cancer and sepsis supported by clinical data and the translation to

278 the advantages and limitations of different sepsis surveillance strategies and consider future direc

279 sm syndrome observed in adult human surgical sepsis survivors.

280 rum and preterm neonatal plasma samples with sepsis suspicion.

281 cidence of infections resistant to empirical sepsis therapy.

282 Neutrophils act as double-edged swords in sepsis; they can help to eradicate microbes, but they al

283 function (gut-liver axis) and by episodes of sepsis to cause cholestasis and IFALD.

284 roteins that correlated highly with clinical sepsis traits, 27 of which had not been previously repor

285 h record evidence of suspected infection and sepsis treatment or organ dysfunction.

286 Rolipram may therefore be a potential novel sepsis treatment, one that would bypass the time-consumi

287 peding clinicians from providing appropriate sepsis treatment.

288 69 patients died in complete remission from sepsis (two [3%]), cardiac arrest (one [1%]), therapy-re

289 reterm babies' plasma samples with suspected sepsis using very low volumes (<10 muL) and in just 5 mi

290 xygen consumption index in the patients with sepsis was 8.4 mL/min/m (2.3-14.5 mL/min/m; p = 0.01).

291 increased plasma IFN-gamma in early clinical sepsis was associated with the later development of seco

292 Improving Pediatric Sepsis Outcomes Sepsis was defined by electronic health record evidence

293 aller for the period from 2014 to 2017, when sepsis was diagnosed more frequently.

294 ion of isolated platelets from patients with sepsis, we identified that patients with sepsis have inc

295 Bacterial translocation and subsequent sepsis were minimal in 7 Gy GIARS mice treated with GL.

296 te Crohn's disease, rheumatoid arthritis, or sepsis were susceptible to both IgA- and IVIG-mediated d

297 ion (LR) identified seven predictors of burn sepsis when controlled for age and burn size (OR 2.8, 95

298 s modest discrimination (AUC = 0.73) between sepsis with organ dysfunction and infection with no orga

299 n Category 27), 2.53 (2.49-2.56); and severe sepsis without shock, 2.48 (2.45-2.51).

300 s adequacy of shorter treatment durations in sepsis would be beneficial.