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1 first but increasing as the infection became septic.
2 re of diagnostic value for the prediction of septic acute kidney injury courses requiring renal repla
3 er candidates for the risk stratification of septic acute kidney injury patients with the need for re
4 The primary endpoint was the development of septic acute kidney injury with the need for renal repla
11 data from seven external datasets containing septic and nonseptic patients, 81% of the differentially
15 gery for trauma (RR 1.9 [1.4-2.6]), previous septic arthritis (RR 4.9 [2.7-7.6]) or inflammatory arth
16 ins were identified and were associated with septic arthritis among black men who have sex with men a
18 s who received arthroscopic knee washout for septic arthritis in England between April 1, 1997, and M
19 system/spine infections, osteomyelitis, and septic arthritis were labeled as IDRIs if discharge code
20 s (infective endocarditis, epidural abscess, septic arthritis, and osteomyelitis), the mean age was 4
22 rial extracorporeal membrane oxygenation for septic cardiomyopathy but also indicate improved hospita
24 clinical outcomes in severe inflammatory and septic conditions.Objectives: Although recent investigat
27 Nonetheless, it is noteworthy that an acute septic episode may harbor antitumoral properties under p
28 as a significant predictor for the number of septic episodes (P = 0.02); independent of age, model of
29 sitively associated with EA, while number of septic episodes was negatively associated (HR = 0.95; 95
30 of hyperinflammation frequently camouflages septic events delaying the initiation of targeted intens
31 nto 6 groups (N = 12/group): 3 control and 3 septic groups depending on the euthanasia time (24 h, 48
33 hether these phenotypic similarities between septic humans and mice are replicated at the circulating
34 ting heparan sulfate in endotoxemic mice and septic humans was enriched in 2-O- and N-sulfated disacc
37 jurisdictions with limited information about septic infrastructure may be able to use geospatial data
39 gaster, to investigate how infection through septic injury modulates nutritional intake and how macro
41 LPS)-induced systemic inflammation (SI; at a septic-like model) in spontaneously hypertensive rats (S
43 t discrimination between liver sections from septic mice and sham-treated mice in contrast to SHG (AU
44 eatment results in a 100% survival in severe septic mice by controlling both infection and hyperinfla
46 d provides an insight on the contribution of septic mice models in the study of multi organ dysfuncti
50 une network was similar in IRF3-KO versus WT septic mice, although the tempo of connectivity differed
53 the identified IsdA mAbs worked in a murine septic model of infection to reduce bacterial burden dur
54 usive hydrogel resins simultaneously adsorbs septic molecules, e.g. lipopolysaccharides (LPS), cytoki
55 d proinflammatory shift was also observed in septic monocytes, signifying that patients suffering fro
58 lop an exhaustive phenotype resembling human septic neutrophils with elevated expression of ICAM1, CD
59 8-5.25) in ICU patients whether admitted for septic or nonseptic causes and 2) the need for renal rep
60 y, we prospectively analyzed PBMCs both from septic patients (n = 10) and lipopolysaccharide stimulat
64 o aid in the rapid and accurate diagnosis of septic patients and to ensure antibiotics are given to p
65 bolic and immune alterations and over 1/3 of septic patients are diabetic, but the mechanism linking
67 gnifying a steeper increase in PSP levels in septic patients as opposed to those exhibiting a nonsept
68 of these sulfation patterns in the plasma of septic patients at intensive care unit (ICU) admission p
71 severity score >= 15) and nonsevere injured septic patients had an odds ratio of 1.39 (95% CI, 1.31-
74 26 studies, compared with healthy controls, septic patients had significantly (p <= 0.05) increased
75 ies, compared with critically ill nonseptic, septic patients had significantly increased checkpoint m
76 ation of serum procalcitonin (PCT) levels in septic patients is facilitated by reviewing the known st
77 onuclear cells were significantly reduced in septic patients on day 1 (p < 0.05), whereas mitochondri
85 contribute to the high mortality rates among septic patients, despite new antimicrobials and resuscit
87 been considerable effort to immunophenotype septic patients, these methods have often not accurately
97 -day mortality decreased among patients with septic shock (22.1% to 15.5%), septic shock with acute r
98 5% male; mean +/- SD, 60 +/- 14 yr old) with septic shock (30%), hemorrhagic shock (15%), cardiogenic
99 10.3%), severe sepsis (20.3% vs 10.3%), and septic shock (33.5% vs 15.9%) was higher in prolonged ac
100 most costly complications were postoperative septic shock (4.0-fold, 95% CI 3.58-4.43) renal insuffic
101 nd chemotherapy (94 patients) were sepsis or septic shock (46 patients [19%] for quizartinib vs 18 [1
102 R had the best discrimination for predicting septic shock (c-statistic 0.90), respiratory failure req
103 The cohorts consisted of 120 patients with septic shock (cohort 1) and 88 patients with S. aureus b
104 rvival benefit was observed in patients with septic shock (HR, 0.80 [CI, .26-2.46]), in NVIE (HR, 0.7
105 ified complications were hepatitis (n = 36), septic shock (n = 22), and pulmonary complications/pneum
106 e ICU admission (OR 5.07, 95% CI 3.18-8.07), septic shock (OR 1.92, 95% CI 0.93-3.98), corticosteroid
107 ST16 (OR 21.4; CI95% 2.3-202.8; p=0,008) and septic shock (OR 11.9; CI95% 4.2-34.1; p<0,001) were ind
108 R 1.943; 95% CI 1.209-3.123), development of septic shock (OR 25.896; 95% CI 8.970-74.765), and the p
109 ence interval [CI], 2.3-202.8; P = .008) and septic shock (OR, 11.9; 95% CI, 4.2-34.1; P < .001) were
110 able intensive care patients with or without septic shock (recommended threshold for RBC transfusion,
112 ation of fluid for infants and children with septic shock (this latter topic was evaluated by evidenc
115 fected patients: 1) patients in the ICU with septic shock and 2) hospitalized patients with Staphyloc
116 hours and first 24 hours after the onset of septic shock and 30-day in-hospital mortality; 2) determ
117 id Treatment in Critically Ill Patients with Septic Shock and Activated Protein C and Corticosteroids
118 id Treatment in Critically Ill Patients with Septic Shock and Activated Protein C and Corticosteroids
119 its potential as a driver of inflammation in septic shock and autoimmune diseases, GSDMD represents a
120 We then analyze plasma from patients with septic shock and find that increasing levels of IL-6 and
121 id Treatment in Critically Ill Patients with Septic Shock and hydrocortisone at a 50 mg IV bolus ever
122 we validated the known genes and pathways in septic shock and identified the unexplored septic shock-
123 o validate this association in children with septic shock and in a juvenile murine model of sepsis.
124 irculating endothelial progenitor cells from septic shock and nonseptic shock patients showed evidenc
125 s in the durvalumab plus tremelimumab group (septic shock and pneumonitis), and one (<1%) patient in
126 ccurred in one patient in the placebo group (septic shock and pulmonary oedema) and one patient in th
130 outcomes in patients with severe sepsis and septic shock as a result of the full implementation of t
131 of vasopressin infusion among patients with septic shock as well as vasoplegic shock after cardiotho
134 ration of HAT therapy among U.S. adults with septic shock before and after study publication and to c
137 d 12 months following PICU admission for the septic shock event, 8%, 11%, 12%, and 13% of patients ha
138 randomized controlled trials in the field of septic shock failed to demonstrate a benefit on mortalit
139 btained serum samples from 529 patients with septic shock from 22 ICUs in Australia and New Zealand.M
141 revealed the role of caspase-11 in mediating septic shock in response to lethal doses of lipopolysacc
142 a central mediator of systemic inflammation, septic shock in the Plasmodium chabaudi-infected mice an
144 pective observational study of children with septic shock in whom the PERSEVERE biomarkers were measu
149 Studies have indicated that patients with septic shock may benefit from extracorporeal membrane ox
150 ntial Organ Failure Assessment scores in the septic shock nonsurvivors patients but not in nonseptic
152 ting consensus criteria for severe sepsis or septic shock on manual chart review were entered into th
156 he timing of antibiotics and mortality among septic shock patients has not been examined among patien
157 mean arterial pressure with noradrenaline in septic shock patients improves density and flow in small
158 ng samples from 10 healthy volunteers and 20 septic shock patients stratified using human leukocyte a
159 es: healthy volunteers, intermediate mHLA-DR septic shock patients, and low mHLA-DR septic shock pati
160 erbate elevated cytokine levels in plasma of septic shock patients, consistent with a safe response.
161 (TNF-alpha) secretion by single monocytes in septic shock patients, to study immune responses by meas
165 ts (n = 274) diagnosed with severe sepsis or septic shock per Sepsis-2 criteria from September to Nov
168 hepatitis related to atezolizumab [n=1] and septic shock related to nab-paclitaxel [n=1]) and one (<
169 hypotensive and was admitted to ICU in frank septic shock requiring inotropes, and with demonstrable
174 t GNB had a significantly lower incidence of septic shock than nontransplant GNB (10.3% vs 30.7%, p =
175 epsis who are at elevated risk of developing septic shock therefore has the potential to save lives b
176 all group of patients with severe sepsis and septic shock treated with hydrocortisone, high-dose asco
177 In 632 patients enrolled in Vasopressin and Septic Shock Trial, Proprotein Convertase Subtilisin/Kex
179 patients with AKI in VASST (Vasopressin and Septic Shock Trial; n = 271), and differences in treatme
183 re initiating therapy, whereas patients with septic shock warrant emergent broad-spectrum antibiotics
184 ng intensity during the first 24 hours after septic shock was associated with increased mortality.
187 ncer patients admitted to ICUs for sepsis or septic shock were extracted from the Groupe de Recherche
190 tcomes of 82 patients (aged >=18 years) with septic shock who received VA-ECMO at five academic ECMO
191 Two deaths were deemed treatment related (septic shock with 60 mg/m(2); pneumonia with 90 mg/m(2))
192 ong all groups (septic shock: 12.6% to 6.7%; septic shock with acute respiratory failure receiving in
193 patients with septic shock (22.1% to 15.5%), septic shock with acute respiratory failure receiving in
195 kers can identify subgroups of patients with septic shock with differential treatment responses to hy
199 id Treatment in Critically Ill Patients with Septic Shock) and $30,911 (Activated Protein C and Corti
202 oclax group (two from pneumonia and one from septic shock) were considered treatment-related; no deat
203 equiring intensive care and/or patients with septic shock), blending together mortality estimates fro
204 t failure, sepsis severity (severe sepsis vs septic shock), obesity, Mortality in Emergency Departmen
206 without the characteristic) are as follows: septic shock, 7.27 (7.19-7.35); metastatic cancer and ac
207 id Treatment in Critically Ill Patients with Septic Shock, adjunctive hydrocortisone therapy showed a
208 ated Protein C and Corticosteroids for Human Septic Shock, adjunctive hydrocortisone therapy showed a
209 groups have a 76.5% and 10.4% prevalence of septic shock, and 43% and 18% mortality, respectively.
212 zyme inhibitors had a higher risk of sepsis, septic shock, and mortality than those receiving angiote
213 hemophagocytic lymphohistiocytosis, sepsis, septic shock, and other conditions were distinctly diffe
215 on score, LogEuroSCORE, acute heart failure, septic shock, and paravalvular complications were risk f
216 the trials were performed in the setting of septic shock, and the most frequent comparator was a com
217 sepsis inpatient admission remain high: for septic shock, approximately 60%; for severe sepsis, appr
218 ng patients with sepsis who will progress to septic shock, as defined by Sepsis- 3 criteria, with the
219 ided resuscitation strategy in patients with septic shock, but the difference in the primary outcome,
221 nting to the emergency department with early septic shock, early goal-directed therapy compared with
222 nal capillary density and/or RBC velocity in septic shock, heart failure, hypovolemia, obstructive sh
223 s for all patients with suspected sepsis and septic shock, ideally within 1 hour of recognition.
224 repinephrine, the first-line vasopressor for septic shock, is not always effective and has important
226 osis and prognosis of acute ischemic stroke, septic shock, lung injuries, insulin resistance in diabe
227 ephrine, the cornerstone vasopressor used in septic shock, may contribute to immune dysregulation and
228 he chlorambucil plus obinutuzumab group (n=1 septic shock, n=1 metastatic skin squamous carcinoma).
230 four clusters following early prediction of septic shock, stratifying by outcome: the highest-risk a
232 0.92-0.98).Conclusions: Among children with septic shock, the PERSEVERE biomarkers predict severe D(
233 acid were not.Conclusions: In patients with septic shock, there was no heterogeneity in effect of ad
235 ntensive care unit (ICU) stay for >24 hours, septic shock, vasoactive agents, positive-pressure venti
280 cytokines was assessed in 195 patients with septic shock.Measurements and Main Results: Norepinephri
281 ated AKI on Day 3 (D(3) SA-AKI) in pediatric septic shock.Methods: We performed secondary analysis of
282 stimate baseline mortality risk in pediatric septic shock.Objectives: To assess the association betwe
283 ty after 14 days decreased among all groups (septic shock: 12.6% to 6.7%; septic shock with acute res
284 nical Modification code for severe sepsis or septic shock; 3,021 of these patients (28%) had an immun
286 s, 38% of the fertilizer sources, 51% of the septic sources, 98% of the atmospheric deposition to the
287 is in systemic viral infections can induce a septic state with leaky capillary syndrome, disseminated
289 ate wells studied, suggesting that household septic systems are the source of this contamination.
290 lity in microbial contamination, the role of septic systems as sources of contamination, and the effe
292 grances), sewage treatment techniques (e.g., septic systems), and ecosystem types (e.g., lakes).
293 site waste treatment systems (OWTS), such as septic systems, present to human health and the environm