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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
5                        In early experimental septic acute kidney injury, fluid bolus therapy transien
6 otential therapeutic strategy for preventing septic AKI.
7 2alpha) axis as a major pathway in mediating septic AKI.
8  of whole blood DNA samples from a cohort of septic and nonseptic critically ill patients.
9                              We assessed, in septic and nonseptic ICU patients, the relation between
10         PSP is able to differentiate between septic and nonseptic patients during acute burn care.
11 data from seven external datasets containing septic and nonseptic patients, 81% of the differentially
12                               Critically ill septic and nonseptic patients.
13 01), black (100% vs 53%; P < .001), and have septic arthritis (35% vs 1%; P < .001).
14                                 Native joint septic arthritis (NJSA) is poorly studied.
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
17                In 10 195 (84%) patients with septic arthritis as the primary admitting diagnosis, 90-
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
21 or infective endocarditis, epidural abscess, septic arthritis, or osteomyelitis.
22 rial extracorporeal membrane oxygenation for septic cardiomyopathy but also indicate improved hospita
23 ks of respiratory, cardiac, anastomotic, and septic complications.
24 clinical outcomes in severe inflammatory and septic conditions.Objectives: Although recent investigat
25 er's patch effector memory CD4(+) T cells in septic CR mice.
26 ease in cells and lipopolysaccharide-induced septic death in mice.
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
32 ng pathogenic effectors may benefit the post-septic host.
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
35 isms that may be triggered simultaneously in septic hypertensive patients.
36 ghts the importance of glucose metabolism in septic inflammation.
37 jurisdictions with limited information about septic infrastructure may be able to use geospatial data
38 nd environmental justice concerns related to septic infrastructure.
39 gaster, to investigate how infection through septic injury modulates nutritional intake and how macro
40                          The consequences of septic knee arthritis in patients undergoing arthroscopi
41 LPS)-induced systemic inflammation (SI; at a septic-like model) in spontaneously hypertensive rats (S
42 ethod for the real-time, label-free study of septic liver damage.
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
45        The protective effects of rolipram on septic mice may result from inhibition of the MAP kinase
46 d provides an insight on the contribution of septic mice models in the study of multi organ dysfuncti
47 arkedly decreased in rmCIRP-injected mice or septic mice treated with LP17.
48                                 In contrast, septic mice treated with LXR antagonist showed increased
49                                              Septic mice were treated with [(C2S, 3S, 4R)-1-O-(alpha-
50 une network was similar in IRF3-KO versus WT septic mice, although the tempo of connectivity differed
51 o the complete recovery of immunocompromised septic mice.
52 posure significantly improved the outcome of septic mice.
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
56 k requiring inotropes, and with demonstrable septic myocardial depression.
57 s) following infection with GBS strains from septic neonates or colonized mothers.
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
61 ription initiation complex, was 74% lower in septic patients (p < 0.001).
62 he platelet transcriptome and translatome in septic patients and healthy donors.
63  changes in platelet gene expression between septic patients and mice subjected to CLP.
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
66                                         Most septic patients are initially encountered in the emergen
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
69                From 256 plasma samples of 48 septic patients at up to seven consecutive time points w
70                                              Septic patients frequently develop cognitive impairment
71  severity score >= 15) and nonsevere injured septic patients had an odds ratio of 1.39 (95% CI, 1.31-
72                                              Septic patients had higher severity of illness scores, c
73                                  A cohort of septic patients had increased cytokine production compar
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
78             More important, neutrophils from septic patients showed increased ABCA1 messenger ribonuc
79                                              Septic patients who died had early, profound, and sustai
80                         We hypothesized that septic patients with bloodstream infections may transiti
81  evaluating the thermoregulatory outcomes of septic patients with hypertension.
82                                    All adult septic patients with positive blood cultures over a 7-ye
83                                    All adult septic patients with positive blood cultures over a peri
84 -based forms of research in order to improve septic patients' morbidity and mortality.
85 contribute to the high mortality rates among septic patients, despite new antimicrobials and resuscit
86                                           In septic patients, plasma concentrations of interleukin (I
87  been considerable effort to immunophenotype septic patients, these methods have often not accurately
88 L-7 restored ex vivo IFN-gamma production in septic patients.
89 en in control, critically ill nonseptic, and septic patients.
90 ry rate <0.05) transcripts in platelets from septic patients.
91 that did not mimic the metabolic settings of septic patients.
92 n guide duration of antibacterial therapy in septic patients.
93  increased checkpoint molecule expression in septic patients.
94 vere Sepsis and Septic Shock-1) enrolled 583 septic patients.
95  of the peritoneum capable of neutralizing a septic polymicrobial insult.
96 ate the expression of TLR 2, 3, 4 and 7 in a septic process.
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,
111  met consensus criteria for severe sepsis or septic shock (reference standard cohort).
112 ation of fluid for infants and children with septic shock (this latter topic was evaluated by evidenc
113                                              Septic shock 48-hour, 3-14-day and greater than 14-day m
114 HLA-A02:01 was associated with lower odds of septic shock [OR 0.52, (0.32-0.82)].
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
127                                Patients with septic shock and S. aureus bacteremia admitted directly
128 ient avoided cost was multiplied by expected septic shock annual incidence.
129       Critically ill patients with sepsis or septic shock are at an increased risk of death.
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
132 ally ventilated, and 42% in severe sepsis or septic shock at infection onset.
133 nter this state are highly likely to develop septic shock at some future time.
134 ration of HAT therapy among U.S. adults with septic shock before and after study publication and to c
135                                              Septic shock carries a high mortality risk.
136  a 6-hour resuscitation in 688 patients with septic shock enrolled in the ProCESS trial.
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
140          A total of 361,323 severe sepsis or septic shock hospital discharges were included.
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
143 logic studies of pediatric severe sepsis and septic shock in this large, multicenter database.
144 pective observational study of children with septic shock in whom the PERSEVERE biomarkers were measu
145                                              Septic shock is a life-threatening condition in which ti
146                                              Septic shock is a systemic inflammation associated with
147                   Cellular Immunotherapy for Septic Shock is the first-in-human clinical trial evalua
148                              Septicemia with septic shock is the most common cause of death, with mor
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
151        In this study, we demonstrate that in septic shock O-GlcNAc stimulation improves global animal
152 ting consensus criteria for severe sepsis or septic shock on manual chart review were entered into th
153 r patients admitted to the ICU for sepsis or septic shock over the last 2 decades.
154           Circulating endothelial cells from septic shock patients are acutely converted into fibrobl
155                                   Sepsis and septic shock patients had higher maximum ferritin levels
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
162 allogeneic mesenchymal stem/stromal cells in septic shock patients.
163 mass might be a useful prognostic factor for septic shock patients.
164 LA-DR septic shock patients, and low mHLA-DR septic shock patients.
165 ts (n = 274) diagnosed with severe sepsis or septic shock per Sepsis-2 criteria from September to Nov
166 e in insured patients with severe sepsis and septic shock post Affordable Care Act.
167                          Among patients with septic shock receiving norepinephrine, administration of
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
170          Abnormal peripheral perfusion after septic shock resuscitation has been associated with orga
171 sus Norepinephrine Infusion in Patients With Septic Shock studies (n=632).
172 nd Simplified Acute Physiology Score II with septic shock survivors (unexposed group).
173 howed discriminatory power between pediatric septic shock survivors and nonsurvivor types.
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
178 ped patients enrolled in the Vasopressin and Septic Shock Trial.
179  patients with AKI in VASST (Vasopressin and Septic Shock Trial; n = 271), and differences in treatme
180 ated Protein C and Corticosteroids for Human Septic Shock trials.
181 organ support-free days outcome reporting in septic shock trials.
182 ated Protein C and Corticosteroids for Human Septic Shock trials.
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.
185           Transcriptomic profile at onset of septic shock was associated with response to corticoster
186                                              Septic shock was the main reason for admission mostly of
187 ncer patients admitted to ICUs for sepsis or septic shock were extracted from the Groupe de Recherche
188 f 506 patients with S. aureus bacteremia and septic shock were included in the analysis.
189  reviewed prospectively enrolled registry of septic shock which had 817 consecutive patients.
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
194       Cure of severe infections, sepsis, and septic shock with antimicrobial drugs is a challenge bec
195 kers can identify subgroups of patients with septic shock with differential treatment responses to hy
196                Hospital survival was 90% for septic shock with left ventricular failure and 64.7% in
197                                  He was in a septic shock with multiple organ failure up on presentat
198  predict mortality and rate of recovery from septic shock with over 90% accuracy.
199 id Treatment in Critically Ill Patients with Septic Shock) and $30,911 (Activated Protein C and Corti
200  complication of atrial fibrillation and one septic shock) and two due to disease progression.
201 ated Protein C and Corticosteroids for Human Septic Shock) per patient.
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
205                       Three months following septic shock, 346 of 389 subjects (88.9%) were alive and
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.
210 severity score 33); 33% developed sepsis, 6% septic shock, and in-hospital mortality was 14%.
211           LPS can cause death as a result of septic shock, and its lipid A core is the target of poly
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
214  hemophagocytic lymphohistiocytosis, sepsis, septic shock, and other diagnoses.
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,
220                              Cardiogenic and septic shock, cardiac arrhythmia, and postsurgical compl
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
225                                     Further, septic shock, late-onset cardiac dysfunction, and multio
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).
229                    Among patients with early septic shock, receipt of HAT was not associated with mor
230  four clusters following early prediction of septic shock, stratifying by outcome: the highest-risk a
231                             In patients with septic shock, the combination of ascorbic acid, corticos
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
234                                           In septic shock, thrombocytopenia is associated with increa
235 ntensive care unit (ICU) stay for >24 hours, septic shock, vasoactive agents, positive-pressure venti
236                       In patients with early septic shock, we compared the association of early HAT t
237 enomedullin and Outcome in Severe Sepsis and Septic Shock-1) enrolled 583 septic patients.
238 n septic shock and identified the unexplored septic shock-related genes and functional groups.
239 for children encountering community-acquired septic shock.
240 t least 1 year following hospitalization for septic shock.
241 the development of post-traumatic sepsis and septic shock.
242 f this combination therapy for patients with septic shock.
243 icated course and mortality in children with septic shock.
244 onth 3 follow-up among children encountering septic shock.
245 may be for patients with suspected sepsis or septic shock.
246 ts a potential new data-driven definition of septic shock.
247 gy Score 2: 54 +/- 20), 53 (54%) experienced septic shock.
248  life disability among children encountering septic shock.
249  Critical Sepsis, was defined, approximating septic shock.
250  coverage to any patient suspected of having septic shock.
251 acterial clearance in the juvenile host with septic shock.
252 ion is detrimental to the juvenile host with septic shock.
253 ong children encountering community-acquired septic shock.
254 ovascular and endothelial alterations during septic shock.
255 omputing risk of transition from sepsis into septic shock.
256 e improved hospital survival in distributive septic shock.
257 ing missed 66 patients with severe sepsis or septic shock.
258 3%), patients had more liver dysfunction and septic shock.
259 s better for patients with severe sepsis and septic shock.
260 enues for a potential therapy of early-stage septic shock.
261 nd incidence of thrombocytopenia are high in septic shock.
262 PS is critical for antibacterial defense and septic shock.
263 y been proposed to confer protection against septic shock.
264  to improve outcomes in cancer patients with septic shock.
265  in development and progression of pediatric septic shock.
266 ine or vasopressin, or to corticosteroids in septic shock.
267 omidine may decrease norepinephrine doses in septic shock.
268 he impending occurrence of severe sepsis and septic shock.
269 ity to adverse outcomes including sepsis and septic shock.
270  a total of 150,845 visits for severe sepsis/septic shock.
271 se, we believe, represents the true onset of septic shock.
272  mortality in children with severe sepsis or septic shock.
273 ECMO) obtained from three large databases of septic shock.
274 s been identified as a potential therapy for septic shock.
275 ent in 28% of children with severe sepsis or septic shock.
276  thiamine vs placebo for adult patients with septic shock.
277 e followed for the development of sepsis and septic shock.
278  antibiotic administration for patients with septic shock.
279 enetic factors and post-traumatic sepsis and septic shock.
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
285              Among this recent cohort of 301 septic SICU patients, 30-day mortality was 9.6%.
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
288             Across 12 studies, compared with septic survivors, nonsurvivors had significantly increas
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
291 hree wells confirmed the impact of household septic systems on well contamination.
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
294 ewers connecting several toilets to communal septic tanks (3-5 USD/person/year).
295                           In 3 gram-negative septic transfusion cases, we performed metagenomic next-
296                       In three Gram-negative septic transfusion cases, we performed mNGS of direct cl
297                                Investigating septic transfusion events is often restricted by the lim
298                             Investigation of septic transfusion events is often restricted by the lim
299 therapeutic opportunity for the treatment of septic vascular leakage.
300 e also performed subgroup analyses comparing septic with nonseptic patients.

 
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