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1 n serum lipopolysaccharide levels (metabolic endotoxemia).
2 esearch into both rotavirus pathogenesis and endotoxemia.
3 inal barrier integrity and reduces metabolic endotoxemia.
4 l endothelial cells and liver in vivo during endotoxemia.
5 appaB only within muscle fibers during acute endotoxemia.
6 ain-inflammation relationship is affected by endotoxemia.
7 chanisms to avoid collateral organ damage in endotoxemia.
8 c function was significantly improved during endotoxemia.
9 uclear factor-kappaB activation in mice with endotoxemia.
10 ease in serum iron during experimental human endotoxemia.
11 tibility to lipopolysaccharide (LPS)-induced endotoxemia.
12 on, cardiac function, and animal survival in endotoxemia.
13 e inhibitor Neu5Gc2en protected mice against endotoxemia.
14 se-mediated hyperinsulinemia associated with endotoxemia.
15 nosuppressive role of macrophage CD40 in LPS endotoxemia.
16 mproves cardiac function and survival during endotoxemia.
17 inflammation often associated with low-grade endotoxemia.
18 tic inflammation in mouse models of NASH and endotoxemia.
19 reduced survival to polymicrobial sepsis and endotoxemia.
20 actor-kappaB pathway were subjected to acute endotoxemia.
21 s well as other conditions such as metabolic endotoxemia.
22 responses of the vascular endothelium during endotoxemia.
23 recently been reported to increase metabolic endotoxemia.
24 t have potential for liver protection during endotoxemia.
25 respiratory dysfunction during experimental endotoxemia.
26 in on skeletal muscle injury in experimental endotoxemia.
27 tissue injury in traumatized animals during endotoxemia.
28 s sympathetic activation during experimental endotoxemia.
29 and the effects of statins in a rat model of endotoxemia.
30 is and in healthy subjects with experimental endotoxemia.
31 5116 pg/mL), were much higher 12 hours after endotoxemia.
32 asma lipopolysaccharides (LPSs) in metabolic endotoxemia.
33 asma Lp-PLA(2) mass declined modestly during endotoxemia.
34 usion encountered in healthy subjects during endotoxemia.
35 ciated with bacterial translocation (BT) and endotoxemia.
36 O contributes importantly to protection from endotoxemia.
37 utoregulation in healthy subjects exposed to endotoxemia.
38 tive in a number of circumstances, including endotoxemia.
39 ome in models of polymicrobial infection and endotoxemia.
40 efense against A. fumigatus infection and to endotoxemia.
41 endotoxin), and therapeutic hypercapnia with endotoxemia.
42 ion but suffered persistent injury following endotoxemia.
43 e of another caspase 1-dependent mediator of endotoxemia.
44 function (5A-aPC) to reduce the mortality of endotoxemia.
45 ctivation of coagulation in a mouse model of endotoxemia.
46 ociated thrombosis and high mortality during endotoxemia.
47 g multiorgan host injury responses in murine endotoxemia.
48 or TLR4(-/-) mice after induction of NEC or endotoxemia.
49 amage and tumor formation by alcohol-induced endotoxemia.
50 ammatory response frequently associated with endotoxemia.
51 oduction in activated macrophages and during endotoxemia.
52 okines and improves survival in experimental endotoxemia.
53 nditions, particularly those associated with endotoxemia.
54 ine and late mediator of mortality in murine endotoxemia.
55 peritoneum, and blood using a mouse model of endotoxemia.
56 tiated mortality to both neonatal sepsis and endotoxemia.
57 esulting in improved tolerance to sepsis and endotoxemia.
58 during both polymicrobial sepsis and sterile endotoxemia.
59 shing IL-18 increased lethality to sepsis or endotoxemia.
60 thetic vasoconstrictor responsiveness during endotoxemia.
61 fects of lipopolysaccharide and for treating endotoxemia.
62 ng hyperinflammation during the first 3 h of endotoxemia.
63 ants of the febrile response to experimental endotoxemia.
64 agulants; thrombocytopenia; neutrophilia and endotoxemia.
65 ologic features in response to mild systemic endotoxemia.
66 d to a dextran sodium sulfate-induced portal endotoxemia.
67 the suppression of hyperinflammation during endotoxemia.
68 on with macrophages in the spleen during LPS endotoxemia.
69 ll migration and increased susceptibility to endotoxemia.
71 our swine were instrumented and subjected to endotoxemia (100 microg/kg), followed by serial plasma s
72 arterial pressure decreased similarly during endotoxemia (-11% +/- 16%) and endotoxemia + hypoxia (-1
75 th 5% CO2 (therapeutic hypercapnia), air and endotoxemia (5 mg/kg endotoxin), and therapeutic hyperca
76 ere hepatic insulin resistance under chronic endotoxemia, accompanied by increased inflammatory respo
77 ur data demonstrate that in a mouse model of endotoxemia activation of the coagulation cascade is ini
78 isorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin re
79 oxin levels and predicted subsequent maximal endotoxemia, after adjusting for other significant covar
80 at in the acute inflammatory response during endotoxemia, aged neutrophils cease returning to the bon
81 uces mortality in lipopolysaccharide-induced endotoxemia and a bacterial infusion mouse sepsis model.
82 rmeability to bacterial products, leading to endotoxemia and a variety of deleterious effects in both
83 inhibits iNOS activity in a murine model of endotoxemia and blocks pain behaviors in a formalin mode
84 oles for beta-arr2 in inflammation following endotoxemia and cecal ligation and puncture (CLP) models
85 y administered leptin increased mortality in endotoxemia and cecal ligation puncture models and was a
89 are resistant to lipopolysaccharide-induced endotoxemia and display a marked inability to mount infl
90 ted against lipopolysaccharide (LPS)-induced endotoxemia and hepatic damage associated with decreased
92 7 (Th17) responses during experimental human endotoxemia and in patients with sepsis admitted to the
94 displayed increased mortality in LPS-induced endotoxemia and increased vascular permeability in respo
100 odify gut microbiota and to reduce metabolic endotoxemia and other obesity-related biochemical abnorm
103 flammatory activity of APC in the setting of endotoxemia and provide clear evidence that the antiinfl
104 preventing ALI in lipopolysaccharide-induced endotoxemia and raise the possibility of an essential ro
105 e, ZAA significantly ameliorated LPS-induced endotoxemia and Salmonella-induced diarrhea in mice.
109 mechanisms were operant in the kidney during endotoxemia and served a cytoprotective role in mitigati
110 rnatively activated macrophages, and develop endotoxemia and severe hepatic and intestinal pathology.
115 tty acids exhibit higher levels of metabolic endotoxemia and systemic low-grade inflammation, while t
116 lin G (IVIG) treatment significantly reduced endotoxemia and the percentage of PD-1(+) CD4 T cells, a
118 metic peptide L-4F in ARDS and gram-negative endotoxemia and warrant further clinical evaluation.
122 rated, exposed to lipopolysaccharide-induced endotoxemia, and injected with caspase 1 inhibitor.
123 ant increases in biomarkers of liver damage, endotoxemia, and MT indexes and a trend for greater hepa
124 at IAP detoxifies bacterial toxins, prevents endotoxemia, and preserves intestinal microbiotal homeos
125 17A and IL-23 both appeared in plasma during endotoxemia, and their neutralization improved survival.
126 an inhibitory effect on gastric iNOS during endotoxemia, and this may represent a potential cytoprot
128 trials targeting populations with documented endotoxemia are more likely to provide an adequate test
129 estinal permeability and decreased metabolic endotoxemia as evidenced by reduced plasma LPS level, an
131 to therapeutic hypercapnia with and without endotoxemia before and at 4, 12, and 24 hrs into the stu
132 Both endotoxemia and combined hypoxia and endotoxemia blunted sympathetic vasoconstrictor responsi
133 n-style diet might, therefore, contribute to endotoxemia by causing changes in gastrointestinal barri
134 followed by induction of abdominal sepsis or endotoxemia by intraperitoneal injection with cecal slur
135 ralization of D-DT protects mice from lethal endotoxemia by reducing the expression of downstream eff
139 days before or after the induction of lethal endotoxemia, cecal ligation and puncture, or fecal perit
145 dying childhood resistance to mortality from endotoxemia, demonstrate that oestrogen is responsible f
146 ay stored autologous RBCs in the presence of endotoxemia does not result in lung injury in humans.
148 y, are not sufficient to reduce mortality in endotoxemia, emphasizing the need for APC's cytoprotecti
150 and early surgery predict the development of endotoxemia; endotoxemia is particularly associated with
151 Lcn2KO mice were markedly more sensitive to endotoxemia, exhibiting elevated indices of organ damage
155 was associated with a decrease in metabolic endotoxemia, glucose insulinotropic peptide, glucose int
156 Concurrent with the role of Cryopyrin in endotoxemia, glyburide significantly delays lipopolysacc
159 that betaArr1 deficiency protects mice from endotoxemia, here we demonstrate that the absence of bet
161 for B cell-derived IL-10 was evident during endotoxemia; however, although B cells dominated lymphoi
162 ilarly during endotoxemia (-11% +/- 16%) and endotoxemia + hypoxia (-10% +/- 15%; both p < 0.05).
164 g vascular conductance, +100% +/- 115%), and endotoxemia + hypoxia (leg blood flow, +67% +/- 120%; le
166 n mice were assessed after acute and chronic endotoxemia (i.e., exposure to inflammatory lipopolysacc
167 quently, all subjects underwent experimental endotoxemia (i.v. administration of 2 ng/kg Escherichia
168 mice) with intact IL-1R8 were protected from endotoxemia, IL-1R8-deficient IL-37tg mice were not.
169 n in beta-cells by hyperlipidemia-associated endotoxemia improves the adaptation of beta-cells to ins
173 duced cytokine levels and organ injury after endotoxemia in aged rats, which was associated with sign
176 okine signaling, suggesting that subclinical endotoxemia in healthy individuals might lead to signifi
177 e nanoparticles (GVNPs) for the treatment of endotoxemia in high-risk patients, using a murine model
179 regulation of Lp-PLA(2) during experimental endotoxemia in humans, probed the source of Lp-PLA(2) in
180 Using intravital microscopy, we found that endotoxemia in mice rapidly induced pulmonary microvascu
182 the cardiac dysfunction caused by sepsis or endotoxemia in mice; this effect may be caused by increa
183 the gut microbiota and preventing metabolic endotoxemia in rats fed a high fat and sucrose diet.
189 erely affected in two models of experimental endotoxemia, including exposure to Escherichia coli lipo
191 toneal neutrophil recruitment during sterile endotoxemia independent of the vagus nerve, without affe
193 s on mTNF-alpha and protect mice from severe endotoxemia induced by lipopolysaccharide (LPS) challeng
194 ptibility to lethal effects of gram-negative endotoxemia induced by lipopolysaccharide (LPS), whereas
195 est, T3 significantly protected mice against endotoxemia induced by lipopolysaccharide i.p. injection
197 hibitor temsirolimus, even after established endotoxemia, induced autophagy and protected against the
200 ion correlated with disease severity scores, endotoxemia, infections, and short-term mortality, thus
202 l inflammation, and its dysregulation during endotoxemia is a novel mechanism for LPS-induced vascula
204 th a postcardiac arrest shock, high level of endotoxemia is independently associated with duration of
205 addition, low-level but persistent metabolic endotoxemia is often found in diabetic and obese subject
206 gery predict the development of endotoxemia; endotoxemia is particularly associated with cardiovascul
211 r than 25, and patients with an intermediate endotoxemia level (>/= 0.4) had more cardiovascular dysf
215 cohort of HIV-negative men with subclinical endotoxemia linked to alterations in CD4/CD8 T cell rati
216 nome-wide association study (GWAS) of evoked endotoxemia (lipopolysaccharide (LPS) 1 ng/kg IV) in hea
220 dels, such as the lipopolysaccharide-induced endotoxemia model and the cecal ligation and puncture (C
224 tory effects, we used the human experimental endotoxemia model to test the hypothesis that a transien
229 ading to diaphragmatic weakness during acute endotoxemia, most likely via effects on multiple inflamm
230 er suppresses the adrenocortical response to endotoxemia nor enhances the accompanying production of
231 Thus, HMGB1 secretion, which is critical for endotoxemia, occurs downstream of inflammasome assembly
234 The present study addressed the effect of endotoxemia on the functional and molecular mechanisms t
235 mer all were increased greatly in mice after endotoxemia or cecal ligation and puncture as compared w
237 ceptor blockade commenced 6 hrs after lethal endotoxemia or fecal peritonitis did not improve surviva
238 grated into an extracorporeal circuit in pig endotoxemia or heparin therapy models, it produces real-
239 om mice with intrarenal (maleate), prerenal (endotoxemia), or postrenal (ureteral obstruction) injury
242 after sepsis; p < 0.001 and 86% vs 12% after endotoxemia; p = 0.013) and significantly reduced viscer
243 ponse to endotoxin, clinical significance of endotoxemia, past failed therapies targeting endotoxin,
244 keywords: sepsis, septicemia, septic shock, endotoxemia, persistent pulmonary hypertension, nitric o
246 appaBalpha super-repressor mice subjected to endotoxemia, proinflammatory cytokines, muscle RING-fing
247 o adaptive changes during human experimental endotoxemia promoting higher levels of adenosine thereby
248 RESEARCH DESIGN AND We performed a 60-h endotoxemia protocol (3 ng/kg intravenous bolus) in heal
249 idation in adipose from an independent human endotoxemia protocol (N = 7, with 0.6 ng/kg LPS) and for
250 DCs from severely malnourished children with endotoxemia provide a rational basis for the anergy foun
251 fatty acids on gut microbiota and metabolic endotoxemia provide insight into the etiology and manage
252 ne system, displayed enhanced sensitivity to endotoxemia, rapid progression of chemical-induced colit
253 monocytes from volunteers with experimental endotoxemia re-instates their capacity for cytokine prod
262 h plasma EL concentrations, and experimental endotoxemia significantly increases plasma EL concentrat
263 challenge, with rapid development of typical endotoxemia signs and extensive organ damage, and elevat
264 we show that vagus nerve stimulation during endotoxemia specifically attenuates TNF production by sp
270 for the P2X1 receptor in LPS-induced lethal endotoxemia through its critical involvement in neutroph
271 itment to liver and LPS-induced death during endotoxemia, thus highlighting a previously unrecognized
273 e demonstrate that hyperlipidemia-associated endotoxemia upregulates miR-155-5p in murine pancreatic
274 n regard to dynamic cerebral autoregulation, endotoxemia was associated with lower middle cerebral ar
277 Traumatic soft-tissue injury with additional endotoxemia was characterized by nutritive perfusion fai
287 % of our study patients, in association with endotoxemia we describe the novel finding of DC maturati
288 study the role of neutrophils in LPS-induced endotoxemia, we developed a new mouse model, PMN(DTR) mi
290 e receptors for coagulation factors in mouse endotoxemia, we found that the protein C receptor (ProcR
291 sing this human in vivo model of subclinical endotoxemia, we furthermore show that plasma LPS leads t
292 hrough genomic interrogation of experimental endotoxemia, we identified and replicated a novel fever
294 Using an LPS-induced mouse model of lethal endotoxemia, we showed that APC administration reduced t
297 and gastrointestinal barrier dysfunction and endotoxemia when mice were forced to consume alcohol.
298 ease in plasma levels of endotoxin activity (endotoxemia), whereas a prudent-style diet reduced level
299 eg vascular conductance were not affected by endotoxemia, whereas both were elevated by adenosine inf
300 lysaccharide (4 or 20 mg/kg, i.p.) to induce endotoxemia with and without recombinant human annexin A
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