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1 n serum lipopolysaccharide levels (metabolic endotoxemia).
2 de in a clinically controlled setting (human endotoxemia).
3 uced colonic mucosal barrier dysfunction and endotoxemia.
4 shing IL-18 increased lethality to sepsis or endotoxemia.
5 thetic vasoconstrictor responsiveness during endotoxemia.
6 ding RNA, was largely recapitulated in human endotoxemia.
7 fects of lipopolysaccharide and for treating endotoxemia.
8 ng hyperinflammation during the first 3 h of endotoxemia.
9 ants of the febrile response to experimental endotoxemia.
10 ologic features in response to mild systemic endotoxemia.
11 d to a dextran sodium sulfate-induced portal endotoxemia.
12 the suppression of hyperinflammation during endotoxemia.
13 on with macrophages in the spleen during LPS endotoxemia.
14 ll migration and increased susceptibility to endotoxemia.
15 inal barrier integrity and reduces metabolic endotoxemia.
16 l endothelial cells and liver in vivo during endotoxemia.
17 appaB only within muscle fibers during acute endotoxemia.
18 ain-inflammation relationship is affected by endotoxemia.
19 chanisms to avoid collateral organ damage in endotoxemia.
20 c function was significantly improved during endotoxemia.
21 uclear factor-kappaB activation in mice with endotoxemia.
22 ease in serum iron during experimental human endotoxemia.
23 tibility to lipopolysaccharide (LPS)-induced endotoxemia.
24 on, cardiac function, and animal survival in endotoxemia.
25 e inhibitor Neu5Gc2en protected mice against endotoxemia.
26 se-mediated hyperinsulinemia associated with endotoxemia.
27 nosuppressive role of macrophage CD40 in LPS endotoxemia.
28 mproves cardiac function and survival during endotoxemia.
29 inflammation often associated with low-grade endotoxemia.
30 tic inflammation in mouse models of NASH and endotoxemia.
31 reduced survival to polymicrobial sepsis and endotoxemia.
32 actor-kappaB pathway were subjected to acute endotoxemia.
33 s well as other conditions such as metabolic endotoxemia.
34 responses of the vascular endothelium during endotoxemia.
35 recently been reported to increase metabolic endotoxemia.
36 t have potential for liver protection during endotoxemia.
37 respiratory dysfunction during experimental endotoxemia.
38 in on skeletal muscle injury in experimental endotoxemia.
39 tissue injury in traumatized animals during endotoxemia.
40 s sympathetic activation during experimental endotoxemia.
41 and the effects of statins in a rat model of endotoxemia.
42 is and in healthy subjects with experimental endotoxemia.
43 5116 pg/mL), were much higher 12 hours after endotoxemia.
44 asma lipopolysaccharides (LPSs) in metabolic endotoxemia.
45 asma Lp-PLA(2) mass declined modestly during endotoxemia.
46 usion encountered in healthy subjects during endotoxemia.
47 ciated with bacterial translocation (BT) and endotoxemia.
48 utoregulation in healthy subjects exposed to endotoxemia.
49 tive in a number of circumstances, including endotoxemia.
50 ome in models of polymicrobial infection and endotoxemia.
51 endotoxin), and therapeutic hypercapnia with endotoxemia.
52 ion but suffered persistent injury following endotoxemia.
53 e of another caspase 1-dependent mediator of endotoxemia.
54 function (5A-aPC) to reduce the mortality of endotoxemia.
55 ccharide- or Acinetobacter baumannii-induced endotoxemia.
56 ctivation of coagulation in a mouse model of endotoxemia.
57 ociated thrombosis and high mortality during endotoxemia.
58 e that included muscle wasting and metabolic endotoxemia.
59 particularly on fructose intake and systemic endotoxemia.
60 educed systemic concentrations of TNF during endotoxemia.
61 from LysM-Cre:BVR (fl/fl) mice in a model of endotoxemia.
62 agulants; thrombocytopenia; neutrophilia and endotoxemia.
63 esearch into both rotavirus pathogenesis and endotoxemia.
64 O contributes importantly to protection from endotoxemia.
65 efense against A. fumigatus infection and to endotoxemia.
66 ammatory response frequently associated with endotoxemia.
67 nditions, particularly those associated with endotoxemia.
68 peritoneum, and blood using a mouse model of endotoxemia.
69 ty and restoring Th17/Tregs polarization and endotoxemia.
70 tiated mortality to both neonatal sepsis and endotoxemia.
71 esulting in improved tolerance to sepsis and endotoxemia.
72 during both polymicrobial sepsis and sterile endotoxemia.
74 our swine were instrumented and subjected to endotoxemia (100 microg/kg), followed by serial plasma s
75 arterial pressure decreased similarly during endotoxemia (-11% +/- 16%) and endotoxemia + hypoxia (-1
76 th 5% CO2 (therapeutic hypercapnia), air and endotoxemia (5 mg/kg endotoxin), and therapeutic hyperca
77 uced TJ disruption, barrier dysfunction, and endotoxemia accompanied by protein thiol oxidation and d
78 ere hepatic insulin resistance under chronic endotoxemia, accompanied by increased inflammatory respo
79 ur data demonstrate that in a mouse model of endotoxemia activation of the coagulation cascade is ini
82 isorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin re
83 oxin levels and predicted subsequent maximal endotoxemia, after adjusting for other significant covar
84 at in the acute inflammatory response during endotoxemia, aged neutrophils cease returning to the bon
85 uces mortality in lipopolysaccharide-induced endotoxemia and a bacterial infusion mouse sepsis model.
86 rmeability to bacterial products, leading to endotoxemia and a variety of deleterious effects in both
87 oles for beta-arr2 in inflammation following endotoxemia and cecal ligation and puncture (CLP) models
88 y administered leptin increased mortality in endotoxemia and cecal ligation puncture models and was a
91 are resistant to lipopolysaccharide-induced endotoxemia and display a marked inability to mount infl
92 ng correlated with IgA deficiency-associated endotoxemia and endotoxin-induced expression of activin
93 ted against lipopolysaccharide (LPS)-induced endotoxemia and hepatic damage associated with decreased
95 7 (Th17) responses during experimental human endotoxemia and in patients with sepsis admitted to the
97 displayed increased mortality in LPS-induced endotoxemia and increased vascular permeability in respo
103 odify gut microbiota and to reduce metabolic endotoxemia and other obesity-related biochemical abnorm
106 flammatory activity of APC in the setting of endotoxemia and provide clear evidence that the antiinfl
107 preventing ALI in lipopolysaccharide-induced endotoxemia and raise the possibility of an essential ro
109 e, ZAA significantly ameliorated LPS-induced endotoxemia and Salmonella-induced diarrhea in mice.
113 mechanisms were operant in the kidney during endotoxemia and served a cytoprotective role in mitigati
117 tty acids exhibit higher levels of metabolic endotoxemia and systemic low-grade inflammation, while t
118 myogenesis through suppression of metabolic endotoxemia and that Zip14 ablation coincides with susta
119 lin G (IVIG) treatment significantly reduced endotoxemia and the percentage of PD-1(+) CD4 T cells, a
121 metic peptide L-4F in ARDS and gram-negative endotoxemia and warrant further clinical evaluation.
125 rated, exposed to lipopolysaccharide-induced endotoxemia, and injected with caspase 1 inhibitor.
126 ant increases in biomarkers of liver damage, endotoxemia, and MT indexes and a trend for greater hepa
127 at IAP detoxifies bacterial toxins, prevents endotoxemia, and preserves intestinal microbiotal homeos
129 17A and IL-23 both appeared in plasma during endotoxemia, and their neutralization improved survival.
131 sing fructose intake and addressing systemic endotoxemia are plausible targets for improving metaboli
132 estinal permeability and decreased metabolic endotoxemia as evidenced by reduced plasma LPS level, an
133 ves survival in a mouse model of LPS-induced endotoxemia as well as decreases progression in a mouse
134 n addition, patients with CVID+AIC had serum endotoxemia associated with a dearth of isotype-switched
136 to therapeutic hypercapnia with and without endotoxemia before and at 4, 12, and 24 hrs into the stu
137 Both endotoxemia and combined hypoxia and endotoxemia blunted sympathetic vasoconstrictor responsi
138 n-style diet might, therefore, contribute to endotoxemia by causing changes in gastrointestinal barri
139 followed by induction of abdominal sepsis or endotoxemia by intraperitoneal injection with cecal slur
140 ralization of D-DT protects mice from lethal endotoxemia by reducing the expression of downstream eff
152 dying childhood resistance to mortality from endotoxemia, demonstrate that oestrogen is responsible f
153 ecretion in vivo, in a MC-dependent model of endotoxemia, demonstrating that TLR4 engagement leads to
154 ay stored autologous RBCs in the presence of endotoxemia does not result in lung injury in humans.
157 and early surgery predict the development of endotoxemia; endotoxemia is particularly associated with
158 Lcn2KO mice were markedly more sensitive to endotoxemia, exhibiting elevated indices of organ damage
159 e observed that mice that survived sepsis or endotoxemia experienced loss of hippocampal long-term po
162 was associated with a decrease in metabolic endotoxemia, glucose insulinotropic peptide, glucose int
165 The role of fructose intake and metabolic endotoxemia has gained attention recently, but data in k
166 that betaArr1 deficiency protects mice from endotoxemia, here we demonstrate that the absence of bet
168 ilarly during endotoxemia (-11% +/- 16%) and endotoxemia + hypoxia (-10% +/- 15%; both p < 0.05).
170 g vascular conductance, +100% +/- 115%), and endotoxemia + hypoxia (leg blood flow, +67% +/- 120%; le
172 n mice were assessed after acute and chronic endotoxemia (i.e., exposure to inflammatory lipopolysacc
173 quently, all subjects underwent experimental endotoxemia (i.v. administration of 2 ng/kg Escherichia
174 mice) with intact IL-1R8 were protected from endotoxemia, IL-1R8-deficient IL-37tg mice were not.
175 vo, and antibody blockade of IFN-gamma after endotoxemia improved survival of secondary candidemia.
176 n in beta-cells by hyperlipidemia-associated endotoxemia improves the adaptation of beta-cells to ins
180 okine signaling, suggesting that subclinical endotoxemia in healthy individuals might lead to signifi
181 e nanoparticles (GVNPs) for the treatment of endotoxemia in high-risk patients, using a murine model
183 regulation of Lp-PLA(2) during experimental endotoxemia in humans, probed the source of Lp-PLA(2) in
184 lungs and liver were markedly reduced during endotoxemia in IL-37Tg mice but not observed in IL-37D20
185 Using intravital microscopy, we found that endotoxemia in mice rapidly induced pulmonary microvascu
188 the cardiac dysfunction caused by sepsis or endotoxemia in mice; this effect may be caused by increa
189 the gut microbiota and preventing metabolic endotoxemia in rats fed a high fat and sucrose diet.
195 toneal neutrophil recruitment during sterile endotoxemia independent of the vagus nerve, without affe
197 ptibility to lethal effects of gram-negative endotoxemia induced by lipopolysaccharide (LPS), whereas
198 est, T3 significantly protected mice against endotoxemia induced by lipopolysaccharide i.p. injection
199 hibitor temsirolimus, even after established endotoxemia, induced autophagy and protected against the
202 ion correlated with disease severity scores, endotoxemia, infections, and short-term mortality, thus
204 l inflammation, and its dysregulation during endotoxemia is a novel mechanism for LPS-induced vascula
207 th a postcardiac arrest shock, high level of endotoxemia is independently associated with duration of
208 addition, low-level but persistent metabolic endotoxemia is often found in diabetic and obese subject
209 gery predict the development of endotoxemia; endotoxemia is particularly associated with cardiovascul
213 thelial injury in animal models of sepsis or endotoxemia leads to shedding of heparan fragments from
215 r than 25, and patients with an intermediate endotoxemia level (>/= 0.4) had more cardiovascular dysf
219 cohort of HIV-negative men with subclinical endotoxemia linked to alterations in CD4/CD8 T cell rati
220 nome-wide association study (GWAS) of evoked endotoxemia (lipopolysaccharide (LPS) 1 ng/kg IV) in hea
222 st (CPT) and had their blood drawn to assess endotoxemia markers LPS binding protein (LBP), soluble C
223 d mitochondrial TFAM abundance in sepsis and endotoxemia, may help to explain the paradox of lacking
226 dels, such as the lipopolysaccharide-induced endotoxemia model and the cecal ligation and puncture (C
234 ading to diaphragmatic weakness during acute endotoxemia, most likely via effects on multiple inflamm
235 er suppresses the adrenocortical response to endotoxemia nor enhances the accompanying production of
236 Thus, HMGB1 secretion, which is critical for endotoxemia, occurs downstream of inflammasome assembly
239 The present study addressed the effect of endotoxemia on the functional and molecular mechanisms t
240 mer all were increased greatly in mice after endotoxemia or cecal ligation and puncture as compared w
242 grated into an extracorporeal circuit in pig endotoxemia or heparin therapy models, it produces real-
244 om mice with intrarenal (maleate), prerenal (endotoxemia), or postrenal (ureteral obstruction) injury
247 after sepsis; p < 0.001 and 86% vs 12% after endotoxemia; p = 0.013) and significantly reduced viscer
248 g both acute (sepsis) and chronic (metabolic endotoxemia) pathologies wherein aberrant TLR4/MD2 activ
249 keywords: sepsis, septicemia, septic shock, endotoxemia, persistent pulmonary hypertension, nitric o
250 vels, improved colonic integrity, normalized endotoxemia, plasma trimethylamine (TMA) levels, and res
253 appaBalpha super-repressor mice subjected to endotoxemia, proinflammatory cytokines, muscle RING-fing
254 o adaptive changes during human experimental endotoxemia promoting higher levels of adenosine thereby
255 fatty acids on gut microbiota and metabolic endotoxemia provide insight into the etiology and manage
256 ne system, displayed enhanced sensitivity to endotoxemia, rapid progression of chemical-induced colit
257 monocytes from volunteers with experimental endotoxemia re-instates their capacity for cytokine prod
265 challenge, with rapid development of typical endotoxemia signs and extensive organ damage, and elevat
267 ptomic analysis of innate lymphocytes during endotoxemia suggested that NKT cells drove IFN-gamma pro
271 for the P2X1 receptor in LPS-induced lethal endotoxemia through its critical involvement in neutroph
272 itment to liver and LPS-induced death during endotoxemia, thus highlighting a previously unrecognized
274 was evoked in a human model of experimental endotoxemia to recruit neutrophil subsets with different
277 e demonstrate that hyperlipidemia-associated endotoxemia upregulates miR-155-5p in murine pancreatic
278 n regard to dynamic cerebral autoregulation, endotoxemia was associated with lower middle cerebral ar
281 Traumatic soft-tissue injury with additional endotoxemia was characterized by nutritive perfusion fai
287 study the role of neutrophils in LPS-induced endotoxemia, we developed a new mouse model, PMN(DTR) mi
289 e receptors for coagulation factors in mouse endotoxemia, we found that the protein C receptor (ProcR
290 sing this human in vivo model of subclinical endotoxemia, we furthermore show that plasma LPS leads t
291 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