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1                                          The endotoxic activities of these LPS-containing liposomes w
2                                          Its endotoxic activity depends on the number and length of a
3 ndothelial cell activation show that E. coli endotoxic activity is not due to just LPS.
4 do(hi) microbiota were related to the higher endotoxic activity of lipopolysaccharide (LPS), we compa
5 ndant Gram-negative protein is essential for endotoxic activity, but that the protein component also
6 helators such as EGTA and greatly diminished endotoxic activity.
7 embrane protein of E. coli is a fully active endotoxic agonist for endothelial cells.
8                  This study investigated the endotoxic and biological properties of purified lipopoly
9 scular mineralocorticoid receptors in murine endotoxic and human septic shock.
10 ontributing studies were conducted using the endotoxic animal model, and evidence from clinically rel
11                        Leukocytes can couple endotoxic challenge to the widespread circulatory and in
12 glucagon release, and glucose lowering under endotoxic conditions, whereas inhibition of the GLP-1 re
13 ferior vena caval occlusion, under basal and endotoxic conditions.
14 pha (IL-1 alpha) release, thereby preventing endotoxic death.
15           Additionally, FFF21 displayed anti-endotoxic effects in vitro.
16 om LPS-responsive cells, a critical step for endotoxic effects.
17 f bacterial virulence that can elicit potent endotoxic effects.
18 sal immune homeostasis, and mice with highly endotoxic Endo(hi) microbiota (a high proportion of Ente
19 H may be involved in the hepatic response to endotoxic insult by counteracting potential inflammatory
20 e production and enhanced protection against endotoxic lethality.
21 was found to be a strong predictor of murine endotoxic lethality.
22 such as phosphatidylcholine and lipid A, the endotoxic lipid component of bacterial lipopolysaccharid
23 of proinflammatory genes that are induced by endotoxic lipopolysaccharide (LPS) in vitro; however, mu
24                                              Endotoxic lipopolysaccharide (LPS) is a proinflammatory
25 to Escherichia coli bacteria versus purified endotoxic lipopolysaccharide (LPS).
26                                  Exposure to endotoxic lipopolysaccharide initiates an insect immune
27                    The lipid A domain of the endotoxic lipopolysaccharide layer of Gram-negative bact
28 lipid A (MPLA), a low toxicity derivative of endotoxic lipopolysaccharide, enhances antibody response
29 trate that, while rickettsiae do not contain endotoxic lipopolysaccharide, they nevertheless initiate
30 ling with the LPS forms studied here as with endotoxic LPS or detoxified monophosphorylated lipid A (
31  LPS structures that differ from the classic endotoxic LPS structures.
32 -deficient mice have reduced survival during endotoxic LPS-induced shock.
33                                 Treatment of endotoxic mice with YW3-56, a peptidylarginine deiminase
34            However, exactly how lipid A, the endotoxic moiety of LPS, activates myeloid lineage cells
35 tion, tissue damage, and mortality following endotoxic or bacterial challenge.
36 development of an effective gene therapy for endotoxic or septic shock.
37 eir reactogenicity by modifying lipid A, the endotoxic part of LPS, through deletion of late acyltran
38 and HAVR remained baseline values during the endotoxic phase (P < 0.05 vs. nontreated group, ANOVA).
39                     Only during the postburn endotoxic phase, iloprost improved hDO2 and hVO2 (140% a
40            However, during the late postburn endotoxic phase, prostacyclin seems to significantly imp
41                                          The endotoxic portion of lipopolysaccharide (LPS), a glycoph
42 osaccharide significantly contributes to the endotoxic potency of the whole rough-type C. canimorsus
43                    Consistent with a reduced endotoxic potential, S. flexneri 2a msbB mutants were at
44  of research, mAbs specific for lipid A (the endotoxic principle of LPS) have not been successfully d
45 ed on antibody sequestration of lipid A (the endotoxic principle of LPS); however, none have been suc
46 a peculiar chemical structure, harbours the 'endotoxic principle' of LPS and is responsible for the e
47 x vivo contractility of aortas obtained from endotoxic rats and improved survival in lethal murine en
48 enteral infusion of KIC improves survival in endotoxic rats, and, if so, the mechanism of this effect
49 age oil diets, as compared with corn oil, in endotoxic rats.
50 efining a role for ceramide in mediating the endotoxic response.
51 t experimental conditions to induce colitis, endotoxic sepsis, and pancreatitis.
52    Upon LPS challenge, merkd animals died of endotoxic shock (15/17, 88.2%), whereas control wild-typ
53 e conditions, norepinephrine infusion during endotoxic shock actually increases renal blood flow and
54 owever, these mice are highly susceptible to endotoxic shock and appear to be compromised in their ab
55 umatic brain injury, diabetes, Parkinsonism, endotoxic shock and arthritis, implicating PARP in the p
56 orming CM-LPS complexes, and protect against endotoxic shock and death in rodent models of gram-negat
57 ve in controlling clinical manifestations of endotoxic shock and death under conditions wherein fluni
58 e found increased production of IL-12 during endotoxic shock and enhanced Th1 cells in TTP knockout m
59 AP12-deficient mice were more susceptible to endotoxic shock and had enhanced resistance to infection
60 icient mice exhibit diminished recovery from endotoxic shock and hyperresponsiveness of a subset of e
61 out (SR-A(-/-)) mice are more susceptible to endotoxic shock and Listeria monocytogenes infection in
62 vents regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal
63 ransfer experiments showed that responses to endotoxic shock and polymicrobial sepsis were transferab
64 -fold higher concentrations of IL-27(p28) in endotoxic shock and polymicrobial sepsis.
65 t from other inflammatory disorders, such as endotoxic shock and rheumatoid arthritis.
66 )-deficient mice display reduced survival to endotoxic shock and sepsis.
67 hypersensitive to lipopolysaccharide-induced endotoxic shock and showed prolonged inflammation in a m
68 cated in serious autoimmune diseases such as endotoxic shock and thus are important therapeutic targe
69 tion may be protective in some patients with endotoxic shock and with diseases characterized by chron
70 onclusion, hypometabolism and hypothermia in endotoxic shock are not consequential to hypoxia but ser
71 pendent cytokine responses and the resultant endotoxic shock are not coupled to SRA-mediated clearanc
72                        Patients in septic or endotoxic shock are sensitive to most anesthetic regimen
73 fective in that they are highly resistant to endotoxic shock as compared with normal responder mice.
74 nces susceptibility and worsens outcome from endotoxic shock by augmenting sympathetic activity, part
75  experiments in a mouse model of LPS-induced endotoxic shock confirmed the proinflammatory potential
76 ve apoptosis of leukocytes during sepsis and endotoxic shock constitutes an important mechanism linke
77 liest drops in cardiac output and DO2 during endotoxic shock did not precede the reduction in VO2 tha
78  action of exogenous low-dose vasopressin in endotoxic shock does not impair blood flow to any of the
79 trite and rings taken from rats subjected to endotoxic shock exhibited reduced endothelium-dependent
80 orrhaged mice were susceptible to sepsis and endotoxic shock from the leaky gut.
81     However, 85% of individuals that develop endotoxic shock from V. vulnificus are males.
82 function in the first 4 h after induction of endotoxic shock in anesthetized canine preparations (n =
83 temic inflammation, organ damage, and lethal endotoxic shock in beta2-knockout mice.
84                     Death due to LPS-induced endotoxic shock in merkd mice was blocked by administrat
85 roptosis, which is critical for induction of endotoxic shock in mice.
86 study examines the effect of parthenolide in endotoxic shock in rodents.
87  and in vivo and increased susceptibility to endotoxic shock in SRA-deficient mice.
88 eficient in MKP-1 were highly susceptible to endotoxic shock in vivo, associated with enhanced produc
89 ion of the cytokines IL-17A and IL-23 during endotoxic shock in young adult male C57BL/6J mice and ha
90 ut of Mkp-1 substantially sensitizes mice to endotoxic shock induced by lipopolysaccharide (LPS) chal
91 t mice, casp-11 mutant mice are resistant to endotoxic shock induced by lipopolysaccharide.
92                                              Endotoxic shock is a life-threatening condition caused b
93                                              Endotoxic shock is a life-threatening consequence of sev
94                                        Acute endotoxic shock is accompanied by an increase in the pro
95 velopment of hypothermia instead of fever in endotoxic shock is consequential to hypoxia.
96 creased survival rates of mutants faced with endotoxic shock may indicate a contribution of grancalci
97 ervention with conventional laparotomy in an endotoxic shock model in the pig.
98 ation, can be recapitulated in mice using an endotoxic shock model.
99                                           In endotoxic shock of C57BL/6J mice, pharmacologic activati
100 ucocorticoid-dependent host defense after an endotoxic shock or bacterial infection.
101                Using a novel rabbit model of endotoxic shock produced by multiple exposures to endoto
102          Gram-negative sepsis and subsequent endotoxic shock remain major health problems in the Unit
103                     In vehicle-treated mice, endotoxic shock resulted in lung injury and was associat
104    The present studies provide evidence that endotoxic shock results from disseminated endothelial ap
105 acterial challenges, possibly at the cost of endotoxic shock risk.
106                                          The endotoxic shock syndrome is characterized by systemic in
107 esistant to lipopolysaccharide (LPS)-induced endotoxic shock than control wild-type mice.
108 ice, which are more resistant to LPS-induced endotoxic shock than wild-type animals.
109  edema, leukocyte infiltration, and signs of endotoxic shock that correlated with higher levels of TN
110  we have developed a model for V. vulnificus endotoxic shock that mimics the sexually dimorphic respo
111 arthenolide exerts beneficial effects during endotoxic shock through inhibition of NF-kappaB.
112 iologic protective factor against the lethal endotoxic shock triggered by an acute inflammatory respo
113       Survival of lipopolysaccharide-induced endotoxic shock was improved in Tph1(-/-) mice.
114                                              Endotoxic shock was induced by administration of Escheri
115                                              Endotoxic shock was induced by bacterial lipopolysacchar
116                                              Endotoxic shock was induced in male B6/129F2/J mice by a
117                        Sensitivity to lethal endotoxic shock was not significantly altered in Bf-defi
118         A clinical picture characteristic of endotoxic shock was observed in most animals as a termin
119 gy reminiscent of lipopolysaccharide-induced endotoxic shock, a type of systemic inflammatory respons
120 how that c-peptide has beneficial effects in endotoxic shock, and this therapeutic effect is associat
121 ammation using three models of inflammation: endotoxic shock, diabetes, and contact hypersensitivity.
122 UF1 knockout mice display symptoms of severe endotoxic shock, including vascular hemorrhage, intravas
123 lling diseases such as rheumatoid arthritis, endotoxic shock, inflammatory bowel disease, osteoporosi
124                       One form of sepsis, or endotoxic shock, is a hyperactivated systemic response c
125 aken to determine if V antigen could prevent endotoxic shock, known to be mediated by excessive produ
126 the antiinflammatory response to LPS-induced endotoxic shock, likely through its essential role in fa
127                            In a rat model of endotoxic shock, lipopolysaccharide-induced HO-1 mRNA an
128                                In a model of endotoxic shock, LPS (35 microg/mouse, i.p.) suppressed
129 ole in various inflammatory diseases such as endotoxic shock, multiple sclerosis, cerebral malaria, a
130      Foremost, both models result in DIC and endotoxic shock, neither of which is likely to respond t
131 y responses and it blocks the hypotension of endotoxic shock, we determined whether TGF-beta1 could b
132 2cre)) resulted in resistance to LPS-induced endotoxic shock, whereas Socs2(-/-) mice were highly sus
133 in the potentially lethal condition known as endotoxic shock, whereby uncontrolled inflammation can l
134  in IL-1beta showed unaltered sensitivity to endotoxic shock, with or without pretreatment with D-gal
135 e induced by SIVsmmPBj4 clinically resembles endotoxic shock, with the development of severe gastroin
136  to induce disease and death in humans in an endotoxic shock-like manner.
137 phrine at 18 hours after induction of murine endotoxic shock.
138 uppressive ODN protect mice from LPS-induced endotoxic shock.
139 tic shock, were intravenously infused during endotoxic shock.
140 ted in a model of lipopolysaccharide-induced endotoxic shock.
141 ful in treating organ injury associated with endotoxic shock.
142 hages, and this function protected mice from endotoxic shock.
143 st from cytokine-induced immunopathology and endotoxic shock.
144 ity reaction and increased susceptibility to endotoxic shock.
145 were resistant to lipopolysaccharide-induced endotoxic shock.
146 ection from lipopolysaccharide (LPS)-induced endotoxic shock.
147 t hypotension that develops in Gram-negative endotoxic shock.
148  and is also essential in protection against endotoxic shock.
149 sistant to the lethal effects of LPS-induced endotoxic shock.
150 mulation by microbial components may lead to endotoxic shock.
151 re susceptible to lipopolysaccharide-induced endotoxic shock.
152 ndering them more susceptible to LPS-induced endotoxic shock.
153  cytokine production within the heart during endotoxic shock.
154 nst V. vulnificus lipopolysaccharide-induced endotoxic shock.
155 ally dimorphic response to Vibrio vulnificus endotoxic shock.
156 ar tone and increases in oxidative stress is endotoxic shock.
157 educed the lethality associated with ensuing endotoxic shock.
158  could protect endotoxin-sensitive mice from endotoxic shock.
159 gulating TNF-alpha secretion and attenuating endotoxic shock.
160 ute to the beneficial effect of TGF-beta1 on endotoxic shock.
161 onsible for the overall host response during endotoxic shock.
162 umption (VO2) in the presence and absence of endotoxic shock.
163  an enhanced susceptibility to pathogens and endotoxic shock.
164 contributes to the hemodynamic compromise of endotoxic shock.
165 tes to the reduction in vascular tone during endotoxic shock.
166 ing protection in this experimental model of endotoxic shock.
167 y relevant model of gram-negative sepsis and endotoxic shock.
168 oration of alpha1-adrenoceptor expression in endotoxic shock.
169 o block the organ damage or lethal effect of endotoxic shock.
170 be involved in the hemodynamic compromise of endotoxic shock.
171 nt for the acidotic mucosal tonometric pH in endotoxic shock.
172  rats and improved survival in lethal murine endotoxic shock.
173 vels of PAF are observed in animal models of endotoxic shock.
174 ascular energetic and contractile failure in endotoxic shock.
175 ng in the microcirculation during septic and endotoxic shock.
176  by the fall in oxygen delivery (DO2) during endotoxic shock.
177 echolamine-producing adrenal glands prior to endotoxic shock.
178 macrophages were sufficient to induce lethal endotoxic shock.
179 nd is protective in an experimental model of endotoxic shock.
180 uch higher levels of IL-17A and IL-23 during endotoxic shock.
181 oving survival in an in vivo murine model of endotoxic shock.
182  leads to greater sensitivity to LPS-induced endotoxic shock.
183  cytokines, but only partial protection from endotoxic shock.
184 o partial recovery of CCL5 production during endotoxic shock.
185 ent of AC7 are hypersensitive to LPS-induced endotoxic shock.
186 d showed reduced CCL5 levels in serum during endotoxic shock.
187 cking caspase 1 are resistant to LPS-induced endotoxic shock.
188 ible to LPS-induced splenocyte apoptosis and endotoxic shock.
189 agocytosis of bacteria and susceptibility to endotoxic shock.
190 m-derived molecules, are more susceptible to endotoxic shock.
191  immune response to an infectious disease or endotoxic shock.
192  ATF3-deficient mice are more susceptible to endotoxic shock.
193 ord complete protection in a murine model of endotoxic shock.
194 l mice are hypersensitive to the LPS-induced endotoxic shock.
195 mal antiinflammatory response to LPS-induced endotoxic shock.
196 ng a murine model of D-galactosamine-induced endotoxic shock.
197 e are markedly hypersensitive to LPS-induced endotoxic shock.
198 back element for cardiovascular tolerance in endotoxic shock.
199 ve immune response to LPS and development of endotoxic shock.
200 e cardiovascular dysfunction associated with endotoxic shock.
201 n macrophages, a major cell type involved in endotoxic shock.
202 ta protect AUF1 knockout mice against lethal endotoxic shock.
203 cytokines that facilitate the development of endotoxic shock.
204  production, and increased susceptibility to endotoxic shock.
205 sive ODN might be of use in the treatment of endotoxic shock.
206 e life-threatening multiple-organ failure of endotoxic shock.
207 ve cells play an important role in mediating endotoxic shock; (ii) tamLITAF(i)-/- mice show a similar
208 ry cytokines and exhibit hypersensitivity to endotoxic shock; these effects are mitigated when the an
209  Phe-126 is indeed the "molecular switch" in endotoxic signaling.
210                                              Endotoxic stimulation induced a respiratory burst with t
211 tion of PAF-like bioactivity) in response to endotoxic stimulation was delayed for several minutes.
212 st of the phospholipid agonists arising from endotoxic stimulation.
213  increased susceptibility of aged animals to endotoxic stress.
214                      The LPS induced neither endotoxic symptoms nor lethality for 96 h, suggesting ne
215 is cascade is mandatory for evolution of the endotoxic syndrome.
216 example, monophosphoryl lipid A, a family of endotoxic TLR4 agonist molecules from bacteria, has rece
217 channel opener drug improved survival in the endotoxic WT but had no effect in the Kir6.1 knockout.

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