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 ution is a potential resuscitation fluid for
endotoxic and septic shock.
11 ontributing studies were conducted using the
endotoxic animal model, and evidence from clinically rel
12 Leukocytes can couple
endotoxic challenge to the widespread circulatory and in
13 cture-function relationships of lipid A, the
endotoxic component of lipopolysaccharide which also ser
14 glucagon release, and glucose lowering under
endotoxic conditions, whereas inhibition of the GLP-1 re
15 ferior vena caval occlusion, under basal and
endotoxic conditions.
16 pha (IL-1 alpha) release, thereby preventing
endotoxic death.
17 Additionally, FFF21 displayed anti-
endotoxic effects in vitro.
18 om LPS-responsive cells, a critical step for
endotoxic effects.
19 f bacterial virulence that can elicit potent
endotoxic effects.
20 sal immune homeostasis, and mice with highly
endotoxic Endo(hi) microbiota (a high proportion of Ente
21 H may be involved in the hepatic response to
endotoxic insult by counteracting potential inflammatory
22 e production and enhanced protection against
endotoxic lethality.
23 was found to be a strong predictor of murine
endotoxic lethality.
24 such as phosphatidylcholine and lipid A, the
endotoxic lipid component of bacterial lipopolysaccharid
25 of proinflammatory genes that are induced by
endotoxic lipopolysaccharide (LPS) in vitro; however, mu
26 Endotoxic lipopolysaccharide (LPS) is a proinflammatory
27 to Escherichia coli bacteria versus purified
endotoxic lipopolysaccharide (LPS).
28 Exposure to
endotoxic lipopolysaccharide initiates an insect immune
29 The lipid A domain of the
endotoxic lipopolysaccharide layer of Gram-negative bact
30 lipid A (MPLA), a low toxicity derivative of
endotoxic lipopolysaccharide, enhances antibody response
31 trate that, while rickettsiae do not contain
endotoxic lipopolysaccharide, they nevertheless initiate
32 ling with the LPS forms studied here as with
endotoxic LPS or detoxified monophosphorylated lipid A (
33 LPS structures that differ from the classic
endotoxic LPS structures.
34 -deficient mice have reduced survival during
endotoxic LPS-induced shock.
35 Mortality by
endotoxic (
LPS) shock is highly time-of-day dependent an
36 Treatment of
endotoxic mice with YW3-56, a peptidylarginine deiminase
37 However, exactly how lipid A, the
endotoxic moiety of LPS, activates myeloid lineage cells
38 tion, tissue damage, and mortality following
endotoxic or bacterial challenge.
39 development of an effective gene therapy for
endotoxic or septic shock.
40 eir reactogenicity by modifying lipid A, the
endotoxic part of LPS, through deletion of late acyltran
41 and HAVR remained baseline values during the
endotoxic phase (P < 0.05 vs. nontreated group, ANOVA).
42 Only during the postburn
endotoxic phase, iloprost improved hDO2 and hVO2 (140% a
43 However, during the late postburn
endotoxic phase, prostacyclin seems to significantly imp
44 The
endotoxic portion of lipopolysaccharide (LPS), a glycoph
45 osaccharide significantly contributes to the
endotoxic potency of the whole rough-type C. canimorsus
46 Consistent with a reduced
endotoxic potential, S. flexneri 2a msbB mutants were at
47 of research, mAbs specific for lipid A (the
endotoxic principle of LPS) have not been successfully d
48 ed on antibody sequestration of lipid A (the
endotoxic principle of LPS); however, none have been suc
49 a peculiar chemical structure, harbours the '
endotoxic principle' of LPS and is responsible for the e
50 x vivo contractility of aortas obtained from
endotoxic rats and improved survival in lethal murine en
51 enteral infusion of KIC improves survival in
endotoxic rats, and, if so, the mechanism of this effect
52 age oil diets, as compared with corn oil, in
endotoxic rats.
53 efining a role for ceramide in mediating the
endotoxic response.
54 t experimental conditions to induce colitis,
endotoxic sepsis, and pancreatitis.
55 Upon LPS challenge, merkd animals died of
endotoxic shock (15/17, 88.2%), whereas control wild-typ
56 e conditions, norepinephrine infusion during
endotoxic shock actually increases renal blood flow and
57 owever, these mice are highly susceptible to
endotoxic shock and appear to be compromised in their ab
58 umatic brain injury, diabetes, Parkinsonism,
endotoxic shock and arthritis, implicating PARP in the p
59 orming CM-LPS complexes, and protect against
endotoxic shock and death in rodent models of gram-negat
60 ve in controlling clinical manifestations of
endotoxic shock and death under conditions wherein fluni
61 e found increased production of IL-12 during
endotoxic shock and enhanced Th1 cells in TTP knockout m
62 AP12-deficient mice were more susceptible to
endotoxic shock and had enhanced resistance to infection
63 icient mice exhibit diminished recovery from
endotoxic shock and hyperresponsiveness of a subset of e
64 out (SR-A(-/-)) mice are more susceptible to
endotoxic shock and Listeria monocytogenes infection in
65 vents regulating the p28 subunit of IL-27 in
endotoxic shock and polymicrobial sepsis following cecal
66 ransfer experiments showed that responses to
endotoxic shock and polymicrobial sepsis were transferab
67 -fold higher concentrations of IL-27(p28) in
endotoxic shock and polymicrobial sepsis.
68 t from other inflammatory disorders, such as
endotoxic shock and rheumatoid arthritis.
69 )-deficient mice display reduced survival to
endotoxic shock and sepsis.
70 hypersensitive to lipopolysaccharide-induced
endotoxic shock and showed prolonged inflammation in a m
71 cated in serious autoimmune diseases such as
endotoxic shock and thus are important therapeutic targe
72 tion may be protective in some patients with
endotoxic shock and with diseases characterized by chron
73 onclusion, hypometabolism and hypothermia in
endotoxic shock are not consequential to hypoxia but ser
74 pendent cytokine responses and the resultant
endotoxic shock are not coupled to SRA-mediated clearanc
75 Patients in septic or
endotoxic shock are sensitive to most anesthetic regimen
76 Mortality by
endotoxic shock as a function of circadian time is indep
77 fective in that they are highly resistant to
endotoxic shock as compared with normal responder mice.
78 nces susceptibility and worsens outcome from
endotoxic shock by augmenting sympathetic activity, part
79 cterial and lipopolysaccharide (LPS)-induced
endotoxic shock by blocking the non-canonical inflammaso
80 experiments in a mouse model of LPS-induced
endotoxic shock confirmed the proinflammatory potential
81 ve apoptosis of leukocytes during sepsis and
endotoxic shock constitutes an important mechanism linke
82 liest drops in cardiac output and DO2 during
endotoxic shock did not precede the reduction in VO2 tha
83 action of exogenous low-dose vasopressin in
endotoxic shock does not impair blood flow to any of the
84 trite and rings taken from rats subjected to
endotoxic shock exhibited reduced endothelium-dependent
85 orrhaged mice were susceptible to sepsis and
endotoxic shock from the leaky gut.
86 However, 85% of individuals that develop
endotoxic shock from V. vulnificus are males.
87 function in the first 4 h after induction of
endotoxic shock in anesthetized canine preparations (n =
88 temic inflammation, organ damage, and lethal
endotoxic shock in beta2-knockout mice.
89 Death due to LPS-induced
endotoxic shock in merkd mice was blocked by administrat
90 roptosis, which is critical for induction of
endotoxic shock in mice.
91 study examines the effect of parthenolide in
endotoxic shock in rodents.
92 and in vivo and increased susceptibility to
endotoxic shock in SRA-deficient mice.
93 eficient in MKP-1 were highly susceptible to
endotoxic shock in vivo, associated with enhanced produc
94 Perforin-2 (P2) is critical for LPS-induced
endotoxic shock in wild-type mice.
95 ion of the cytokines IL-17A and IL-23 during
endotoxic shock in young adult male C57BL/6J mice and ha
96 ut of Mkp-1 substantially sensitizes mice to
endotoxic shock induced by lipopolysaccharide (LPS) chal
97 t mice, casp-11 mutant mice are resistant to
endotoxic shock induced by lipopolysaccharide.
98 Endotoxic shock is a life-threatening condition caused b
99 Endotoxic shock is a life-threatening consequence of sev
100 Acute
endotoxic shock is accompanied by an increase in the pro
101 velopment of hypothermia instead of fever in
endotoxic shock is consequential to hypoxia.
102 creased survival rates of mutants faced with
endotoxic shock may indicate a contribution of grancalci
103 ervention with conventional laparotomy in an
endotoxic shock model in the pig.
104 In an
endotoxic shock model, HNRNPA2B1-deficient mice exhibit
105 ation, can be recapitulated in mice using an
endotoxic shock model.
106 In
endotoxic shock of C57BL/6J mice, pharmacologic activati
107 ucocorticoid-dependent host defense after an
endotoxic shock or bacterial infection.
108 Using a novel rabbit model of
endotoxic shock produced by multiple exposures to endoto
109 Gram-negative sepsis and subsequent
endotoxic shock remain major health problems in the Unit
110 In vehicle-treated mice,
endotoxic shock resulted in lung injury and was associat
111 The present studies provide evidence that
endotoxic shock results from disseminated endothelial ap
112 An in vivo model of
endotoxic shock revealed that, in comparison with wild t
113 acterial challenges, possibly at the cost of
endotoxic shock risk.
114 X) was not sufficient to reverse LPS-induced
endotoxic shock susceptibility or restore IL-10 release.
115 The
endotoxic shock syndrome is characterized by systemic in
116 esistant to lipopolysaccharide (LPS)-induced
endotoxic shock than control wild-type mice.
117 ice, which are more resistant to LPS-induced
endotoxic shock than wild-type animals.
118 edema, leukocyte infiltration, and signs of
endotoxic shock that correlated with higher levels of TN
119 we have developed a model for V. vulnificus
endotoxic shock that mimics the sexually dimorphic respo
120 -33 protects animals from lipopolysaccharide
endotoxic shock through attenuated neutrophil extravasat
121 arthenolide exerts beneficial effects during
endotoxic shock through inhibition of NF-kappaB.
122 iologic protective factor against the lethal
endotoxic shock triggered by an acute inflammatory respo
123 Survival of lipopolysaccharide-induced
endotoxic shock was improved in Tph1(-/-) mice.
124 Endotoxic shock was induced by administration of Escheri
125 Endotoxic shock was induced by bacterial lipopolysacchar
126 Endotoxic shock was induced in male B6/129F2/J mice by a
127 Sensitivity to lethal
endotoxic shock was not significantly altered in Bf-defi
128 A clinical picture characteristic of
endotoxic shock was observed in most animals as a termin
129 gy reminiscent of lipopolysaccharide-induced
endotoxic shock, a type of systemic inflammatory respons
130 how that c-peptide has beneficial effects in
endotoxic shock, and this therapeutic effect is associat
131 ammation using three models of inflammation:
endotoxic shock, diabetes, and contact hypersensitivity.
132 During lipopolysaccharide (LPS)-induced
endotoxic shock, HLJ1 knockout mice shows reduced organ
133 UF1 knockout mice display symptoms of severe
endotoxic shock, including vascular hemorrhage, intravas
134 lling diseases such as rheumatoid arthritis,
endotoxic shock, inflammatory bowel disease, osteoporosi
135 One form of sepsis, or
endotoxic shock, is a hyperactivated systemic response c
136 aken to determine if V antigen could prevent
endotoxic shock, known to be mediated by excessive produ
137 the antiinflammatory response to LPS-induced
endotoxic shock, likely through its essential role in fa
138 In a rat model of
endotoxic shock, lipopolysaccharide-induced HO-1 mRNA an
139 In a model of
endotoxic shock, LPS (35 microg/mouse, i.p.) suppressed
140 ole in various inflammatory diseases such as
endotoxic shock, multiple sclerosis, cerebral malaria, a
141 Foremost, both models result in DIC and
endotoxic shock, neither of which is likely to respond t
142 that U90926 expression is protective during
endotoxic shock, potentially mediated by the paracrine a
143 y responses and it blocks the hypotension of
endotoxic shock, we determined whether TGF-beta1 could b
144 2cre)) resulted in resistance to LPS-induced
endotoxic shock, whereas Socs2(-/-) mice were highly sus
145 in the potentially lethal condition known as
endotoxic shock, whereby uncontrolled inflammation can l
146 in IL-1beta showed unaltered sensitivity to
endotoxic shock, with or without pretreatment with D-gal
147 e induced by SIVsmmPBj4 clinically resembles
endotoxic shock, with the development of severe gastroin
148 to induce disease and death in humans in an
endotoxic shock-like manner.
149 nt mice were more susceptible to LPS-induced
endotoxic shock.
150 sive ODN might be of use in the treatment of
endotoxic shock.
151 e life-threatening multiple-organ failure of
endotoxic shock.
152 uppressive ODN protect mice from LPS-induced
endotoxic shock.
153 tic shock, were intravenously infused during
endotoxic shock.
154 ted in a model of lipopolysaccharide-induced
endotoxic shock.
155 ful in treating organ injury associated with
endotoxic shock.
156 ng a murine model of D-galactosamine-induced
endotoxic shock.
157 hages, and this function protected mice from
endotoxic shock.
158 st from cytokine-induced immunopathology and
endotoxic shock.
159 ity reaction and increased susceptibility to
endotoxic shock.
160 were resistant to lipopolysaccharide-induced
endotoxic shock.
161 ection from lipopolysaccharide (LPS)-induced
endotoxic shock.
162 t hypotension that develops in Gram-negative
endotoxic shock.
163 and is also essential in protection against
endotoxic shock.
164 sistant to the lethal effects of LPS-induced
endotoxic shock.
165 mulation by microbial components may lead to
endotoxic shock.
166 re susceptible to lipopolysaccharide-induced
endotoxic shock.
167 ndering them more susceptible to LPS-induced
endotoxic shock.
168 cytokine production within the heart during
endotoxic shock.
169 nst V. vulnificus lipopolysaccharide-induced
endotoxic shock.
170 ally dimorphic response to Vibrio vulnificus
endotoxic shock.
171 ar tone and increases in oxidative stress is
endotoxic shock.
172 educed the lethality associated with ensuing
endotoxic shock.
173 could protect endotoxin-sensitive mice from
endotoxic shock.
174 gulating TNF-alpha secretion and attenuating
endotoxic shock.
175 ute to the beneficial effect of TGF-beta1 on
endotoxic shock.
176 onsible for the overall host response during
endotoxic shock.
177 an enhanced susceptibility to pathogens and
endotoxic shock.
178 contributes to the hemodynamic compromise of
endotoxic shock.
179 tes to the reduction in vascular tone during
endotoxic shock.
180 ing protection in this experimental model of
endotoxic shock.
181 ation and promoted the recovery of mice from
endotoxic shock.
182 y relevant model of gram-negative sepsis and
endotoxic shock.
183 o block the organ damage or lethal effect of
endotoxic shock.
184 be involved in the hemodynamic compromise of
endotoxic shock.
185 nt for the acidotic mucosal tonometric pH in
endotoxic shock.
186 rats and improved survival in lethal murine
endotoxic shock.
187 vels of PAF are observed in animal models of
endotoxic shock.
188 ascular energetic and contractile failure in
endotoxic shock.
189 ng in the microcirculation during septic and
endotoxic shock.
190 umption (VO2) in the presence and absence of
endotoxic shock.
191 ory genes and show resistance to LPS-induced
endotoxic shock.
192 nnate immunity, macrophages, and LPS-induced
endotoxic shock.
193 of light and myeloid clocks on mortality by
endotoxic shock.
194 y to influenza A virus (IAV) and LPS-induced
endotoxic shock.
195 ssociated with hemorrhagic, cardiogenic, and
endotoxic shock.
196 cterial lipopolysaccharide (LPS), a model of
endotoxic shock.
197 ver a key role for this lncRNA in modulating
endotoxic shock.
198 by the fall in oxygen delivery (DO2) during
endotoxic shock.
199 phrine at 18 hours after induction of murine
endotoxic shock.
200 macrophages were sufficient to induce lethal
endotoxic shock.
201 nd is protective in an experimental model of
endotoxic shock.
202 uch higher levels of IL-17A and IL-23 during
endotoxic shock.
203 oration of alpha1-adrenoceptor expression in
endotoxic shock.
204 oving survival in an in vivo murine model of
endotoxic shock.
205 leads to greater sensitivity to LPS-induced
endotoxic shock.
206 cytokines, but only partial protection from
endotoxic shock.
207 o partial recovery of CCL5 production during
endotoxic shock.
208 ent of AC7 are hypersensitive to LPS-induced
endotoxic shock.
209 d showed reduced CCL5 levels in serum during
endotoxic shock.
210 cking caspase 1 are resistant to LPS-induced
endotoxic shock.
211 echolamine-producing adrenal glands prior to
endotoxic shock.
212 ible to LPS-induced splenocyte apoptosis and
endotoxic shock.
213 agocytosis of bacteria and susceptibility to
endotoxic shock.
214 m-derived molecules, are more susceptible to
endotoxic shock.
215 immune response to an infectious disease or
endotoxic shock.
216 ATF3-deficient mice are more susceptible to
endotoxic shock.
217 ord complete protection in a murine model of
endotoxic shock.
218 l mice are hypersensitive to the LPS-induced
endotoxic shock.
219 mal antiinflammatory response to LPS-induced
endotoxic shock.
220 e are markedly hypersensitive to LPS-induced
endotoxic shock.
221 back element for cardiovascular tolerance in
endotoxic shock.
222 ve immune response to LPS and development of
endotoxic shock.
223 e cardiovascular dysfunction associated with
endotoxic shock.
224 n macrophages, a major cell type involved in
endotoxic shock.
225 ta protect AUF1 knockout mice against lethal
endotoxic shock.
226 cytokines that facilitate the development of
endotoxic shock.
227 production, and increased susceptibility to
endotoxic shock.
228 ve cells play an important role in mediating
endotoxic shock; (ii) tamLITAF(i)-/- mice show a similar
229 ry cytokines and exhibit hypersensitivity to
endotoxic shock; these effects are mitigated when the an
230 Phe-126 is indeed the "molecular switch" in
endotoxic signaling.
231 Endotoxic stimulation induced a respiratory burst with t
232 tion of PAF-like bioactivity) in response to
endotoxic stimulation was delayed for several minutes.
233 st of the phospholipid agonists arising from
endotoxic stimulation.
234 increased susceptibility of aged animals to
endotoxic stress.
235 The LPS induced neither
endotoxic symptoms nor lethality for 96 h, suggesting ne
236 is cascade is mandatory for evolution of the
endotoxic syndrome.
237 example, monophosphoryl lipid A, a family of
endotoxic TLR4 agonist molecules from bacteria, has rece
238 channel opener drug improved survival in the
endotoxic WT but had no effect in the Kir6.1 knockout.