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.