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1 nt mice were more susceptible to LPS-induced endotoxic shock.
2 re susceptible to lipopolysaccharide-induced endotoxic shock.
3 ndering them more susceptible to LPS-induced endotoxic shock.
4  cytokine production within the heart during endotoxic shock.
5 nst V. vulnificus lipopolysaccharide-induced endotoxic shock.
6 ally dimorphic response to Vibrio vulnificus endotoxic shock.
7 ar tone and increases in oxidative stress is endotoxic shock.
8 educed the lethality associated with ensuing endotoxic shock.
9  could protect endotoxin-sensitive mice from endotoxic shock.
10 gulating TNF-alpha secretion and attenuating endotoxic shock.
11 ute to the beneficial effect of TGF-beta1 on endotoxic shock.
12 onsible for the overall host response during endotoxic shock.
13  an enhanced susceptibility to pathogens and endotoxic shock.
14 contributes to the hemodynamic compromise of endotoxic shock.
15 tes to the reduction in vascular tone during endotoxic shock.
16 ing protection in this experimental model of endotoxic shock.
17 y relevant model of gram-negative sepsis and endotoxic shock.
18 o block the organ damage or lethal effect of endotoxic shock.
19 umption (VO2) in the presence and absence of endotoxic shock.
20 be involved in the hemodynamic compromise of endotoxic shock.
21 nt for the acidotic mucosal tonometric pH in endotoxic shock.
22  rats and improved survival in lethal murine endotoxic shock.
23 vels of PAF are observed in animal models of endotoxic shock.
24 ascular energetic and contractile failure in endotoxic shock.
25 ng in the microcirculation during septic and endotoxic shock.
26 ory genes and show resistance to LPS-induced endotoxic shock.
27 nnate immunity, macrophages, and LPS-induced endotoxic shock.
28  of light and myeloid clocks on mortality by endotoxic shock.
29 y to influenza A virus (IAV) and LPS-induced endotoxic shock.
30 ssociated with hemorrhagic, cardiogenic, and endotoxic shock.
31 cterial lipopolysaccharide (LPS), a model of endotoxic shock.
32 ver a key role for this lncRNA in modulating endotoxic shock.
33  by the fall in oxygen delivery (DO2) during endotoxic shock.
34 ation and promoted the recovery of mice from endotoxic shock.
35 macrophages were sufficient to induce lethal endotoxic shock.
36 nd is protective in an experimental model of endotoxic shock.
37 phrine at 18 hours after induction of murine endotoxic shock.
38 uch higher levels of IL-17A and IL-23 during endotoxic shock.
39 oving survival in an in vivo murine model of endotoxic shock.
40  leads to greater sensitivity to LPS-induced endotoxic shock.
41  cytokines, but only partial protection from endotoxic shock.
42 o partial recovery of CCL5 production during endotoxic shock.
43 ent of AC7 are hypersensitive to LPS-induced endotoxic shock.
44 d showed reduced CCL5 levels in serum during endotoxic shock.
45 cking caspase 1 are resistant to LPS-induced endotoxic shock.
46 ible to LPS-induced splenocyte apoptosis and endotoxic shock.
47 agocytosis of bacteria and susceptibility to endotoxic shock.
48 m-derived molecules, are more susceptible to endotoxic shock.
49  immune response to an infectious disease or endotoxic shock.
50 oration of alpha1-adrenoceptor expression in endotoxic shock.
51  ATF3-deficient mice are more susceptible to endotoxic shock.
52 ord complete protection in a murine model of endotoxic shock.
53 l mice are hypersensitive to the LPS-induced endotoxic shock.
54 mal antiinflammatory response to LPS-induced endotoxic shock.
55 echolamine-producing adrenal glands prior to endotoxic shock.
56 e are markedly hypersensitive to LPS-induced endotoxic shock.
57 back element for cardiovascular tolerance in endotoxic shock.
58 ve immune response to LPS and development of endotoxic shock.
59 e cardiovascular dysfunction associated with endotoxic shock.
60 n macrophages, a major cell type involved in endotoxic shock.
61 ta protect AUF1 knockout mice against lethal endotoxic shock.
62 cytokines that facilitate the development of endotoxic shock.
63  production, and increased susceptibility to endotoxic shock.
64 sive ODN might be of use in the treatment of endotoxic shock.
65 e life-threatening multiple-organ failure of endotoxic shock.
66 uppressive ODN protect mice from LPS-induced endotoxic shock.
67 tic shock, were intravenously infused during endotoxic shock.
68 ng a murine model of D-galactosamine-induced endotoxic shock.
69 ted in a model of lipopolysaccharide-induced endotoxic shock.
70 ful in treating organ injury associated with endotoxic shock.
71 hages, and this function protected mice from endotoxic shock.
72 st from cytokine-induced immunopathology and endotoxic shock.
73 ity reaction and increased susceptibility to endotoxic shock.
74 were resistant to lipopolysaccharide-induced endotoxic shock.
75 ection from lipopolysaccharide (LPS)-induced endotoxic shock.
76 t hypotension that develops in Gram-negative endotoxic shock.
77  and is also essential in protection against endotoxic shock.
78 sistant to the lethal effects of LPS-induced endotoxic shock.
79 mulation by microbial components may lead to endotoxic shock.
80    Upon LPS challenge, merkd animals died of endotoxic shock (15/17, 88.2%), whereas control wild-typ
81 gy reminiscent of lipopolysaccharide-induced endotoxic shock, a type of systemic inflammatory respons
82 e conditions, norepinephrine infusion during endotoxic shock actually increases renal blood flow and
83 owever, these mice are highly susceptible to endotoxic shock and appear to be compromised in their ab
84 umatic brain injury, diabetes, Parkinsonism, endotoxic shock and arthritis, implicating PARP in the p
85 orming CM-LPS complexes, and protect against endotoxic shock and death in rodent models of gram-negat
86 ve in controlling clinical manifestations of endotoxic shock and death under conditions wherein fluni
87 e found increased production of IL-12 during endotoxic shock and enhanced Th1 cells in TTP knockout m
88 AP12-deficient mice were more susceptible to endotoxic shock and had enhanced resistance to infection
89 icient mice exhibit diminished recovery from endotoxic shock and hyperresponsiveness of a subset of e
90 out (SR-A(-/-)) mice are more susceptible to endotoxic shock and Listeria monocytogenes infection in
91 vents regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal
92 ransfer experiments showed that responses to endotoxic shock and polymicrobial sepsis were transferab
93 -fold higher concentrations of IL-27(p28) in endotoxic shock and polymicrobial sepsis.
94 t from other inflammatory disorders, such as endotoxic shock and rheumatoid arthritis.
95 )-deficient mice display reduced survival to endotoxic shock and sepsis.
96 hypersensitive to lipopolysaccharide-induced endotoxic shock and showed prolonged inflammation in a m
97 cated in serious autoimmune diseases such as endotoxic shock and thus are important therapeutic targe
98 tion may be protective in some patients with endotoxic shock and with diseases characterized by chron
99 how that c-peptide has beneficial effects in endotoxic shock, and this therapeutic effect is associat
100 onclusion, hypometabolism and hypothermia in endotoxic shock are not consequential to hypoxia but ser
101 pendent cytokine responses and the resultant endotoxic shock are not coupled to SRA-mediated clearanc
102                        Patients in septic or endotoxic shock are sensitive to most anesthetic regimen
103                                 Mortality by endotoxic shock as a function of circadian time is indep
104 fective in that they are highly resistant to endotoxic shock as compared with normal responder mice.
105 nces susceptibility and worsens outcome from endotoxic shock by augmenting sympathetic activity, part
106 cterial and lipopolysaccharide (LPS)-induced endotoxic shock by blocking the non-canonical inflammaso
107  experiments in a mouse model of LPS-induced endotoxic shock confirmed the proinflammatory potential
108 ve apoptosis of leukocytes during sepsis and endotoxic shock constitutes an important mechanism linke
109 ammation using three models of inflammation: endotoxic shock, diabetes, and contact hypersensitivity.
110 liest drops in cardiac output and DO2 during endotoxic shock did not precede the reduction in VO2 tha
111  action of exogenous low-dose vasopressin in endotoxic shock does not impair blood flow to any of the
112 trite and rings taken from rats subjected to endotoxic shock exhibited reduced endothelium-dependent
113 orrhaged mice were susceptible to sepsis and endotoxic shock from the leaky gut.
114     However, 85% of individuals that develop endotoxic shock from V. vulnificus are males.
115      During lipopolysaccharide (LPS)-induced endotoxic shock, HLJ1 knockout mice shows reduced organ
116 ve cells play an important role in mediating endotoxic shock; (ii) tamLITAF(i)-/- mice show a similar
117 function in the first 4 h after induction of endotoxic shock in anesthetized canine preparations (n =
118 temic inflammation, organ damage, and lethal endotoxic shock in beta2-knockout mice.
119                     Death due to LPS-induced endotoxic shock in merkd mice was blocked by administrat
120 roptosis, which is critical for induction of endotoxic shock in mice.
121 study examines the effect of parthenolide in endotoxic shock in rodents.
122  and in vivo and increased susceptibility to endotoxic shock in SRA-deficient mice.
123 eficient in MKP-1 were highly susceptible to endotoxic shock in vivo, associated with enhanced produc
124  Perforin-2 (P2) is critical for LPS-induced endotoxic shock in wild-type mice.
125 ion of the cytokines IL-17A and IL-23 during endotoxic shock in young adult male C57BL/6J mice and ha
126 UF1 knockout mice display symptoms of severe endotoxic shock, including vascular hemorrhage, intravas
127 ut of Mkp-1 substantially sensitizes mice to endotoxic shock induced by lipopolysaccharide (LPS) chal
128 t mice, casp-11 mutant mice are resistant to endotoxic shock induced by lipopolysaccharide.
129 lling diseases such as rheumatoid arthritis, endotoxic shock, inflammatory bowel disease, osteoporosi
130                                              Endotoxic shock is a life-threatening condition caused b
131                                              Endotoxic shock is a life-threatening consequence of sev
132                                        Acute endotoxic shock is accompanied by an increase in the pro
133 velopment of hypothermia instead of fever in endotoxic shock is consequential to hypoxia.
134                       One form of sepsis, or endotoxic shock, is a hyperactivated systemic response c
135 aken to determine if V antigen could prevent endotoxic shock, known to be mediated by excessive produ
136  to induce disease and death in humans in an endotoxic shock-like manner.
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 creased survival rates of mutants faced with endotoxic shock may indicate a contribution of grancalci
141 ervention with conventional laparotomy in an endotoxic shock model in the pig.
142                                        In an endotoxic shock model, HNRNPA2B1-deficient mice exhibit
143 ation, can be recapitulated in mice using an endotoxic shock model.
144 ole in various inflammatory diseases such as endotoxic shock, multiple sclerosis, cerebral malaria, a
145      Foremost, both models result in DIC and endotoxic shock, neither of which is likely to respond t
146                                           In endotoxic shock of C57BL/6J mice, pharmacologic activati
147 ucocorticoid-dependent host defense after an endotoxic shock or bacterial infection.
148  that U90926 expression is protective during endotoxic shock, potentially mediated by the paracrine a
149                Using a novel rabbit model of endotoxic shock produced by multiple exposures to endoto
150          Gram-negative sepsis and subsequent endotoxic shock remain major health problems in the Unit
151                     In vehicle-treated mice, endotoxic shock resulted in lung injury and was associat
152    The present studies provide evidence that endotoxic shock results from disseminated endothelial ap
153                          An in vivo model of endotoxic shock revealed that, in comparison with wild t
154 acterial challenges, possibly at the cost of endotoxic shock risk.
155 X) was not sufficient to reverse LPS-induced endotoxic shock susceptibility or restore IL-10 release.
156                                          The endotoxic shock syndrome is characterized by systemic in
157 esistant to lipopolysaccharide (LPS)-induced endotoxic shock than control wild-type mice.
158 ice, which are more resistant to LPS-induced endotoxic shock than wild-type animals.
159  edema, leukocyte infiltration, and signs of endotoxic shock that correlated with higher levels of TN
160  we have developed a model for V. vulnificus endotoxic shock that mimics the sexually dimorphic respo
161 ry cytokines and exhibit hypersensitivity to endotoxic shock; these effects are mitigated when the an
162 -33 protects animals from lipopolysaccharide endotoxic shock through attenuated neutrophil extravasat
163 arthenolide exerts beneficial effects during endotoxic shock through inhibition of NF-kappaB.
164 iologic protective factor against the lethal endotoxic shock triggered by an acute inflammatory respo
165       Survival of lipopolysaccharide-induced endotoxic shock was improved in Tph1(-/-) mice.
166                                              Endotoxic shock was induced by administration of Escheri
167                                              Endotoxic shock was induced by bacterial lipopolysacchar
168                                              Endotoxic shock was induced in male B6/129F2/J mice by a
169                        Sensitivity to lethal endotoxic shock was not significantly altered in Bf-defi
170         A clinical picture characteristic of endotoxic shock was observed in most animals as a termin
171 y responses and it blocks the hypotension of endotoxic shock, we determined whether TGF-beta1 could b
172 2cre)) resulted in resistance to LPS-induced endotoxic shock, whereas Socs2(-/-) mice were highly sus
173 in the potentially lethal condition known as endotoxic shock, whereby uncontrolled inflammation can l
174  in IL-1beta showed unaltered sensitivity to endotoxic shock, with or without pretreatment with D-gal
175 e induced by SIVsmmPBj4 clinically resembles endotoxic shock, with the development of severe gastroin

 
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