ライフサイエンスコーパス: endotoxic shock

1 phrine at 18 hours after induction of murine endotoxic shock.

2 cytokine production within the heart during endotoxic shock.

3 nst V. vulnificus lipopolysaccharide-induced endotoxic shock.

4 ally dimorphic response to Vibrio vulnificus endotoxic shock.

5 ar tone and increases in oxidative stress is endotoxic shock.

6 educed the lethality associated with ensuing endotoxic shock.

7 could protect endotoxin-sensitive mice from endotoxic shock.

8 umption (VO2) in the presence and absence of endotoxic shock.

9 gulating TNF-alpha secretion and attenuating endotoxic shock.

10 ute to the beneficial effect of TGF-beta1 on endotoxic shock.

11 onsible for the overall host response during endotoxic shock.

12 an enhanced susceptibility to pathogens and endotoxic shock.

13 contributes to the hemodynamic compromise of endotoxic shock.

14 tes to the reduction in vascular tone during endotoxic shock.

15 ing protection in this experimental model of endotoxic shock.

16 y relevant model of gram-negative sepsis and endotoxic shock.

17 o block the organ damage or lethal effect of endotoxic shock.

18 be involved in the hemodynamic compromise of endotoxic shock.

19 nt for the acidotic mucosal tonometric pH in endotoxic shock.

20 by the fall in oxygen delivery (DO2) during endotoxic shock.

21 rats and improved survival in lethal murine endotoxic shock.

22 vels of PAF are observed in animal models of endotoxic shock.

23 ascular energetic and contractile failure in endotoxic shock.

24 ng in the microcirculation during septic and endotoxic shock.

25 macrophages were sufficient to induce lethal endotoxic shock.

26 oration of alpha1-adrenoceptor expression in endotoxic shock.

27 nd is protective in an experimental model of endotoxic shock.

28 uch higher levels of IL-17A and IL-23 during endotoxic shock.

29 oving survival in an in vivo murine model of endotoxic shock.

30 echolamine-producing adrenal glands prior to endotoxic shock.

31 leads to greater sensitivity to LPS-induced endotoxic shock.

32 cytokines, but only partial protection from endotoxic shock.

33 o partial recovery of CCL5 production during endotoxic shock.

34 ent of AC7 are hypersensitive to LPS-induced endotoxic shock.

35 d showed reduced CCL5 levels in serum during endotoxic shock.

36 cking caspase 1 are resistant to LPS-induced endotoxic shock.

37 ible to LPS-induced splenocyte apoptosis and endotoxic shock.

38 agocytosis of bacteria and susceptibility to endotoxic shock.

39 m-derived molecules, are more susceptible to endotoxic shock.

40 immune response to an infectious disease or endotoxic shock.

41 ATF3-deficient mice are more susceptible to endotoxic shock.

42 ng a murine model of D-galactosamine-induced endotoxic shock.

43 ord complete protection in a murine model of endotoxic shock.

44 l mice are hypersensitive to the LPS-induced endotoxic shock.

45 mal antiinflammatory response to LPS-induced endotoxic shock.

46 e are markedly hypersensitive to LPS-induced endotoxic shock.

47 back element for cardiovascular tolerance in endotoxic shock.

48 ve immune response to LPS and development of endotoxic shock.

49 e cardiovascular dysfunction associated with endotoxic shock.

50 n macrophages, a major cell type involved in endotoxic shock.

51 ta protect AUF1 knockout mice against lethal endotoxic shock.

52 cytokines that facilitate the development of endotoxic shock.

53 production, and increased susceptibility to endotoxic shock.

54 sive ODN might be of use in the treatment of endotoxic shock.

55 e life-threatening multiple-organ failure of endotoxic shock.

56 uppressive ODN protect mice from LPS-induced endotoxic shock.

57 tic shock, were intravenously infused during endotoxic shock.

58 ted in a model of lipopolysaccharide-induced endotoxic shock.

59 ful in treating organ injury associated with endotoxic shock.

60 hages, and this function protected mice from endotoxic shock.

61 st from cytokine-induced immunopathology and endotoxic shock.

62 ity reaction and increased susceptibility to endotoxic shock.

63 were resistant to lipopolysaccharide-induced endotoxic shock.

64 ection from lipopolysaccharide (LPS)-induced endotoxic shock.

65 t hypotension that develops in Gram-negative endotoxic shock.

66 and is also essential in protection against endotoxic shock.

67 sistant to the lethal effects of LPS-induced endotoxic shock.

68 mulation by microbial components may lead to endotoxic shock.

69 re susceptible to lipopolysaccharide-induced endotoxic shock.

70 ndering them more susceptible to LPS-induced endotoxic shock.

71 Upon LPS challenge, merkd animals died of endotoxic shock (15/17, 88.2%), whereas control wild-typ

72 gy reminiscent of lipopolysaccharide-induced endotoxic shock, a type of systemic inflammatory respons

73 e conditions, norepinephrine infusion during endotoxic shock actually increases renal blood flow and

74 owever, these mice are highly susceptible to endotoxic shock and appear to be compromised in their ab

75 umatic brain injury, diabetes, Parkinsonism, endotoxic shock and arthritis, implicating PARP in the p

76 orming CM-LPS complexes, and protect against endotoxic shock and death in rodent models of gram-negat

77 ve in controlling clinical manifestations of endotoxic shock and death under conditions wherein fluni

78 e found increased production of IL-12 during endotoxic shock and enhanced Th1 cells in TTP knockout m

79 AP12-deficient mice were more susceptible to endotoxic shock and had enhanced resistance to infection

80 icient mice exhibit diminished recovery from endotoxic shock and hyperresponsiveness of a subset of e

81 out (SR-A(-/-)) mice are more susceptible to endotoxic shock and Listeria monocytogenes infection in

82 vents regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal

83 ransfer experiments showed that responses to endotoxic shock and polymicrobial sepsis were transferab

84 -fold higher concentrations of IL-27(p28) in endotoxic shock and polymicrobial sepsis.

85 t from other inflammatory disorders, such as endotoxic shock and rheumatoid arthritis.

86 )-deficient mice display reduced survival to endotoxic shock and sepsis.

87 hypersensitive to lipopolysaccharide-induced endotoxic shock and showed prolonged inflammation in a m

88 cated in serious autoimmune diseases such as endotoxic shock and thus are important therapeutic targe

89 tion may be protective in some patients with endotoxic shock and with diseases characterized by chron

90 how that c-peptide has beneficial effects in endotoxic shock, and this therapeutic effect is associat

91 onclusion, hypometabolism and hypothermia in endotoxic shock are not consequential to hypoxia but ser

92 pendent cytokine responses and the resultant endotoxic shock are not coupled to SRA-mediated clearanc

93 Patients in septic or endotoxic shock are sensitive to most anesthetic regimen

94 fective in that they are highly resistant to endotoxic shock as compared with normal responder mice.

95 nces susceptibility and worsens outcome from endotoxic shock by augmenting sympathetic activity, part

96 experiments in a mouse model of LPS-induced endotoxic shock confirmed the proinflammatory potential

97 ve apoptosis of leukocytes during sepsis and endotoxic shock constitutes an important mechanism linke

98 ammation using three models of inflammation: endotoxic shock, diabetes, and contact hypersensitivity.

99 liest drops in cardiac output and DO2 during endotoxic shock did not precede the reduction in VO2 tha

100 action of exogenous low-dose vasopressin in endotoxic shock does not impair blood flow to any of the

101 trite and rings taken from rats subjected to endotoxic shock exhibited reduced endothelium-dependent

102 orrhaged mice were susceptible to sepsis and endotoxic shock from the leaky gut.

103 However, 85% of individuals that develop endotoxic shock from V. vulnificus are males.

104 ve cells play an important role in mediating endotoxic shock; (ii) tamLITAF(i)-/- mice show a similar

105 function in the first 4 h after induction of endotoxic shock in anesthetized canine preparations (n =

106 temic inflammation, organ damage, and lethal endotoxic shock in beta2-knockout mice.

107 Death due to LPS-induced endotoxic shock in merkd mice was blocked by administrat

108 roptosis, which is critical for induction of endotoxic shock in mice.

109 study examines the effect of parthenolide in endotoxic shock in rodents.

110 and in vivo and increased susceptibility to endotoxic shock in SRA-deficient mice.

111 eficient in MKP-1 were highly susceptible to endotoxic shock in vivo, associated with enhanced produc

112 ion of the cytokines IL-17A and IL-23 during endotoxic shock in young adult male C57BL/6J mice and ha

113 UF1 knockout mice display symptoms of severe endotoxic shock, including vascular hemorrhage, intravas

114 ut of Mkp-1 substantially sensitizes mice to endotoxic shock induced by lipopolysaccharide (LPS) chal

115 t mice, casp-11 mutant mice are resistant to endotoxic shock induced by lipopolysaccharide.

116 lling diseases such as rheumatoid arthritis, endotoxic shock, inflammatory bowel disease, osteoporosi

117 Endotoxic shock is a life-threatening condition caused b

118 Endotoxic shock is a life-threatening consequence of sev

119 Acute endotoxic shock is accompanied by an increase in the pro

120 velopment of hypothermia instead of fever in endotoxic shock is consequential to hypoxia.

121 One form of sepsis, or endotoxic shock, is a hyperactivated systemic response c

122 aken to determine if V antigen could prevent endotoxic shock, known to be mediated by excessive produ

123 to induce disease and death in humans in an endotoxic shock-like manner.

124 the antiinflammatory response to LPS-induced endotoxic shock, likely through its essential role in fa

125 In a rat model of endotoxic shock, lipopolysaccharide-induced HO-1 mRNA an

126 In a model of endotoxic shock, LPS (35 microg/mouse, i.p.) suppressed

127 creased survival rates of mutants faced with endotoxic shock may indicate a contribution of grancalci

128 ervention with conventional laparotomy in an endotoxic shock model in the pig.

129 ation, can be recapitulated in mice using an endotoxic shock model.

130 ole in various inflammatory diseases such as endotoxic shock, multiple sclerosis, cerebral malaria, a

131 Foremost, both models result in DIC and endotoxic shock, neither of which is likely to respond t

132 In endotoxic shock of C57BL/6J mice, pharmacologic activati

133 ucocorticoid-dependent host defense after an endotoxic shock or bacterial infection.

134 Using a novel rabbit model of endotoxic shock produced by multiple exposures to endoto

135 Gram-negative sepsis and subsequent endotoxic shock remain major health problems in the Unit

136 In vehicle-treated mice, endotoxic shock resulted in lung injury and was associat

137 The present studies provide evidence that endotoxic shock results from disseminated endothelial ap

138 acterial challenges, possibly at the cost of endotoxic shock risk.

139 The endotoxic shock syndrome is characterized by systemic in

140 esistant to lipopolysaccharide (LPS)-induced endotoxic shock than control wild-type mice.

141 ice, which are more resistant to LPS-induced endotoxic shock than wild-type animals.

142 edema, leukocyte infiltration, and signs of endotoxic shock that correlated with higher levels of TN

143 we have developed a model for V. vulnificus endotoxic shock that mimics the sexually dimorphic respo

144 ry cytokines and exhibit hypersensitivity to endotoxic shock; these effects are mitigated when the an

145 arthenolide exerts beneficial effects during endotoxic shock through inhibition of NF-kappaB.

146 iologic protective factor against the lethal endotoxic shock triggered by an acute inflammatory respo

147 Survival of lipopolysaccharide-induced endotoxic shock was improved in Tph1(-/-) mice.

148 Endotoxic shock was induced by administration of Escheri

149 Endotoxic shock was induced by bacterial lipopolysacchar

150 Endotoxic shock was induced in male B6/129F2/J mice by a

151 Sensitivity to lethal endotoxic shock was not significantly altered in Bf-defi

152 A clinical picture characteristic of endotoxic shock was observed in most animals as a termin

153 y responses and it blocks the hypotension of endotoxic shock, we determined whether TGF-beta1 could b

154 2cre)) resulted in resistance to LPS-induced endotoxic shock, whereas Socs2(-/-) mice were highly sus

155 in the potentially lethal condition known as endotoxic shock, whereby uncontrolled inflammation can l

156 in IL-1beta showed unaltered sensitivity to endotoxic shock, with or without pretreatment with D-gal

157 e induced by SIVsmmPBj4 clinically resembles endotoxic shock, with the development of severe gastroin