ライフサイエンスコーパス: multiple organ failure

1 pre-existing injury, potentially leading to multiple organ failure).

2 hallenge in a baboon model of sepsis-induced multiple organ failure.

3 ntribute to the development of shock-induced multiple organ failure.

4 Most deaths occurred early after multiple organ failure.

5 rculation to distant organs, where it causes multiple organ failure.

6 e coexisting conditions including sepsis and multiple organ failure.

7 independent predictor of excess mortality in multiple organ failure.

8 ntrinsically involved in the pathogenesis of multiple organ failure.

9 systemic inflammatory response syndrome and multiple organ failure.

10 ibutes to the pathological manifestations of multiple organ failure.

11 in response to inflammation, infection, and multiple organ failure.

12 a may affect the severity and progression of multiple organ failure.

13 barrier, predisposing patients to sepsis and multiple organ failure.

14 lay an important role in the pathogenesis of multiple organ failure.

15 ose and (except one) died within 58 hrs with multiple organ failure.

16 appaB activation, in experimental sepsis and multiple organ failure.

17 ve state serve to trigger the development of multiple organ failure.

18 tion and appropriate treatment of sepsis and multiple organ failure.

19 ailure, and possibly a delayed recovery from multiple organ failure.

20 pal mediator of sepsis, often with resulting multiple organ failure.

21 NE in inflammatory disorders such as ALI and multiple organ failure.

22 ths from exsanguination and late deaths from multiple organ failure.

23 s to acute respiratory distress syndrome and multiple organ failure.

24 cell activation and inflammation, as well as multiple organ failure.

25 on the role of the gut in the generation of multiple organ failure.

26 inant meningococcemia, refractory shock, and multiple organ failure.

27 ents considered to be at risk for developing multiple organ failure.

28 ic ischemia, and the patient rapidly died of multiple organ failure.

29 se in tissue injury, a presumed harbinger of multiple organ failure.

30 ng parenchymal lymphocytic infiltration with multiple organ failure.

31 nduces hyperinflammation, ultimately causing multiple organ failure.

32 er OHCA, cyclosporine does not prevent early multiple organ failure.

33 rfusion, systemic inflammatory response, and multiple organ failure.

34 of systemic inflammatory response underlying multiple organ failure.

35 rfusion, systemic inflammatory response, and multiple organ failure.

36 pital mortality, venous thromboembolism, and multiple organ failure.

37 sponse to infection that often culminates in multiple organ failure.

38 iver abscess, (7) endophthalmitis, , and (8) multiple organ failure.

39 the pathogenesis of critical illness-induced multiple organ failure.

40 ents with acute-on-chronic liver failure and multiple organ failure.

41 severe trauma, which predisposes patients to multiple organ failure.

42 a role in the pathophysiology of sepsis and multiple organ failure.

43 vidence of a "second-hit"-induced late-onset multiple organ failure.

44 ratory failure that is often associated with multiple organ failure.

45 intravascular coagulation, septic shock, and multiple organ failure.

46 mild to severe and possibly lead to death by multiple organ failure.

47 econdary conditions such as septic shock and multiple-organ failure.

48 oscopic necrosectomy did not cause new-onset multiple organ failure (0% vs 50%, RD, 0.50; 95% CI, 0.1

49 te of deaths from exsanguination (9% to 1%), multiple organ failure (12% to 1%), and death within 24

50 atio, 0.15; 95% CI, 0.03-0.60) and new-onset multiple-organ failure (15.6% vs 39.1%; P = .008; risk r

51 Multiple organ failure (16.1%) and sepsis (9.6%) were th

52 f death in both trial groups were sepsis and multiple organ failure (31 [10%] vs 30 [10%]), and the m

53 rsus-host disease, and the patient died from multiple organ failure 4 months after transplantation.

54 ent; p = 0.004), especially in patients with multiple organ failure (acute-on-chronic liver failure g

55 h increased risk of cardiovascular death and multiple-organ failure (adjusted hazard ratio, 2.07 [1.3

56 c hypotension, in order to prevent "delayed" multiple organ failure after hemostasis and all-out resu

57 nce and pattern of systemic inflammation and multiple organ failure after major trauma.

58 icantly smaller risk of lung dysfunction and multiple organ failure among the group receiving antipla

59 re following liver transplantation will have multiple organ failure and a high rate of mortality unle

60 leukocytes and has been associated with the multiple organ failure and adult respiratory distress sy

61 Between causes of death, multiple organ failure and brain death affected respecti

62 as a consequence of the rapid development of multiple organ failure and cerebral edema.

63 ciated with severe disease pathology such as multiple organ failure and cerebral malaria.

64 hereby uncontrolled inflammation can lead to multiple organ failure and death of the infected host.

65 complement cascades that could contribute to multiple organ failure and death.

66 re to develop sepsis, which may culminate in multiple organ failure and death.

67 atients, this inflammatory response leads to multiple organ failure and death.

68 bolism that delays recovery or even leads to multiple organ failure and death.

69 nd chemokine interactions, which might limit multiple organ failure and decrease mortality in hemorrh

70 sociated with a significantly higher risk of multiple organ failure and fewer ventilator-free days.

71 % of those with a score of > or =2 developed multiple organ failure and half of them died from sepsis

72 ory response to bacterial infection, causing multiple organ failure and high mortality.

73 e phase with IGF-1/BP-3 response may prevent multiple organ failure and improve clinical outcomes aft

74 omen, with increased age, in the presence of multiple organ failure and in patients with intra-abdomi

75 bundles has fortunately led to a decline in multiple organ failure and in-hospital mortality.

76 formation, and hypotension that can lead to multiple organ failure and lethal shock, as well as desq

77 ns may be associated with a decrease in late multiple organ failure and morbidity.

78 gulopathy and later propensity to infection, multiple organ failure and mortality are associated with

79 Multiple organ failure and mortality rates were 34.8% an

80 is associated with poor outcomes, including multiple organ failure and mortality.

81 endent protective effect of female gender on multiple organ failure and nosocomial infection rates re

82 associated with a 43% and 23% lower risk of multiple organ failure and nosocomial infection, respect

83 he highest TNF-alpha concentration developed multiple organ failure and required continuous venovenou

84 One recipient died of multiple organ failure and sepsis.

85 kidney injury often occurs in the context of multiple organ failure and sepsis.

86 tion from which numerous patients die due to multiple organ failure and septic shock.

87 eralized inflammatory state that can lead to multiple organ failure and shock.

88 candidemic septic shock sustained persistent multiple organ failure and showed delayed recovery from

89 major secondary causative agents of delayed multiple organ failure and subsequent death after OPW ex

90 comial infection did not increase subsequent multiple organ failure and there was no evidence of a "s

91 dict those individuals at increased risk for multiple-organ failure and death and therefore assist in

92 all, 63% developed lung dysfunction, 19% had multiple organ failure, and 21% died.

93 natomical severity of injury, development of multiple organ failure, and 30-day survival were determi

94 in rats and was associated with hypotension, multiple organ failure, and 50% mortality.

95 as well as more frequent infections, sepsis, multiple organ failure, and death (p < 0.05).

96 condition that can manifest as septic shock, multiple organ failure, and death.

97 knockout mice develop severe hypotension and multiple organ failure, and exhibit a remarkable increas

98 d metabolic responses, prevalence of sepsis, multiple organ failure, and mortality than burn patients

99 Overall mortality, multiple organ failure, and nosocomial infection rates f

100 evaluate the effects of gender on mortality, multiple organ failure, and nosocomial infection, after

101 cations, but mostly due to the occurrence of multiple organ failure, and occurred after a median time

102 tality rate, a high likelihood of associated multiple organ failure, and possibly a delayed recovery

103 d with a decreased risk of lung dysfunction, multiple organ failure, and possibly mortality in high-r

104 ection characterized by marked coagulopathy, multiple organ failure, and rapid tissue destruction and

105 results in a systemic inflammatory response, multiple-organ failure, and death.

106 rimarily driven by cardiovascular causes and multiple-organ failure, and may thus identify a vulnerab

107 ation support was withdrawn in 70 (70%) with multiple organ failure as the indication in 58 (83%) pat

108 play an important role in the development of multiple organ failure associated with severe sepsis.

109 age II group, 9 died (8% of all deaths) from multiple organ failure associated with their underlying

110 nts with candidemia and septic shock were in multiple organ failure at days 3, 7, and 14; patients wi

111 ilure of three of more organs and sequential multiple organ failure but not mortality.

112 Ebola virus disease complicated by multiple organ failure can be survivable with the applic

113 arenchymal cell apoptosis is contributing to multiple organ failure cannot be determined from the pre

114 d acute liver failure patients compared with multiple organ failure, chronic liver disease, and healt

115 gan failure and showed delayed recovery from multiple organ failure compared with patients with bacte

116 ital-free days (P < 0.05), with no change in multiple organ failure deaths.

117 ia, acute respiratory distress syndrome, and multiple organ failure (Denver 2 score>3) for both child

118 by the Denver multiple organ failure score), multiple organ failure (Denver multiple organ failure sc

119 Hemorrhagic shock often progresses to multiple organ failure despite conventional resuscitatio

120 Overall, 29% of patients had multiple organ failure develop.

121 Multiple organ failure developed in 14% of the survivors

122 Multiple organ failure developed in 31% of patients with

123 ondary endpoints included the development of multiple organ failure, duration of mechanical ventilati

124 lay a fundamental role in the development of multiple organ failure during sepsis.

125 injury in rodent models of inflammation and multiple organ failure elicited by intraperitoneal injec

126 species colonization at multiple sites, and multiple organ failure, empirical treatment with micafun

127 uired sepsis, multiple Candida colonization, multiple organ failure, exposed to broad-spectrum antiba

128 Multiple organ failure following a variety of insults, i

129 olonged response, however, may contribute to multiple organ failure, hypermetabolism, complications,

130 lative protection from acute lung injury and multiple organ failure in children.

131 tion of microvascular thrombi contributes to multiple organ failure in human cases of gram-negative b

132 y innate immune cells is thought to initiate multiple organ failure in murine models of sepsis.

133 42% (11/26); causes of death were sepsis or multiple organ failure in nine and hemorrhage in two pat

134 tions are associated with the development of multiple organ failure in pediatric sepsis.

135 The incidence of multiple organ failure in pediatric trauma victims is lo

136 t they also contribute to the development of multiple organ failure in sepsis.

137 microvasculature from injury and preventing multiple organ failure in sepsis.

138 ocytes are implicated in the pathogenesis of multiple organ failure in sepsis.

139 y injured patients to sepsis and the ensuing multiple organ failure in the clinical situation.

140 e Staphylococcus haemolyticus, septic shock, multiple organ failure including acute respiratory distr

141 nt patients, complicated by septic shock and multiple organ failure, including acute renal injury and

142 Male sex, multiple organ failure, increasing percentage of pancrea

143 ogy and Chronic Health Evaluation II scores, Multiple Organ Failure index, and Glasgow Coma Score, in

144 We propose that, first, multiple organ failure induced by critical illness is pr

145 end point of major complications (new-onset multiple organ failure, intra-abdominal bleeding, entero

146 Multiple organ failure is a major threat to the survival

147 There is moderate evidence that multiple organ failure is a risk factor for delirium.

148 Multiple organ failure is associated with subsequent nos

149 Sepsis-induced multiple organ failure is the major cause of mortality a

150 ged widely, from mild respiratory disease to multiple organ failure leading to death.

151 included respiratory infection, sepsis, and multiple organ failure, length of stay and mortality; ad

152 ions that include fever and rash, as well as multiple organ failure (liver, kidney, lungs, and/or hea

153 Secondary outcomes were multiple organ failure, lung injury, and sepsis.

154 Patients with multiple organ failure may be at risk for unusual pigmen

155 er understanding of the role of adenosine in multiple organ failure may facilitate the development of

156 olic hepatitis (AH) frequently progresses to multiple organ failure (MOF) and death.

157 Postinjury multiple organ failure (MOF) may result from overwhelmin

158 Outcomes measured were mortality, multiple organ failure (MOF), venous thromboembolism, in

159 ry is the strongest independent predictor of multiple organ failure (MOF).

160 emia occur in children dying with sepsis and multiple organ failure (MOF).

161 without new onset thrombocytopenia but with multiple organ failure (MOF).

162 Outcomes of interest included multiple organ failure (MOF, Marshall MOD score > 5) and

163 ced acute liver failure (n = 13), nonhepatic multiple organ failure (n = 28), chronic liver disease (

164 ncluded postcardiac surgery (n = 58), sepsis/multiple organ failure (n = 32), respiratory disease (n

165 important to apply mechanical support before multiple organ failure occurs.

166 e system participate in the life-threatening multiple-organ failure of endotoxic shock.

167 nfidence interval (CI): 0.09-0.55; P <0.01), multiple organ failure (OR = 0.15; 95% CI: 0.04-0.62; P

168 2.167, 95% CI: 1.234-13.140, p = 0.005), and multiple organ failure (OR = 3.067, 95% CI: 1.184-15.150

169 s thromboembolism (OR, 1.73; p < 0.001), and multiple organ failure (OR, 1.38; p = 0.02).

170 Females had less multiple organ failure [OR: 1.18 (95% CI, 1.05-1.33); P

171 t receiving it (lung dysfunction p = 0.0116, multiple organ failure p = 0.0291).

172 p < 0.001), endophthalmitis (p = 0.003), and multiple organ failure (p < 0.001).

173 erative intensive care stay (P = 0.014), and multiple organ failure (P < 0.001); operation before 200

174 ng high-dose catecholamines and had signs of multiple organ failure: pH 7.16 (6.68-7.39), blood lacta

175 y for predicting subsequent mortality and/or multiple organ failure, plasma lactate >or=3.85 mmol/L w

176 nosocomial infection, whereas persistence of multiple organ failure predicted mortality.

177 arrow, heart, and liver transplants, died of multiple organ failure, probably unrelated to TMA.

178 Overall, the multiple organ failure rate was 27%.

179 Multiple organ failure remains common after severe injur

180 these critically ill patients with impending multiple organ failure requires a team approach with exp

181 tion of patients with cirrhosis manifests as multiple organ failure requiring admission to an intensi

182 deteriorate and within 3 weeks had developed multiple organ failure requiring ventilation, haemofiltr

183 ilure score), multiple organ failure (Denver multiple organ failure score >3), and mortality.

184 c Health Evaluation II score (P = 0.03), the Multiple Organ Failure score (P = 0.01), or presence of

185 red blood cells within 24 hours, and Denver multiple organ failure score at 72 hours as independent

186 MODS was defined as a Denver Multiple Organ Failure score of 4 or greater.

187 unction (defined as grades 2-3 by the Denver multiple organ failure score), multiple organ failure (D

188 005), greater organ failure severity (Denver multiple organ failure score, 3.5 +/- 2.4 vs 0.8 +/- 1.1

189 on persisted after adjustment for APACHE II, Multiple Organ Failure score, or the combined covariates

190 ultiple organ dysfunction score and with the multiple organ failure score.

191 KIM-1 increased in tandem with APACHE II and Multiple Organ Failure scores.

192 ons, acute respiratory distress syndrome, or multiple organ failure scores.

193 nd developed for severe critical illness and multiple organ failure secondary to Ebola virus infectio

194 cascade of complications of septic shock and multiple organ failure seen in Gram-negative bacterial i

195 Males are more susceptible to multiple organ failure, sepsis, and mortality after trau

196 ent modalities, length of stay, and outcome (multiple organ failure, sepsis, mortality rates) were as

197 hondrial damage is an important component of multiple organ failure syndrome, a highly lethal complic

198 gut ischemia leading to the exacerbation of multiple organ failure syndrome.

199 Thrombocytopenia-associated multiple organ failure (TAMOF) is a poorly understood sy

200 septic shock and thrombocytopenia-associated multiple organ failure (TAMOF), and in those without new

201 nces, cause cell and tissue damage and hence multiple organ failure, the clinical hallmark of sepsis.

202 n of mitochondrial biogenesis as a potential multiple organ failure therapy.

203 erapies to sustain patients with diverse and multiple organ failures, thus providing patients with a

204 apoptosis of neutrophils is associated with multiple organ failure under those conditions.

205 cluding acute respiratory distress syndrome, multiple organ failure, venous thromboembolism, sepsis,

206 (30-day and 90-day mortality, development of multiple organ failure, ventilator-free days, renal fail

207 Multiple organ failure was a frequent cause of death dur

208 n size for mortality, sepsis, infection, and multiple organ failure was approximately 60% total body

209 Development of multiple organ failure was early (median time, 2 days),

210 Multiple organ failure was significantly less likely to

211 characteristics, 28-day mortality rates, and multiple organ failure were compared for the two cohorts

212 decreased incidence and different pattern of multiple organ failure when compared with adults.

213 Patients with multiple organ failure who have undergone hepatectomy re

214 g with Candida infections, two patients with multiple organ failure who received high-dose fluconazol

215 as having capillary leak syndrome (n = 24), multiple organ failure with death from sepsis (n = 37),

216 One study observed an increase in multiple organ failure with higher ratios, whereas no st

217 zed endothelial dysfunction, contributing to multiple organ failure with increased morbidity and mort

218 failure with death from sepsis (n = 37), or multiple organ failure with recovery (n = 57) or as well

219 icant tissue damage and frequently result in multiple organ failure, with >70% mortality.