ライフサイエンスコーパス: liver dysfunction

1 , debilitating fibroses, and obesity-related liver dysfunction.

2 s on both the cancer stage and the extent of liver dysfunction.

3 e aminotransferase levels were suggestive of liver dysfunction.

4 cy; 50% of patients with this condition have liver dysfunction.

5 abnormal glucose metabolism, and progressive liver dysfunction.

6 ous, including gastric dilatation and severe liver dysfunction.

7 ess than 25% appears to reduce postoperative liver dysfunction.

8 (HIV) infection is commonly associated with liver dysfunction.

9 i-HCV and HCV RNA and serially evaluated for liver dysfunction.

10 s and tetralogy of Fallot) in the absence of liver dysfunction.

11 titis C virus-positive organs, and degree of liver dysfunction.

12 edicting increases in biochemical indexes of liver dysfunction.

13 recurrent line infections, and intermittent liver dysfunction.

14 r a median of 6 days because of renal and/or liver dysfunction.

15 elevations if there was no other evidence of liver dysfunction.

16 ion is warranted when treating patients with liver dysfunction.

17 ality and major CVD, as well as myopathy and liver dysfunction.

18 lung recipients with an equivalent degree of liver dysfunction.

19 ochondrial disorder that includes diagnostic liver dysfunction.

20 clearance contributes to cardiovascular and liver dysfunction.

21 by a neurodevelopmental disorder (NDD) with liver dysfunction.

22 proteins, which corresponded with its severe liver dysfunction.

23 rapeutic strategies targeting age-associated liver dysfunction.

24 ity, concomitant metabolic abnormalities and liver dysfunction.

25 in aggregates within hepatocytes, leading to liver dysfunction.

26 immunotherapy in HCC patients with relevant liver dysfunction.

27 a phenotype of NDD, dysmorphic features, and liver dysfunction.

28 d by lipotoxicity, fibrosis, and progressive liver dysfunction.

29 esults in the setting of volume overload and liver dysfunction.

30 ditions of cardiac arrest, cancer, renal and liver dysfunction.

31 ules) were not associated with postoperative liver dysfunction.

32 n1-deficient mice with age, and mice develop liver dysfunction.

33 signs of cholestatic jaundice, pruritis, or liver dysfunction.

34 al effect of BAs on testis physiology during liver dysfunction.

35 sistance and obesity, as well as progressive liver dysfunction.

36 s as a novel cause of permanent diabetes and liver dysfunction.

37 to evaluate its' potential relationship with liver dysfunction.

38 Endstage Liver Disease (MELD) as a gauge of liver dysfunction.

39 with increased cell death, and commensurate liver dysfunction.

40 ion, renal insufficiency, iron overload, and liver dysfunction.

41 otal parenteral nutrition and others develop liver dysfunction.

42 d is thought to contribute to age-associated liver dysfunction.

43 on, whereas abnormalities involving hepatic (liver dysfunction, 13.0% [95% CI, 10.8%-15.3%]), skeleta

44 n rash (38%), peripheral eosinophilia (38%), liver dysfunction (15%), and proteinuria (22%).

45 rence 15 (95% confidence interval 1 to 29)), liver dysfunction (21 trials, odds ratio 1.33 (1.12 to 1

46 Anemia (107 [47.3%]), history of liver dysfunction (62 [27.4%]), and gallstones (53 [23.5

47 Assessment of liver dysfunction according to the MELD scoring system p

48 Reperfusion injury can cause liver dysfunction after cold storage and warm ischemia.

49 Rather, liver dysfunction after eHx results from a transient, p2

50 evels of thrombospondin 1 (TSP-1), predicted liver dysfunction after resection.

51 erval: 1.126-2.89; P =0.01), and of enhanced liver dysfunction after stage 2 (odds ratio=1.93; 95% co

52 uency of rejection, and the reversibility of liver dysfunction after transplant.

53 c infections, diabetic lesions and causes of liver dysfunction after transplantation, among other top

54 We propose that these changes reflect liver dysfunction and also that they can be used to disc

55 In the ACLF model, the severity of liver dysfunction and brain edema was attenuated by recA

56 at often leads to cirrhosis and consequently liver dysfunction and death.

57 Seven patients died with persistent liver dysfunction and either multiorgan failure or sepsi

58 o include Fah die perinatally as a result of liver dysfunction and exhibit a complex syndrome charact

59 perfusion injury (IRI), which often leads to liver dysfunction and failure.

60 lation and platelet activation contribute to liver dysfunction and fibrosis, but mechanisms initiatin

61 and were associated with the development of liver dysfunction and focal radiation-induced liver dise

62 Ongoing monitoring for liver dysfunction and hematologic toxicity is critical t

63 nt worldwide and has become a major cause of liver dysfunction and hepatocellular carcinoma.

64 Severe, reversible neonatal liver dysfunction and hypoglycemia were seen in >40% of

65 at age 4 mo with recurrent episodes of acute liver dysfunction and hypoglycemia, with otherwise minor

66 idimensional construct that is distinct from liver dysfunction and incorporates endurance, strength,

67 t confounder of sIL-2R levels independent of liver dysfunction and inflammation.

68 bserved in two affected individuals included liver dysfunction and microcytic anemia, while one had f

69 lasma fibrinogen levels were associated with liver dysfunction and mortality in patients undergoing l

70 d cosmetics, can cause health issues such as liver dysfunction and nausea when consumed excessively.

71 ter accounting for factors such as degree of liver dysfunction and patient performance status.

72 ed during the first 48 h with development of liver dysfunction and pulmonary dysfunction (falling art

73 creased hepatic degeneration associated with liver dysfunction and reduced ability to proliferate.

74 rtality rates in patients with primary acute liver dysfunction and secondary acute liver dysfunction

75 phenotype (n = 2667; 13%), patients had more liver dysfunction and septic shock.

76 icated in patients with significant renal or liver dysfunction and should be temporarily discontinued

77 opsy is necessary to exclude viral causes of liver dysfunction and to confirm characteristic abnormal

78 Patients with liver dysfunction and/or symptomatic disease are eligibl

79 of the reduction of SIRT1 in age-associated liver dysfunctions and provide a potential tool for the

80 d the occurrence of kidney, lung, heart, and liver dysfunctions and the severity of the inflammatory

81 d hepatic fibrosis (a pathological marker of liver dysfunction) and that postnatal supplementation wi

82 BALB/c mice also developed lymphadenopathy, liver dysfunction, and decreased NK cell numbers.

83 nsistent with early indications of diabetes, liver dysfunction, and disruption of gut microbiome home

84 tatus influenced the incidence of rejection, liver dysfunction, and graft survival in HCV+ recipients

85 nal donors, degree of recipient preoperative liver dysfunction, and longer survival after LT.

86 ociation Classes III and IV at presentation, liver dysfunction, and previous myocardial infarction.

87 One month later, the patient experienced liver dysfunction, and pulmonary opacity was observed on

88 involving hypomyelination and microcephaly, liver dysfunction, and recurrent autoinflammation.

89 care unit (ICU) and hospital stay, prolonged liver dysfunction, and septic complications.

90 s severe acute kidney injury and cholestatic liver dysfunction appeared less prevalent with tight glu

91 Iron-loading, viral infection and liver dysfunction are determined to be the major regulat

92 ous symptoms of DM1, lipid abnormalities and liver dysfunction are frequent but remain understudied.

93 Liver dysfunctions are classified into acute and chronic

94 soybean oil, it resulted in hepatomegaly and liver dysfunction as did olive oil, which has a similar

95 versions, which are established measures of liver dysfunction, as a tool to assess heart transplanta

96 Trif/IRF-3 pathway is a target to ameliorate liver dysfunction associated with chronic EtOH.

97 HCC in the setting of NASH have less severe liver dysfunction at HCC diagnosis and better OS after c

98 was to determine differences in severity of liver dysfunction at HCC diagnosis and long-term surviva

99 ic changes were not a consequence of general liver dysfunction because acute SLC25A47 depletion in ad

100 identified for the effect of atorvastatin on liver dysfunction, but the dose-response relationships f

101 However, liver resection in the setting of liver dysfunction caused by biliary obstruction can be a

102 We hypothesize that liver dysfunction caused by Plasmodium infection is resp

103 (runts) exhibits a pronounced male prevalent liver dysfunction characterized by downregulated amino a

104 the presence of infection, and the degree of liver dysfunction (Child-Turcotte-Pugh or Model for End-

105 Cholestatic liver dysfunction (CLD) and biliary sludge often occur d

106 clinical manifestations include cytopenias, liver dysfunction, coagulopathy resembling disseminated

107 ir glycosylation and lead to stunted growth, liver dysfunction, coagulopathy, hypoglycemia, and intes

108 Only the presence of pemphigus or liver dysfunction correlated with a bad prognosis.

109 s in the plasma metabolome are suggestive of liver dysfunction, could provide insights into the under

110 egaly, neurologic dysfunction, coagulopathy, liver dysfunction, cytopenias, hypertriglyceridemia, hyp

111 e identification of mechanisms of kidney and liver dysfunction/disease often present in individuals w

112 gnancy is required in women who present with liver dysfunction during pregnancy.

113 bridge-to-transplant) in patients with acute liver dysfunction (e.g. acute liver failure (ALF), acute

114 Thus, early liver dysfunction, elevated serum creatinine, and low ma

115 are high in this patient population of acute liver dysfunction, especially in combination with case-r

116 In all four patients with advanced liver dysfunction, fibrosis and cholestasis regressed wi

117 Emc6 LKO mice exhibited progressive liver dysfunction, fibrosis and spontaneous carcinogenes

118 IR model that closely recapitulates clinical liver dysfunction following liver resection.

119 No patient had evidence of liver dysfunction; four patients had neurological abnorm

120 ult of toxicity (3% v 1%, with patients with liver dysfunction [>/= grade 2 liver function tests] at

121 Patients with liver dysfunction have increased susceptibility to funga

122 he liver of a mouse model with mitochondrial liver dysfunction (i.e. the hepatocyte-specific prohibit

123 er concentrations and biochemical markers of liver dysfunction in a nationally representative sample.

124 ling data describing the time progression of liver dysfunction in a rat model of acute hepatic failur

125 through the cell cycle, were associated with liver dysfunction in animals infected with the Ad5Ikappa

126 d there was no associated increased risk for liver dysfunction in any stratum.

127 erated postnatal growth increase the risk of liver dysfunction in later life.

128 line/d was established for the prevention of liver dysfunction in men, as assessed by measuring serum

129 dicate that BIM is an important regulator of liver dysfunction in obesity and a novel therapeutic tar

130 data may explain the frequent development of liver dysfunction in patients exposed to multiple bacter

131 Refractory liver dysfunction in patients receiving parenteral nutri

132 determinant of disease severity and risk of liver dysfunction in patients with EPP or XLP.

133 liver disease is the most frequent cause of liver dysfunction in pregnancy and provides a real threa

134 However, most liver dysfunction in pregnancy is pregnancy-related and

135 he commonest cause of hepatic tenderness and liver dysfunction in pregnancy, and 2%-12% of cases are

136 Liver dysfunction in SCD is likely to escalate as life s

137 Prevalence of liver dysfunction in SCD is unknown, with estimates of 1

138 that brain death does not cause significant liver dysfunction in the donor before organ removal.

139 tified Neo1 as a potential target to prevent liver dysfunction in the future.

140 NASH) is the most common etiology of chronic liver dysfunction in the United States and can progress

141 disease (NAFLD) is the most common cause of liver dysfunction in the Western world and is increasing

142 or preventing elevations in serum markers of liver dysfunction in this population under the condition

143 acute liver dysfunction and secondary acute liver dysfunction (in the context of cardiothoracic surg

144 ure could be more widely applied, with early liver dysfunction indicating the need for transplant eva

145 t significantly reduced bowel hemorrhage and liver dysfunction induced by 20 mg/kg LPS, but it had no

146 that LECA is an important determinant of the liver dysfunction induced by gut I/R.

147 cking 12-HETE production inhibits IR-induced liver dysfunction, inflammation and cell death in mice a

148 For example, liver dysfunction is a common phenotype observed in spac

149 In severe sepsis, liver dysfunction is characterized by cholestasis, steat

150 Liver dysfunction is common in burn patients and gut dys

151 reatment of choice in the presence of severe liver dysfunction is no longer valid; novel antidiabetic

152 gnificance of these findings with respect to liver dysfunction is not yet clear.

153 e.g., heart infection and myocardial injury, liver dysfunction, kidney damage, as well as neurologica

154 of 21 patients suffering from postoperative liver dysfunction (LD) after liver resection and 27 matc

155 patients were followed up for postoperative liver dysfunction (LD), morbidity, and mortality.

156 liver function were used to evaluate LR and liver dysfunction (LD).

157 ered in light of HCC tumor burden, degree of liver dysfunction, life expectancy, and patient preferen

158 perfusion (I/R) elicits neutrophil-dependent liver dysfunction, little is known about the kinetics of

159 cerebellar abnormalities, failure to thrive, liver dysfunction, lower extremity edema and dysmorphic

160 Finally, the effect of GFT505 on liver dysfunction markers was assessed in a combined ana

161 In addition, GFT505 improved liver dysfunction markers, decreased hepatic lipid accum

162 The pathogenesis of liver dysfunction may be, at least in part, related to v

163 It has been proposed that liver dysfunction may contribute to the development of t

164 icrog/dL; P </= .001), and increased risk of liver dysfunction (median ePPIX levels for those with li

165 users in age, sex distribution, severity of liver dysfunction, median duration of abstinence, or Uni

166 of bleeding, for whom other causes, such as liver dysfunction, medication effect, disseminated intra

167 e severe complications ( P =0.03) and higher liver dysfunction (MELD) P =0.0001) than females.

168 ncentration of hepatic enzymes are linked to liver dysfunction, metabolic and cardiovascular diseases

169 uency of ELS utilization in cases of primary liver dysfunction (mortality rates: 68.39% versus 40.63%

170 report seven individuals who presented with liver dysfunction multifactorial coagulation deficiency

171 o treatment-related adverse events, of which liver dysfunction (n=4) and rash (n=4) were most common.

172 eatohepatitis (NASH) may develop progressive liver dysfunction necessitating liver transplantation (O

173 these oils against cardiovascular diseases, liver dysfunction, obesity and diabetes are presented wi

174 nes are likely to play a pivotal role in the liver dysfunction observed in space-flown rodents, and t

175 potency of Toc-HDO results in a reduction of liver dysfunction observed in the parent ASO at a simila

176 ical and surgical patients without synthetic liver dysfunction or a history of oral anticoagulant use

177 Subclinical celiac disease can cause cryptic liver dysfunction or be associated with autoimmune hepat

178 Gene expression did not correlate with liver dysfunction or body composition.

179 mopoietic stem-cell infusion did not improve liver dysfunction or fibrosis and might be associated wi

180 atic uptake of hydrophobic bile acids during liver dysfunction, or disorders of lipoprotein metabolis

181 ld, were pregnant, had evidence of kidney or liver dysfunction, or reported a history of alcohol abus

182 se (VOD); (2) the impact of HCV infection on liver dysfunction, other than VOD, occurring between 21

183 eview, we summarize current evidence linking liver dysfunction-particularly metabolic dysfunction-ass

184 l factors, including tumor burden, degree of liver dysfunction, performance status, and patient's lon

185 e symptoms and organ damage (eg, cytopenias, liver dysfunction, portal hypertension, malabsorption, a

186 e results suggest that PCS in the absence of liver dysfunction produces testicular atrophy by reducti

187 ction was unleashed, and this coincided with liver dysfunction reflected by a failure to maintain hyd

188 Studies linking transcriptomics with liver dysfunction rely on tools which exploit correlatio

189 toms, clinically confirmed muscle disorders, liver dysfunction, renal insufficiency, diabetes, and ey

190 multiple health effects, from skin rashes to liver dysfunction, reproductive toxicity and cancer.

191 erefore, were undertaken to characterize the liver dysfunction seen in mice with this same mutation.

192 l in DILI ALF is determined by the degree of liver dysfunction, specifically baseline levels of bilir

193 expressing ATF3 in the liver had symptoms of liver dysfunction such as high levels of serum bilirubin

194 ients also suffer from various metabolic and liver dysfunctions such as increased susceptibility to m

195 ing for patient characteristics and level of liver dysfunction, survival in simultaneous LLT was comp

196 mplication rates and increased postoperative liver dysfunction than have standard hepatic resections

197 Acute liver failure (ALF) causes severe liver dysfunction that can lead to multi-organ failure a

198 , including dysnatremia, kidney failure, and liver dysfunction, the same day as the EEG.

199 alysis assesses survival of HCC patients and liver dysfunction treated with immunotherapy-based regim

200 Of the four with severe liver dysfunction, two have undergone successful retrans

201 d to end-stage renal failure and progressive liver dysfunction, underwent hepatorenal transplantation

202 In 6 other patients, causes of severe liver dysfunction unrelated to pregnancy were found.

203 act of persistent intravascular hemolysis on liver dysfunction using the mouse malaria model.

204 function (median ePPIX levels for those with liver dysfunction vs normal liver function, 2016 vs 1510

205 Such liver dysfunction was associated with severe hypoglycemi

206 Onset of liver dysfunction was at 294 days (range, 74-747 days) a

207 Onset of liver dysfunction was at 35 days (range, 11 to 406 days)

208 Liver dysfunction was determined based on model for end-

209 Liver dysfunction was initially manifested by the elevat

210 Severe reversible liver dysfunction was noted in 15% to 25%.

211 Grade 3 or higher liver dysfunction was noted in 23 of 1612 patients in th

212 Liver dysfunction was slightly increased in the R+ group

213 ciency in the brain or if it is secondary to liver dysfunction, we generated a mouse model with a bra

214 To facilitate study of NPC-associated liver dysfunction, we have developed a novel mouse model

215 Pretransplantation factors associated with liver dysfunction were a diagnosis of aggressive maligna

216 Postoperative complications including liver dysfunction were compared between the groups.

217 Patients with hemodynamic instability or liver dysfunction were excluded.

218 ency operation, coronary artery disease, and liver dysfunction were independent determinants of late

219 vascular disease, anemia, prior stroke, and liver dysfunction were independent risk factors of major

220 f pulmonary toxic effects and of thyroid and liver dysfunction were not significantly increased in th

221 Cardiac and liver dysfunction were significantly attenuated in femal

222 iet could predict whether they would develop liver dysfunction when deprived of dietary choline.

223 ne could predict whether humans will develop liver dysfunction when deprived of dietary choline.

224 aused a transitory attenuation of kidney and liver dysfunction, which was ultimately associated with

225 cosylation characterized by coagulopathy and liver dysfunction with abnormal serum N-glycans.

226 een suggested as a gene therapy protocol for liver dysfunction with aging, may not be tumorigenic in

227 reatment of hematological diseases developed liver dysfunction with histological features suggestive