ライフサイエンスコーパス: liver dysfunction

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

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

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

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

5 edicting increases in biochemical indexes of liver dysfunction.

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

7 recurrent line infections, and intermittent liver dysfunction.

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

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

10 ion is warranted when treating patients with liver dysfunction.

11 ules) were not associated with postoperative liver dysfunction.

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

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

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

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

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

17 with increased cell death, and commensurate liver dysfunction.

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

19 otal parenteral nutrition and others develop liver dysfunction.

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

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

22 e aminotransferase levels were suggestive of liver dysfunction.

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

24 abnormal glucose metabolism, and progressive liver dysfunction.

25 ous, including gastric dilatation and severe liver dysfunction.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 Refractory liver dysfunction in patients receiving parenteral nutri

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 Liver dysfunction was determined based on model for end-

134 Liver dysfunction was initially manifested by the elevat

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

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

137 Liver dysfunction was slightly increased in the R+ group

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

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

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

141 Patients with hemodynamic instability or liver dysfunction were excluded.

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

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

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

145 Cardiac and liver dysfunction were significantly attenuated in femal

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

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

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

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

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