ライフサイエンスコーパス: hepatomegaly

1 oting hepatocyte proliferation, resulting in hepatomegaly.

2 ressed on mature hepatocytes induces massive hepatomegaly.

3 -2'-deoxyuridine into hepatocyte nuclei, and hepatomegaly.

4 tment also resulted in hepatic steatosis and hepatomegaly.

5 phic regeneration was accelerated and led to hepatomegaly.

6 The most common sign of NASH is hepatomegaly.

7 pathy, splenomegaly, thymic enlargement, and hepatomegaly.

8 18 patients who underwent liver imaging had hepatomegaly.

9 lar retention of nascent proteins leading to hepatomegaly.

10 kinase subunit, but did not have diabetes or hepatomegaly.

11 omplications such as cholestatic jaundice or hepatomegaly.

12 rm protocol, possibly the result of systemic hepatomegaly.

13 ration of cholangiocytes, ultimately causing hepatomegaly.

14 controlled regenerative response and drives hepatomegaly.

15 ition to LT, poor tumor differentiation, and hepatomegaly.

16 ents presented hormone secretion and 55% had hepatomegaly.

17 de dyslipidemia, elevated transaminases, and hepatomegaly.

18 termination of the regeneration process and hepatomegaly.

19 increased serum cytokine levels, and develop hepatomegaly.

20 epatic dysfunction, portal hypertension, and hepatomegaly.

21 n this study we examined its role in chronic hepatomegaly.

22 blast exceeding marrow blast percentage, and hepatomegaly.

23 BOP-induced proliferation of hepatocytes and hepatomegaly.

24 iliary sludge, one (2%) fatty liver and none hepatomegaly.

25 to Aoah(-/-) mice and prevented LPS-induced hepatomegaly.

26 zed beta-catenin transgenic mice also showed hepatomegaly.

27 Amongst the patients, 32 (64%) had hepatomegaly, 15 (30%) cholelithiasis and 3 (6%) biliary

28 evels also were higher in children with firm hepatomegaly [176.6 (129.6, 240.7) pg/mg] than in normal

29 features included fever (8 patients), tender hepatomegaly (5 of 8), hypoxemia (2 of 8), septic pulmon

30 lymphadenopathy (100%), splenomegaly (72%), hepatomegaly (50%), and edema (28%).

31 At 3 months, cP(f/f)78(f/f) livers showed hepatomegaly, activation of lipogenic genes, exacerbated

32 ed the following predictors of poor outcome: hepatomegaly, age more than 45 years, and any amount of

33 either finding (38%), intermediate risk with hepatomegaly alone (40%), and high risk with both (21%;

34 Reversible, dose-dependent hepatomegaly also occurs when animals are given intraven

35 the peroxisome proliferator WY-14643 caused hepatomegaly, alterations in mRNAs encoding proteins tha

36 significant difference in the prevalence of hepatomegaly and cholelithiasis between the patients and

37 cystic kidney disease, can result in massive hepatomegaly and debilitating symptoms.

38 t presents with abdominal discomfort, tender hepatomegaly and elevated transaminases.

39 creased fatty acid synthesis, accompanied by hepatomegaly and fatty liver phenotype.

40 tion of hepatic P450s were observed, whereas hepatomegaly and fatty liver were only observed in the l

41 ecific Albumin-Cre;Vps34(f/f) mice developed hepatomegaly and hepatic steatosis, and impaired protein

42 nd alcohol feeding in HIF1dPA mice increased hepatomegaly and hepatic triglyceride compared with WT m

43 cell tumors in nude mice results in dramatic hepatomegaly and hepatocyte hyperplasia in the absence o

44 6 months of age, transgenic mice had obvious hepatomegaly and histological evidence of dysplasia in t

45 Cholic acid feeding reverses hepatomegaly and hypertriglyceridemia but not adrenomega

46 sting impaired lipid storage with subsequent hepatomegaly and hypertriglyceridemia.

47 SD6) defines a group of disorders that cause hepatomegaly and hypoglycemia with reduced liver phospho

48 hed diet significantly reduced the degree of hepatomegaly and induction of target genes encoding enzy

49 han conventional soybean oil, it resulted in hepatomegaly and liver dysfunction as did olive oil, whi

50 t difference between the villages or between hepatomegaly and normal groups [539.7 (436.7, 666.9) vs.

51 the Pkhd1-null mouse develops massive cystic hepatomegaly and proximal tubule dilation, whereas the m

52 signaling effector YAP/TAZ to promote severe hepatomegaly and rapid HCC initiation and progression.

53 ng in uncontrolled hepatocyte proliferation, hepatomegaly and rapid lethality despite maintenance of

54 Hepatomegaly and small calcified spleen are typical find

55 EtOH-treated larvae develop hepatomegaly and steatosis accompanied by changes in the

56 e inclusion of cholesterol in the WD induced hepatomegaly and steatosis in both HCR and LCR rats, whi

57 ecific Hnf4a knock-out mouse develops severe hepatomegaly and steatosis resulting in premature death,

58 nges correlated with reduced body adiposity, hepatomegaly and steatosis, and postprandial plasma insu

59 gative association between presentation with hepatomegaly and the levels of the regulatory cytokines

60 e to peroxisome proliferators that can drive hepatomegaly and tumor development in rodents.

61 clinical problem that can result in massive hepatomegaly and various complications, leading to signi

62 derate or severe), most had mild or moderate hepatomegaly, and 20% had mild anemia.

63 onset of leukemia, reduced splenomegaly and hepatomegaly, and a longer survival than TCL1+/wtMIFwt/w

64 and is associated with hypertriglyceridemia, hepatomegaly, and disordered glucose metabolism.

65 ing infancy, resulting in failure to thrive, hepatomegaly, and hepatic failure, and an average life e

66 atocyte proliferation, in the development of hepatomegaly, and in survival during chronic inflammatio

67 )-induced liver damage, serum ALT elevation, hepatomegaly, and lipid accumulation.

68 cantly reduced triglycerides, transaminases, hepatomegaly, and liver fat content.

69 -/-) mice with lymphoma showed splenomegaly, hepatomegaly, and lymphadenopathy with involvement of bo

70 sis with maturing neutrophils, splenomegaly, hepatomegaly, and myeloid infiltration into peripheral t

71 nt at diagnosis, presence of splenomegaly or hepatomegaly, and presence of more than 15% blasts in th

72 nation these mice present with splenomegaly, hepatomegaly, and severe lymphadenopathy.

73 r wall thickness, pleural effusion, ascites, hepatomegaly, and splenomegaly are highly suggestive of

74 lar infiltration, multifocal liver necrosis, hepatomegaly, and splenomegaly were found in B6 mice, bu

75 iferator-activated receptor alpha results in hepatomegaly, and these nuclear receptors are implicated

76 cuolar protein sorting gene vps18 results in hepatomegaly associated with large, vesicle-filled hepat

77 gates de novo PtdIns synthesis, resulting in hepatomegaly at 5 days postfertilization.

78 els for hepatic pathologies, we screened for hepatomegaly at day 5 of embryogenesis in 297 zebrafish

79 ng induction therapy (P =.027) and having no hepatomegaly at diagnosis (P =.009) was associated with

80 wed that grades 1 or 2 GVHD (P =.008) and no hepatomegaly at diagnosis (P =.014) were associated with

81 ncreased by the presence of splenomegaly and hepatomegaly but individual findings are of limited util

82 to the IL-10 receptor increased LPS-induced hepatomegaly by as much as 50%.

83 ropathy and gastric atony, and resolution of hepatomegaly by computed tomographic scan.

84 This hepatomegaly cannot be explained solely by lipid accumul

85 eroderma, hyperpigmentation, hypertrichosis, hepatomegaly, cardiac abnormalities and musculoskeletal

86 AD deficiency may present with hypoglycemia, hepatomegaly, cardiomyopathy, and myopathy.

87 A computed tomographic scan revealed massive hepatomegaly caused by multiple cysts of variable sizes,

88 In this study, hepatomegaly, cholelithiasis and biliary sludge were the

89 Multivariate analysis identified male sex, hepatomegaly, CNS-2 status, and age younger than 2 or ol

90 ease, can present with abdominal pain, acute hepatomegaly, coagulopathy, hyperbilirubinemia, and fulm

91 he cardinal lesion of this disease is marked hepatomegaly due to leukemic proliferation and infiltrat

92 titis (NASH) is a condition characterized by hepatomegaly, elevated serum aminotransferase levels, an

93 d none of the hepatotoxic phenotypes such as hepatomegaly, elevation in serum bile acids, increase of

94 Selective patients with massive hepatomegaly from PLD benefit from operative interventio

95 ge, sex, Rai and Binet stages, splenomegaly, hepatomegaly, hemoglobin (Hgb) level, beta-2 microglobul

96 ignificant 43% increase in the prevalence of hepatomegaly/hepatosplenomegaly for every natural-log-un

97 restingly, control-fed PXR-KO mice exhibited hepatomegaly, hyperinsulinemia, and hyperleptinemia but

98 se (G6Pase) system (e.g. growth retardation, hepatomegaly, hyperlipidemia, and renal dysfunction) are

99 ties included abdominal pain in 11 (73%) and hepatomegaly in 10 (67%) patients, and abnormal liver fu

100 atoxin was associated with childhood chronic hepatomegaly in 2002.

101 Pain was relieved in 71% and hepatomegaly in 59% of group 1 patients, as compared wit

102 lymphadenopathy in 89%, splenomegaly and/or hepatomegaly in 90%.

103 hasone almost completely prevented prolonged hepatomegaly in Aoah(-/-) mice, whereas neutralizing TNF

104 ests that a possible mechanism for childhood hepatomegaly in areas where both malaria and schistosomi

105 f this study was to test the hypothesis that hepatomegaly in burned children can be attenuated or rev

106 ry molecules are unable to prevent prolonged hepatomegaly in mice that cannot inactivate LPS.

107 in a plasmid under a CMV promoter results in hepatomegaly in mice.

108 Considering hepatomegaly in Ob group, RLV was also normalized to bod

109 ), produces rapid hepatocyte hyperplasia and hepatomegaly in the absence of hepatic injury.

110 n and cholate-dependent, cholesterol-induced hepatomegaly in the FGFR4 (-/-) mice suggested that acti

111 HGF gene delivery failed to induce hepatomegaly in these beta-catenin conditionally null mi

112 WY-14,643 treatment induced hepatomegaly in wild type (WT) mice that was also accomp

113 mor initiation but paradoxically exacerbates hepatomegaly induced by Nf2 loss, which can be suppresse

114 role of GPC3 in hepatocyte proliferation and hepatomegaly induced by the xenobiotic mitogens phenobar

115 Hepatomegaly is a sign of many liver disorders.

116 was based on the hypothesis that HGF-induced hepatomegaly is mediated, at least in part, by activatio

117 emic complications (arthritis, splenomegaly, hepatomegaly, leukocytosis, and acute-phase reaction) (P

118 Key features include hepatomegaly, lipid storage, elevated serum liver enzyme

119 0.29; 95% CI, 0.20-0.39); or the absence of hepatomegaly (LR, 0.37; 95% CI, 0.24-0.51).

120 e previously examined for associations among hepatomegaly, malaria, and schistosomiasis.

121 hese included splenomegaly, lymphadenopathy, hepatomegaly, multifocal hepatitis, anemia, altered traf

122 involvement with polyneuropathy (n = 2), and hepatomegaly (n = 1).

123 sy in those with normal ALT were unexplained hepatomegaly (n = 21) and evaluation as a potential dono

124 terized by growth retardation, hypoglycemia, hepatomegaly, nephromegaly, hyperlipidemia, hyperuricemi

125 rol, but lacked the mutation and had neither hepatomegaly nor growth failure.

126 Presentation with a firm type of chronic hepatomegaly of multifactorial etiology is common among

127 Transient hepatomegaly often accompanies acute bacterial infection

128 mia (57/63), elevated interleukin 6 (57/63), hepatomegaly or splenomegaly (52/67), fever (33/64), oed

129 athological changes, including splenomegaly, hepatomegaly, or granulomatous disease.

130 G levels, HIV-1 RNA levels, lymphadenopathy, hepatomegaly, or splenomegaly.

131 (P =.004), lower hemoglobin level (P =.001), hepatomegaly (P =.05), and high beta2M level (P =.00005)

132 Common causes of an epigastric mass include hepatomegaly, pancreatic pseudocyst and epigastric herni

133 yed typical pleiotropic responses, including hepatomegaly, peroxisome proliferation in hepatocytes, a

134 BDNF reduced the hepatomegaly present in db/db mice, in association with

135 We found that recovery from LPS-induced hepatomegaly requires a host enzyme, acyloxyacyl hydrola

136 defined as having two of the following: (1) hepatomegaly+/-splenomegaly; (2)>6 months elevation of A

137 with cough, fever, otitis media, pneumonia, hepatomegaly, splenomegaly, and hospitalization in HIV-i

138 persistent angiofollicular lymphadenopathy, hepatomegaly, splenomegaly, and hypergammaglobulinemia.

139 nsion of primitive mononuclear cells causing hepatomegaly, splenomegaly, severe anemia, and death.

140 rmin improved fatty liver disease, reversing hepatomegaly, steatosis and aminotransferase abnormaliti

141 3; 95% confidence interval [CI], 2.0-4.7) or hepatomegaly (summary LR, 2.4; 95% CI, 1.6-3.6) make mal

142 a low carbohydrate diet resulted in massive hepatomegaly that progressed rapidly to diffuse multifoc

143 The NPC mouse develops significant hepatomegaly that reaches 8% of body weight at 5 to 6 we

144 toxic responses that we examined, including hepatomegaly, thymic involution, and cleft palate format

145 normal liver growth but potently suppresses hepatomegaly/tumorigenesis resulting from YAP overexpres

146 17 patients; 41%), complete disappearance of hepatomegaly (two of seven patients; 29%), > or = 50% re

147 f the human HGF gene delivery in mice led to hepatomegaly via beta-catenin activation in the liver in

148 Hepatocyte growth was reduced and hepatomegaly was absent in p38alpha-deficient mice durin

149 Hepatomegaly was found in 34% and splenomegaly in 56% of

150 Wy14,643-induced hepatomegaly was partially inhibited in hepatocyte RXRal

151 including splenomegaly, lymphadenopathy, and hepatomegaly were associated with no maternal HAART vers

152 These mice developed hepatomegaly, which was the result of hepatocyte hypertr

153 y obese, middle-aged women with asymptomatic hepatomegaly who are diabetic or hyperlipidemic and pres

154 All patients suffered from symptomatic hepatomegaly with 85% being functionally impaired (Easte

155 Ultrasound showed a severe hepatomegaly with multiple lesions.

156 basis of the diagnostic clinical findings of hepatomegaly with or without life-threatening symptoms,

157 nd weakness, nausea and vomiting, and tender hepatomegaly, with a range of neurological symptoms from