ライフサイエンスコーパス: hepatomegaly

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

2 zed beta-catenin transgenic mice also showed hepatomegaly.

3 ressed on mature hepatocytes induces massive hepatomegaly.

4 -2'-deoxyuridine into hepatocyte nuclei, and hepatomegaly.

5 tment also resulted in hepatic steatosis and 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 ging from asymptomatic to highly symptomatic hepatomegaly.

11 -for-age z scores) and increased measures of hepatomegaly.

12 isplay severe liver disease characterized by hepatomegaly.

13 epatic dysfunction, portal hypertension, and hepatomegaly.

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

15 oting hepatocyte proliferation, resulting in hepatomegaly.

16 phic regeneration was accelerated and led to hepatomegaly.

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

18 omplications such as cholestatic jaundice or hepatomegaly.

19 rm protocol, possibly the result of systemic hepatomegaly.

20 ration of cholangiocytes, ultimately causing hepatomegaly.

21 controlled regenerative response and drives hepatomegaly.

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

23 ents presented hormone secretion and 55% had hepatomegaly.

24 de dyslipidemia, elevated transaminases, and hepatomegaly.

25 termination of the regeneration process and hepatomegaly.

26 increased serum cytokine levels, and develop hepatomegaly.

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

28 blast exceeding marrow blast percentage, and hepatomegaly.

29 BOP-induced proliferation of hepatocytes and hepatomegaly.

30 erformed in19 patients, 14 of them (74%) had hepatomegaly, 10 patients (53%) had granular pattern or

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

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

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

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

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

36 e cellular rejection of the liver, jaundice, hepatomegaly, acute hepatic failure and hepatic porphyri

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

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

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

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

41 Resolution of hepatomegaly and a reduction in spleen volume were obser

42 8 days]): five acute deaths were a result of hepatomegaly and associated toxicities; two were a resul

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

44 ystic rats with UDCA-HDAC6i #1 reduced their hepatomegaly and cystogenesis, increased UDCA concentrat

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

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

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

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

49 pe progresses with age and is accompanied by hepatomegaly and hepatic cholesterol crystal deposition.

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

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

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

53 estigated a direct role of Yap in CAR-driven hepatomegaly and hepatocyte proliferation using hepatocy

54 uption, dramatically reduced TCPOBOP-induced hepatomegaly and hepatocyte proliferation.

55 6 months of age, transgenic mice had obvious hepatomegaly and histological evidence of dysplasia in t

56 fasting hypoglycemia, hypertriglyceridemia, hepatomegaly and HS.

57 Cholic acid feeding reverses hepatomegaly and hypertriglyceridemia but not adrenomega

58 sting impaired lipid storage with subsequent hepatomegaly and hypertriglyceridemia.

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

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

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

62 uced cholestatic liver injury, which induced hepatomegaly and liver injury as compared to control die

63 a frequent feature, usually presenting with hepatomegaly and mild liver enzymes abnormalities, which

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

65 complications such as swallowing difficulty, hepatomegaly and portal hypertension.

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

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

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

69 Hepatomegaly and small calcified spleen are typical find

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

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

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

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

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

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

76 onal changes but also suppresses YAP-induced hepatomegaly and tumorigenesis.

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

78 hepatic venous pressure gradient and either hepatomegaly and/or splenomegaly were present in all pat

79 hepatic venous pressure gradient and either hepatomegaly and/or splenomegaly were present in all pat

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

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

82 ive (49 of 69 patients) and 86% specific for hepatomegaly, and a maximal 3D linear threshold of 24 cm

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 ChREBP induction in GSD 1a liver aggravates hepatomegaly because of further accumulation of glycogen

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

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

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

104 if a baseline measurement is not available, hepatomegaly can be defined as greater than 2 SDs above

105 This hepatomegaly cannot be explained solely by lipid accumul

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

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

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

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

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

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

112 nclusion A simple weight-based threshold for hepatomegaly derived by using a fully automated CT-based

113 ical inhibition of mTORC1 partially reversed hepatomegaly, ductular reaction, fibrosis, inflammatory

114 Patients with GSD 1a exhibit severe hepatomegaly due to glycogen and triglyceride (TG) accum

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

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

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

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

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

120 fasting hypoglycemia, hypertriglyceridemia, hepatomegaly, hepatic steatosis (HS), and increased live

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

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

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

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

125 atoxin was associated with childhood chronic hepatomegaly in 2002.

126 trasound in 39% (9) of patients, followed by hepatomegaly in 26% (6).

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

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

129 Chop deletion prevented liver steatosis and hepatomegaly in aged HFD-fed mice without affecting basa

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

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

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

133 spectively, elafibranor tended to exacerbate hepatomegaly in Lep(ob)/Lep(ob)-NASH mice.

134 to cause robust hepatocyte proliferation and hepatomegaly in mice along with induction of drug metabo

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

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

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

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

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

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

141 predict the potency ranges for PFAS-induced hepatomegaly in vivo.

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

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

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

145 1 inhibition almost completely abrogates the hepatomegaly induced by YAP overexpression.

146 Hepatomegaly is a sign of many liver disorders.

147 -compatible fresh platelet transfusions; (3) hepatomegaly is best defined as an absolute increase of

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

149 Background Imaging assessment for hepatomegaly is not well defined and currently uses subo

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

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

152 manifested sinusoidal ischemia, progressive hepatomegaly, liver injury, hyperbilirubinemia, and incr

153 0.29; 95% CI, 0.20-0.39); or the absence of hepatomegaly (LR, 0.37; 95% CI, 0.24-0.51).

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

155 l hepatomegaly threshold volume was derived: hepatomegaly (mL) = 14.0 x (weight [kg]) + 979.

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

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

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

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

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

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

162 Transient hepatomegaly often accompanies acute bacterial infection

163 d with pre-emptive chemotherapy for evolving hepatomegaly or other baseline comorbidities in infants

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

165 g infants with symptoms secondary to massive hepatomegaly or with unfavorable tumor biology are at hi

166 028), nadir platelets (OR, 1.9; P = .00068), hepatomegaly (OR, 2.9; P = .012), and increasing age (OR

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

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

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

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

171 (in contrast to decreased density in NAFLD), hepatomegaly, periportal edema, and ascites.

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

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

174 atment of infants younger than 2 months with hepatomegaly, regardless of symptoms.

175 inferior vena cava in patients with massive hepatomegaly related to PLD: the exposure left lateral s

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

177 in Clcn7 variant exhibited hypopigmentation, hepatomegaly resulting from abnormal storage, and enlarg

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

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

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

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

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

183 3; 95% confidence interval [CI], 2.0-4.7) or hepatomegaly (summary LR, 2.4; 95% CI, 1.6-3.6) make mal

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

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

186 a linear weight-based upper limit of normal hepatomegaly threshold volume was derived: hepatomegaly

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

188 of function, and resulted in progression of hepatomegaly to steatosis, then hepatic injury phenotype

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

190 17 patients; 41%), complete disappearance of hepatomegaly (two of seven patients; 29%), > or = 50% re

191 We found that BRAF(V600E) expression caused hepatomegaly, vascular congestion, and ductal reactions,

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

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

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

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

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

197 ut not female mice, resulted in diet-induced hepatomegaly, which was associated with decreased expres

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

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

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

201 Ultrasound showed a severe hepatomegaly with multiple lesions.

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

203 organ volume and to establish thresholds for hepatomegaly with use of a validated deep learning artif

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

205 induces robust hepatocyte proliferation and hepatomegaly without any liver injury or tissue loss.

206 estrictive features are present; unexplained hepatomegaly without imaging abnormalities; peripheral n