ライフサイエンスコーパス: normal liver

1 tion of early stages of liver dysplasia from normal liver.

2 ic liver has a higher mutational burden than normal liver.

3 essed in approximately 74% cases compared to normal liver.

4 underwent ultrasonography (US)-guided IRE of normal liver.

5 astases were more susceptible to SLSRFA than normal liver.

6 30 and P<0.0455, respectively) than in human normal liver.

7 t to cause dysplasia and HCC in a previously normal liver.

8 growth responses compared to hepatocytes in normal liver.

9 tumor tissue from HCC patients compared with normal liver.

10 ably higher in human HCC lines compared with normal liver.

11 nts and 8 Fz genes and Fzb were expressed in normal liver.

12 rlap in gene expression patterns compared to normal liver.

13 out tumors was compared with pooled RNA from normal liver.

14 lic functions along the portocentral axis in normal liver.

15 s reduced to Vitamin C (VitC) rapidly in the normal liver.

16 PPP2R2C, and TRAF2) in HCC as compared with normal liver.

17 signal intensity of a region of interest in normal liver.

18 go either RF or IRE ablation of noncancerous normal liver.

19 essed in adipose tissue, but undetectable in normal liver.

20 or case and other FL-HCC cases compared with normal liver.

21 ared to the matched peritumorous liver or to normal liver.

22 an cirrhotic peritumoral tissue, compared to normal liver.

23 unctional similarities to bile duct cells in normal liver.

24 ion was increased in human HCC compared with normal livers.

25 s those given a restricted standard diet had normal livers.

26 ctivation, had variable expression levels in normal livers.

27 generation (13% vs 26.4%) but negligible in "normal" liver.

28 was greatest in diseased human liver versus normal liver (32.2 cells/field versus 20.5 cells/field [

29 In normal livers, 4.19 +/- 0.53% of the PB dose was recover

30 ne a baseline PET/CT examination and who had normal livers according to imaging and biochemical test

31 thin the physiological range (~5-20%) of the normal liver acinus, the estrogen-enhanced growth phenot

32 accounts for the anticipated higher tumor-to-normal liver activity concentration ratio, dose point-ke

33 used adenoviral vectors to express Nor-1 in normal liver (Ad/CMV/V5-Nor-1), or reduce its level with

34 lated ischemic-reperfusion injury (15), and "normal" liver adjacent to colorectal cancer metastasis (

35 -old mice display many, but not all signs of normal liver ageing as early as 1 month after treatment,

36 Further analysis of a total of 19 normal liver and 57 HCC specimens showed that down-regul

37 apacity to transactivate its target genes in normal liver and during obstructive cholestasis.

38 unctional autophagy and is indispensable for normal liver and heart function.

39 P1B1 mRNA and protein were only found in the normal liver and hepatocytes.

40 tic, vascular, and sinusoidal endothelium in normal liver and in patients with HCV infection.

41 Our patient had normal liver and intestinal function tests and no signs

42 ear of this procedure, the patient maintains normal liver and kidney function and refers significant

43 th restoration of his circulating C3 levels, normal liver and kidney function at 26 months of follow-

44 pitope-tagged fibrocystin has histologically normal liver and kidneys at 14 mo.

45 tion maps at single-base resolution in human normal liver and lung as well as paired tumor tissues.

46 In normal liver and over a broad age range, cholangiocytes

47 ved graft functions at 2-year follow-up with normal liver and pancreas function.

48 ally expressed on primary hepatocytes within normal liver and pegylated forms of IL-29 and IFN-alpha

49 of transaminase levels between patients with normal liver and pure steatosis did not reveal significa

50 All patients had normal liver and renal function.

51 es, thereby promoting immune surveillance in normal liver and renewal of effector responses in chroni

52 n in the 5' end of pro-pol were expressed in normal liver and showed relatively low levels of derepre

53 In marked contrast, uptake in normal liver and spleen decreased markedly as affinity d

54 (b) Uptake in normal liver and spleen is specific (dependent on phosph

55 t is expressed in FL-HCC but not in adjacent normal liver and that arises as the result of a ~400-kil

56 derived from preexisting hepatocytes in the normal liver and that liver progenitor cells contributed

57 the 3 analyses, measurements of SUV(max) in normal liver and tumor lesions were compared.

58 or clinical and/or K19 analysis included six normal livers and biopsy specimens from 10 patients with

59 gnificantly more proliferative than those in normal livers and expressed high levels of RB/E2F target

60 to HCC and normal liver tissue derived from normal livers and hepatic resections.

61 ion in bile duct epithelium when compared to normal livers and livers affected by other noncholestati

62 N were markedly increased in AH, compared to normal livers and other types of chronic liver diseases,

63 these conditions, Ceacam1a-/- mice displayed normal livers and spinal cords.

64 tocellular carcinoma), RTL-W1 (rainbow trout normal liver), and primary rainbow trout hepatocytes exp

65 embrane serine protease that is expressed in normal liver, and at lower levels in kidney, pancreas, a

66 was overexpressed in >90% cases, compared to normal liver, and LSF expression level showed significan

67 acellular matrix (ECM) and distortion of the normal liver architecture.

68 analysis of BECs from PBC liver compared to normal liver are significantly different, suggesting tha

69 thin the tumors was greater than that within normal liver, as detected with the handheld imaging syst

70 Of 27 potential donors with normal livers at CT and acceptable LAI levels, four (15%

71 rences in maximum tolerable absorbed dose to normal liver between (90)Y radioembolization and externa

72 gh levels of hepatitis B virus (HBV) DNA and normal liver biochemistry, with minimal or no fibrosis.

73 remained HCV RNA-negative; five (7.5%) had a normal liver biopsy; 54 (82%) had fibrosis (stage 2 or 3

74 atic glucose metabolism in the presence of a normal liver/brain insulin ratio (3:1) is unknown.

75 Myofibroblasts are not present in the normal liver but activate and proliferate in response to

76 that Foxl1 is expressed in rare cells in the normal liver but is dramatically induced in the livers o

77 given that there are no CD22(+) cells in the normal liver, but nonspecific uptake of ADCs by liver si

78 Analysis of normal livers by cDNA microarrays disclosed 2418 unique

79 RF ablation of normal liver can stimulate distant subcutaneous tumor gr

80 arcinoma cell line) and HL-7701 cells (human normal liver cell line) by a confocal imaging technique.

81 latory factor (Gdown1) in the maintenance of normal liver cell transcription through constraints on c

82 in the promoter was further examined in one normal liver cell, eight HCC cell lines, eight HCC tissu

83 Differential activity was observed on normal liver cells and at different stages of oval cell

84 pressed exclusively in this subpopulation of normal liver cells and was highly enriched relative to o

85 d within the LIFR promoter that is active in normal liver cells correlate with increased and decrease

86 s on HCC cells and ATRA-PLLA did not inhibit normal liver cells, as expected because ATRA selectively

87 uced resistance to Fas-mediated apoptosis in normal liver cells.

88 nts with early AATD, and among patients with normal liver, cirrhosis, and hepatocellular carcinoma de

89 compared with nonneoplastic surrounding and normal livers coincidently with the suppression of at le

90 s (156 differentially expressed genes versus normal liver) consistent with remodeling toward differen

91 Normal liver contained rare COL15A1-immunoreactive cells

92 Normal liver-derived hepatocytes (NLDH) and cirrhotic li

93 s designed to explore differentiation during normal liver development and regeneration after toxic in

94 (TGF-beta) pathways have been implicated in normal liver development as well as in cancer formation.

95 Wnt/beta-catenin activation is observed in normal liver development, regeneration, and liver cancer

96 ng similar features to those observed during normal liver development, we sought to investigate the r

97 els for ALT in healthy weight, metabolically normal, liver disease-free, NHANES pediatric participant

98 After RF ablation of normal liver, distant R3230 tumors were substantially la

99 on dose to tumor of 35.5 +/- 9.4 Gy and mean normal liver dose of 26.4 +/- 6.8 Gy.

100 rmal liver enzymes and 2.8% among those with normal liver enzymes, compared with only 0.6% among HCV-

101 C workers with high cumulative exposures and normal liver enzymes.

102 Normal liver evaluations were similar, except with margi

103 Normal liver expresses MAT1A, which is silenced in hepat

104 e liver in 78% (28/36) of cases, and 86% had normal liver function (Child class A).

105 n was excellent, and the child is well, with normal liver function 2 months posttransplant.

106 All treated recipients had normal liver function after a 6-month follow-up and are

107 lacetoacetate hydrolase gene (Fah-/-) regain normal liver function after transplantation of Fah+/+ bo

108 P1 from hepatocytes yields mice that exhibit normal liver function and are indistinguishable from lit

109 hemoconcentrated (hemoglobin 16 g/dl), with normal liver function and coagulation testing.

110 This review provides an overview of normal liver function and development and focuses on the

111 Liver fibrosis interferes with normal liver function and facilitates hepatocellular car

112 He acquired full enteral tolerance and normal liver function and has never shown evidence of al

113 res were present in some patients, including normal liver function and Leigh syndrome (subacute necro

114 BV) e antigen-positive viremic patients with normal liver function and the incorporation of new bioma

115 ed AUC) did not differ between patients with normal liver function and those with LD.

116 is trial were on tacrolimus monotherapy with normal liver function tests (LFTs).

117 ts with no or minimal hepatic injury who had normal liver function tests (LTs) (referred to herein as

118 g grafts (all liver transplant patients with normal liver function tests).

119 fter treatment, all patients had improved or normal liver function tests, resolution of C4d depositio

120 All seven patients had normal liver function tests, skin rash, and diagnosis of

121 ; lactate dehydrogenase (LDH), 397 IU/L; and normal liver function tests.

122 rt may require rethinking our definition of "normal liver function tests." Chronic viral hepatitis B

123 Fifteen patients with normal liver function were enrolled as controls.

124 X levels for those with liver dysfunction vs normal liver function, 2016 vs 1510 microg/dL; P = .003)

125 ro, and also after implantation in mice with normal liver function, 60% of the time.

126 al node biopsy, no excessive vitamin intake, normal liver function, negative chest x-ray, and no othe

127 In patients with normal liver function, recurrence was also significantly

128 similation and cytoplasmic PAP hydrolysis to normal liver function.

129 tly established in immunocompetent mice with normal liver function.

130 s essential for human copper homeostasis and normal liver function.

131 NKT-cell development, and the maintenance of normal liver function.

132 rvival of hepatocytes and the maintenance of normal liver function.

133 catenin may also control multiple aspects of normal liver function.

134 ual NF- kappaB activity but are healthy with normal liver function.

135 onine, betaine, and folate) is important for normal liver function.

136 y and rapid lethality despite maintenance of normal liver function.

137 splant patients who are alive currently have normal liver functions.

138 Thus, beta-catenin is essential for normal liver growth and development.

139 nant-negative TEAD molecule does not perturb normal liver growth but potently suppresses hepatomegaly

140 limited radiation tolerance of the adjacent normal liver has prohibited wider use of radiation thera

141 s that do not target antigens present in the normal liver have a relatively low frequency of SOS, but

142 Stem cells from normal livers have a low mutational burden and limited d

143 croarray repositories for gene expression in normal liver, hepatitis C virus (HCV) cirrhosis, HCV-rel

144 Chow-fed TG and KO mice had normal liver histologic findings and body weight.

145 ith subjects with the metabolic syndrome and normal liver histology (n = 17), both NAFL (n = 21) and

146 e steatosis, compared to obese subjects with normal liver histology (P = 0.002 and P = 0.003, respect

147 0 kg/m(2)) patients: (1) obese normal group (normal liver histology), (2) simple steatosis (SS), (3)

148 ertension, and insulin resistance but showed normal liver histology.

149 bolic syndrome and NASH versus controls with normal liver histology.

150 ver enzymes, no fall in platelet counts, and normal liver histology.

151 primarily maintained by self-renewal during normal liver homeostasis, as well as in response to a wi

152 contribute to hepatocyte regeneration during normal liver homeostasis, in response to surgical or tox

153 esis in the liver with no apparent effect on normal liver homeostasis, the work paves the way for the

154 -regulated in these mice that play a role in normal liver homeostasis.

155 o-apoptotic effects of TGF-beta1 involved in normal liver homeostasis.

156 rome P450 expression at comparable levels to normal liver in vitro.

157 We characterized these cells in normal liver, in carbon tetrachloride-injured liver, and

158 Similarly, unlike LSECs in normal livers, in fibrosis, LSECs do not veto dendritic

159 The normal liver is characterized by immunologic tolerance.

160 bronectin splicing in endothelial cells from normal liver is in part promoter-dependent.

161 V(max) in tumor lesions, whereas SUV(max) in normal liver is significantly lower after treatment.

162 totoxicity assay that modeled disease niche, normal liver, kidney, and bone marrow.

163 Furthermore, whereas in normal livers, LSECs are active in the generation of T r

164 PH, delayed hepatocyte mitosis, but overall normal liver mass restoration.

165 n at 10 mg/kg ip with little or no effect on normal liver mass.

166 We determined that normal liver matrix stiffness was around 150 Pa and incr

167 c mice expressing HCV core protein, and from normal liver mitochondria incubated with recombinant cor

168 Specimens from normal liver (n = 5), PSC (n = 20), and PSC-associated C

169 An algorithm for segregating lesions into normal liver, NAFLD, or nonalcoholic steatohepatitis (NA

170 In normal livers, Nogo-B expression was found in nonparench

171 mRNA) and protein were detectable neither in normal liver nor in cultured hepatoblasts, but were read

172 Overexpression of Nor-1 in normal livers of mice induced proliferation of quiescent

173 Ten patients (20%) had normal or nearly normal livers on long-term follow-up biopsy.

174 there was no detectable RCR vector spread to normal liver or bone marrow by quantitative PCR analysis

175 m of FOXO3 in HCV-infected livers but not in normal liver or nonalcoholic steatohepatitis.

176 ficant differences in SUV(max) were found in normal liver or tumor lesions dependent on the interval

177 ficantly higher PAI-1 values than those with normal liver (P < 0.001).

178 increased in patients with AH compared with normal livers (P </= 0.01), chronic hepatitis C (P </= 0

179 mulation of Tc-99m-RBC in hemangiomas and in normal liver parenchyma (HEM/liv), and to verify, whethe

180 s of microsphere accumulation and regions of normal liver parenchyma that demonstrated no apparent mi

181 between the surgical resection clips and the normal liver parenchyma.

182 ta1-integrin has no obvious consequences for normal livers, partial hepatectomy leads to severe liver

183 We found that normal liver pDCs were weak in stimulating T cells, yet

184 ntiation of new hepatocyte lineages makes to normal liver physiology are unknown.

185 The function of miRNAs in normal liver physiology is largely unknown.

186 iscrimination of pathological processes from normal liver processes with high specificity and sensiti

187 ribution was quantified on SPECT as tumor-to-normal-liver ratio (TNR).

188 SPECT/CT-derived mean tumor-to-normal liver ratios varied widely across all planning ta

189 The selective delivery spares surrounding normal liver, reducing the risk of liver failure.

190 patocellular carcinoma; however, its role in normal liver regeneration and hepatocyte proliferation i

191 Down-regulation of Tob1 is required for normal liver regeneration, and Tob1 controls hepatocyte

192 or interfered with several key components of normal liver regeneration, significantly inhibiting prog

193 M1 (FoxM1) expression, which is required for normal liver regeneration, was suppressed by D10 treatme

194 atocyte proliferation, and are necessary for normal liver regeneration.

195 ment of BM LSEC progenitors is necessary for normal liver regeneration.

196 systemic adipose stores may be essential for normal liver regeneration.

197 hanges in systemic adipose metabolism during normal liver regeneration.

198 se events may be essential for initiation of normal liver regeneration.

199 Foxm1b) transcription factor is required for normal liver regeneration.

200 Conversely, predominance of MET favors more normal liver regeneration.

201 patic steatosis may actually be required for normal liver regeneration.

202 atic PPARgamma activity may be essential for normal liver regeneration.

203 tion and signaling pathways important during normal liver regeneration.

204 ar receptor-dependent bile acid signaling in normal liver regeneration.

205 ly regulated during and may be essential for normal liver regeneration.

206 d that complement activation is required for normal liver regeneration.

207 te-derived secreted protein, is required for normal liver regeneration.

208 ignals as regulated during and essential for normal liver regeneration.

209 e, CD1d(-/-) and Jalpha281(-/-) mice, showed normal liver regeneration.

210 (+)/cytokeratin-19(-) and contain all of the normal liver repopulation capacity found in fetal liver.

211 Further analysis of normal liver revealed a minor alternative splicing varia

212 in HCC liver biopsy specimens compared with normal liver RNA.

213 Human fibrotic and normal liver samples were analysed immunohistochemically

214 In addition, normal liver samples were compared with each other to de

215 tosis had reduced PEDF levels, compared with normal liver samples.

216 minished in fibrotic rat liver compared with normal liver; similarly, miR 19b expression was markedly

217 Normal liver sinusoidal endothelial cells (LSECs) promot

218 smooth muscle actin, whereas fatty liver and normal liver specimens do not express IL-13Ralpha2.

219 expression is increased in PBC livers versus normal liver specimens.

220 rformed on 18 additional primary CCAs and 12 normal liver specimens.

221 Normal liver stiffness maintained functional gene regula

222 The 95th percentile of normal liver stiffness was 2.8 kPa.

223 Purpose To determine normal liver stiffness, and associated normal ranges for

224 normal-liver SUV, ratio of T SUV max to mean normal-liver SUV, and score combining tumor volume and T

225 r (T SUV max), ratio of T SUV max to maximal normal-liver SUV, ratio of T SUV max to mean normal-live

226 ty concentration equal to or higher than the normal liver (T/N ratio >/= 1).

227 d by continuing corticosteroid therapy until normal liver test results and normal liver tissue are wi

228 Provided normal liver tests and the absence of cardiac arrest in

229 terial was insufficient in 1 patient; 11 had normal liver tests; and 2 patients had developed alcohol

230 In normal liver, the major cellular source of HGF is the he

231 hepatocytes proliferate at any given time in normal liver, the mechanisms involved in the maintenance

232 Despite high levels of SMN protein in normal liver, there is no comprehensive study of liver p

233 In normal liver, Thy-1(+) cells are a heterogeneous populat

234 has recently been shown to be essential for normal liver, thyroid and forebrain development.

235 We used quantitative RT-PCR in a cohort of normal liver tissue (n = 8), hepatitis C virus (HCV)-ind

236 s significantly higher than in corresponding normal liver tissue (P < 0.001).

237 therapy until normal liver test results and normal liver tissue are within normal limits, institutin

238 blastomas (HPBL), tissue adjacent to HCC and normal liver tissue derived from normal livers and hepat

239 s did not increase the proliferation rate in normal liver tissue even when the protein was localized

240 Compared with normal liver tissue from healthy individuals, the amount

241 m patients with AH or alcoholic cirrhosis or normal liver tissue from hepatic resection.

242 tumor or target volume outline while sparing normal liver tissue from high-dose radiation.

243 naire data from healthy volunteers (n = 11), normal liver tissue from public repositories and patient

244 Analysis of tumors and surrounding normal liver tissue in DEN-treated HNF4alpha knockout mi

245 icrodissected tumor tissue and corresponding normal liver tissue of 156 patients with Klatskin tumors

246 A minority of patients had normal or nearly normal liver tissue on long-term follow-up biopsy.

247 2 tumors versus that in adjacent and distant normal liver tissue primarily by constricting normal dis

248 n acellular liver tissue cubes (ALTCs) using normal liver tissue unsuitable for transplantation.

249 iver tissues with HCC and related cirrhosis; normal liver tissue was used as control.

250 ncer patients, as well as non-cancer-related normal liver tissue, we first determined changes in gene

251 In contrast, FHL2 expression was absent in normal liver tissue.

252 o differentiate areas of liver fibrosis from normal liver tissue.

253 and hepatic arterial fraction for tumors and normal liver tissue.

254 APRIL/BCMA is enhanced in HCC, compared with normal liver tissue.

255 d for the tumor and the adjacent and distant normal liver tissue.

256 distant (68.0 vs 28.3 mL/min/100 g, P = .02) normal liver tissue.

257 Low levels of TACE were detected in normal liver tissue.

258 ithin the HCC region but not in the adjacent normal liver tissue.

259 cations at varied powers in two locations in normal liver tissue.

260 mal human embryonic liver cell line CL-48 or normal liver tissue.

261 (grade 3), or lower than (grade 4) uptake in normal liver tissue.

262 2-fold higher expression in HCC compared to normal liver tissue.

263 nt structural or functional perturbations of normal liver tissue.

264 idal endothelial markers similar to those in normal liver tissue.

265 s studies focused on the effect of aging in "normal" liver tissue, but these studies were compromised

266 .0%-98.0%, respectively), a higher tumour-to-normal-liver-tissue signal ratio (5.33 versus 1.45) and

267 imals were sacrificed and HDV replication in normal liver tissues and in center masses of HCCs was ev

268 r in hepatocellular carcinoma tumors than in normal liver tissues and that pFOXA2 (S107/111) expressi

269 Imaging was performed in normal liver tissues and tumors before and after IRE.

270 Normal liver tissues showed methylation primarily in gro

271 47 samples including 27 HCC and 20 adjacent normal liver tissues using the Illumina HumanMethylation

272 s well as 42 independent HCV cirrhotic and 6 normal liver tissues were studied using high-density oli

273 ar carcinoma tissues, compared with adjacent normal liver tissues.

274 on appears to be comparable in most HCCs and normal liver tissues.

275 tocellular carcinomas compared with matching normal liver tissues.

276 bundant in HCV-positive livers compared with normal liver tissues.

277 n and 10 nontumoral cirrhotic tissues and 10 normal liver tissues.

278 o the cancer cell lines and not the adjacent normal liver tissues.

279 ts expression is very low or undetectable in normal liver tissues.

280 kinase 1 (CHK1) were higher in HCCs than in normal liver tissues.

281 SLSRFA completely and safely ablates normal liver to a depth of at least 4 mm at 45 W/4 cm tr

282 lation zone, the margin, and the surrounding normal liver to calculate a TRC ratio, which was then co

283 wise increase in the mean TAG/DAG ratio from normal livers to NAFL to NASH (7 versus 26 versus 31, P

284 likely to be C282Y homozygotes if they have normal liver transaminase activities.

285 Normal liver uptake (SUV(mean)) showed an average differ

286 was recorded for lesions, and SUV(mean) for normal liver uptake.

287 ased median ratio of hepatic tumor uptake to normal-liver uptake was 3.9 (range, 1.8-22.2).

288 Ablation depth in normal liver varied from 3 to 20 mm.

289 n vitro observations, we demonstrate that in normal liver VEGFR-2 is activated and BMP4 expression is

290 The fraction of affected normal liver volume ranged from 0.07 to 0.30.

291 ure of enhancement at T1-weighted imaging in normal liver was 53 degrees -57 degrees C.

292 A-4 in some HCC tissues and their absence in normal liver was established by immunohistochemistry sta

293 Results: The median SUV(max) in normal liver was significantly higher before treatment (

294 n analysis of the HCV-HCC tumors compared to normal livers, we found an important number of genes rel

295 ity-surface area product (PS) for tumors and normal liver were calculated from phase 1 with and witho

296 MR imaging parameters between the tumor and normal liver were compared with paired Wilcoxon test.

297 lesterol ester, and phospholipid contents in normal livers were quantified and compared to those of N

298 HCCs and matching noncancerous liver and 22 normal livers, were analyzed for methylation.

299 IGF2 is paternally expressed, as well as in normal liver where gene expression is biallelic.

300 liver diseases relative to its expression in normal liver, which suggests a role for the TWEAK/Fn14 p