ライフサイエンスコーパス: normal liver

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

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

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

4 go either RF or IRE ablation of noncancerous 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 essed in adipose tissue, but undetectable in normal liver.

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

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

17 an cirrhotic peritumoral tissue, compared to normal liver.

18 unctional similarities to bile duct cells in normal liver.

19 lic functions along the portocentral axis in normal liver.

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

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

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

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

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

25 ctivation, had variable expression levels in normal livers.

26 Whole organ levels of GP73 were low in normal livers.

27 ic livers was lower than in experiments with normal livers.

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

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

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

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

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

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

45 dy weight and fertility but shows remarkably normal liver and muscle metabolite levels.

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

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

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

49 All patients had normal liver and renal function.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 tumors was significantly higher than that in normal liver ( approximately 3-fold) in rats receiving p

65 in blood flow and bile production, preserved normal liver architecture, and significantly reduced liv

66 y Hnf4alpha in hepatocytes are essential for normal liver architecture, including the organization of

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 Analysis of normal livers by cDNA microarrays disclosed 2418 unique

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

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

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

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

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

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

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

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

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

87 antly higher expression of both receptors in normal liver compared with an HCC specimen.

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

89 Normal liver contained rare COL15A1-immunoreactive cells

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

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

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

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

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

95 orodibenzo-p-dioxin as well as regulation of normal liver development.

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

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

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

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

100 in younger persons and those with repeatedly normal liver enzymes.

101 Normal liver evaluations were similar, except with margi

102 Normal liver expresses MAT1A, which is silenced in hepat

103 ted IGF-I messenger RNA (mRNA) expression in normal liver from tumor-burdened animals in the absence

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

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

113 istory and were hemodynamically stable, with normal liver function and short hospital stay.

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 Expression of A20 preserves normal liver function as assessed by prothrombin time.

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

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

119 The patient has subsequently maintained normal liver function tests on low-dose prednisone alone

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

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

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

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

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

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

126 period; however, all donors have maintained normal liver function without long-term complications.

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

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

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

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

131 tly established in immunocompetent mice with normal liver function.

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

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

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

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

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

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

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

139 similation and cytoplasmic PAP hydrolysis to normal liver function.

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

141 In normal livers, GP73 was constitutively expressed by bili

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

143 nsduced hepatocytes expanded clonally during normal liver growth and secreted enzyme with mannose 6-p

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

145 edly increased yCD expression in tumors over normal liver (>4-fold) measured both by levels of mRNA a

146 of transplanted cells to proliferate in the normal liver hampers cell therapy.

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

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

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

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

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

152 0 kg/m(2)) patients: (1) obese normal group (normal liver histology), (2) simple steatosis (SS), (3)

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

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

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

156 thy, had normal transaminase levels, and had normal liver histology.

157 on of aminotransferase levels and relatively normal liver histology.

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

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

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

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

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

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

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

165 The normal liver is characterized by immunologic tolerance.

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

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

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

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

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

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

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

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

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

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

176 In normal livers, NTG and SNAP induced similar vasorelaxant

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 Interleukin-6 (IL-6) is required for normal liver regeneration, but the specific cellular sou

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

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

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

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

199 hanges in systemic adipose metabolism during normal liver regeneration.

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

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

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

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

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

205 tion and signaling pathways important during normal liver regeneration.

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

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

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

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

210 -dependent fashion, and IL-6 is required for normal liver regeneration.

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

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

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

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

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

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

217 Human fibrotic and normal liver samples were analysed immunohistochemically

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

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

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

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

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

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

224 Normal liver stiffness maintained functional gene regula

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

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

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

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

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

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

231 In the normal liver, the interleukin (IL)-6/STAT-3 pathway is t

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

233 achieve very low levels of expression in the normal liver, the major organ responsible for blood clea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 2 tumors versus that in adjacent and distant normal liver tissue primarily by constricting normal dis

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

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

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

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

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

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

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

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

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

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

260 2-fold higher expression in HCC compared to normal liver tissue.

261 nt structural or functional perturbations of normal liver tissue.

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

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

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

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

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

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

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

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

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

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

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

283 lower vasorelaxant responses, compared with normal livers, to both NTG (P <.0001) and SNAP (P =.0020

284 iral and nonviral human liver disease and in normal livers, to identify its cellular sources, and to

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

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

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

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

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

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

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

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

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

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

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

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

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

298 gher level of NQO1 transcripts compared with normal liver, whereas biliary NQO2 levels were significa

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

300 e with mutations in SCD-1 had histologically normal livers with significantly reduced triglyceride st