ライフサイエンスコーパス: liver

1 red from all other organs except kidneys and liver.

2 stimulates de novo lipogenesis (DNL) in the liver.

3 to mice induces >80% editing of Pcsk9 in the liver.

4 was observed in the small intestine and the liver.

5 otential to metastasize to sites such as the liver.

6 ncreased autoaggression activity against the liver.

7 uses lipid accumulation and apoptosis in the liver.

8 n ABCC6 mutants transiently expressed in the liver.

9 ally inert feathers and metabolically active liver.

10 he four other major SULTs found in brain and liver.

11 g a series of competition experiments in the liver.

12 ance of drugs and foreign compounds from the liver.

13 in the pelvic region with metastases to the liver.

14 lipid metabolism and its loss leads to fatty liver.

15 mean overestimation of 9.3% +/- 7.1% in the liver.

16 ed the immune cell content of the spleen and liver.

17 g units were found in the lungs, spleen, and liver.

18 with hepatocellular carcinoma and cirrhotic livers.

19 e-6-phosphatase, above the levels in control livers.

20 of genes encoding these proteins in control livers.

21 enitor cells in vitro and in embryonic mouse livers.

22 erfusion fluid and matched to 5 RBC-perfused livers.

23 bit the trophozoite proliferation in amoebic liver abscess induced in hamster.

24 tected a decrease in FFA accumulation in the liver after mice were given injections of deoxycholic ac

25 nversion surgery were disease limited to the liver and a higher median number of cycles (close to 12)

26 (SnPP) decreased heme-iron recycling in the liver and ameliorated anemia in the Th3/(+) mice.

27 fness measurement across larger areas of the liver and can be performed in a single breath hold.

28 nc-KDM5D-4 in key processes related to fatty liver and cellular inflammation associated with atherosc

29 ecreased T cell numbers and functions in the liver and lymphoid tissues.

30 22,23-dihydroavermectin B1a in fat, kidney, liver and muscle bovine tissues using UHPLC-MS/MS.

31 Metabolomic analysis of the liver and plasma shows a positive correlation between ob

32 is factor-alpha, interleukins, hemogram, and liver and renal function tests were performed at days 0

33 synthesized primarily and abundantly in the liver and secreted through the kidneys, exhibit male-bia

34 nt Y699 site is significantly reduced in the liver and skeletal muscles of Cry-deficient mice.

35 TM6SF2 is expressed predominantly in liver and small intestine, sites for triglyceride-rich l

36 nonuclear phagocyte system (MPS) such as the liver and spleen.

37 DBAN after it was linked with cancer of the liver and stomach in rodents.

38 ssion and the metabolome were studied in the livers and plasma from these mice.

39 genic mice that expressed KCP in the kidney, liver, and adipose tissues were resistant to developing

40 g revealed numerous metastases in the lungs, liver, and brain.

41 onal, immune, respiratory, gastrointestinal, liver, and endocrine systems, by influencing cellular si

42 Skeletal muscle, liver, and plasma samples were analyzed by gas chromatog

43 ugated phosphorothioate modified ASOs in the liver as evidenced by the loss of activity of GalNAc con

44 The liver as transplantation site for human pancreatic islet

45 ocietal perspective across a range of HCV(+) liver availability rates.

46 Viral serology, viral load, and liver biochemistry were performed at regular intervals d

47 ase over a 10-year period that had undergone liver biopsies (n = 363) were scored for the presence of

48 d with progression from steatosis to NASH in liver biopsies.

49 Six patients on therapy underwent a liver biopsy for flow cytometric analysis.

50 We obtained liver biopsy samples from 69 patients with chronic HCV i

51 ere consistent across subsamples of the same liver but differed between muscle subsamples and between

52 -lyase levels in tissues such as adipose and liver, but the impact of diet on acetyl-CoA and histone

53 ver tumorigenesis and clarify the classes of liver cancer based on molecular features and how they af

54 er CD133, which is located on the surface of liver cancer cells.

55 Unspecified liver cancer decreased over time and constituted <10% of

56 ntries with potentially increasing trends of liver cancer for preventive actions.

57 sorafenib patients had more Barcelona Clinic Liver Cancer stage D ( P < .001), higher Model for End-S

58 were early-stage tumors by Barcelona Clinic Liver Cancer, Cancer of the Liver Italian Program, and t

59 as a potential therapeutic agent for primary liver cancer.

60 The estimated annual number of liver cancers increased over time, but the standardized

61 er time and constituted <10% of all reported liver cancers.

62 ulture system, wherein primary human healthy liver cells form long-term expanding organoids that reta

63 H2.35 liver cells with shRNA knockdown of ANLN formed tumors m

64 on targeted to candidate enhancers active in liver cells, enriched for the binding sites of the FOXA1

65 ne, displaying the highest toxicity in HepG2 liver cells.

66 importing citrate from the circulation into liver cells.

67 The serum and liver cholesterol and TAG levels in rats fed with 1,3-DA

68 d chronic liver infection, which may lead to liver cirrhosis and hepatocellular carcinoma.

69 AP activity in human patients diagnosed with liver cirrhosis and to determine the effectiveness of a

70 Portal vein hypertension (PVH) in liver cirrhosis complicated with portal venous thrombosi

71 estimated as the incidence rate of alcoholic liver cirrhosis in these patients relative to the genera

72 Advanced stages of liver cirrhosis lead to a dramatically increased mortali

73 Liver cirrhosis was already present in 62 patients at fi

74 HBV is a major cause of viral hepatitis, liver cirrhosis, and hepatocellular carcinoma.

75 liver infections other than HBV and HDV, or liver cirrhosis.

76 Liver collagen fractional synthesis rate (FSR) and plasm

77 (heterogeneity P<0.001), but RRs for serious liver complications appeared higher in women (heterogene

78 ls in the UK for patients with unresectable, liver-confined hepatocellular carcinoma.

79 Mouse liver contains two natural killer (NK) cell populations,

80 In addition, tumor-to-liver contrast was superior in the parametric Ki images

81 % of total 5-phosphorylated guide strands in liver, correlating with a 2.7 log10 reduction of HBsAg.

82 naling and increase retention of HSCs in the liver could increase their antifibrotic activities and b

83 Here, we have used mouse liver CRMs involved in regulatory activities of the hepa

84 ease (MELD) score within 3 months of initial liver CT imaging between January 3, 2006, and May 30, 20

85 Heavy alcohol use can lead to progressive liver damage, especially in individuals with chronic hep

86 ategy for preventing and treating IR-induced liver damage.

87 , and 29% had at least 1 previous episode of liver decompensation.

88 y, we demonstrated that development of fatty liver depends on adipocyte GH signaling.

89 Liver-derived stem cells are in clinical development for

90 ssing in hepatocytes and thus the outcome of liver-directed gene therapy using AAV vectors and showed

91 rly non-AIDS infections (10.8, 9.8-12.0) and liver disease (3.7, 3.3-4.2).

92 ary outcomes were improvement in severity of liver disease (change in MELD) at 3 months and the trend

93 ients with cirrhosis and Model for End-Stage Liver Disease (MELD) score within 3 months of initial li

94 impair renal function in non alcoholic fatty liver disease (NAFLD) by altering inflammatory signallin

95 often found increased in nonalcoholic fatty liver disease (NAFLD); however, if this is due to increa

96 e Lille (P < 0.0001) and Model for End-Stage Liver Disease (P < 0.0001) scores were independent progn

97 iffusion parameters in patients with chronic liver disease and to compare the diagnostic accuracy of

98 wing recurrence included model for end-stage liver disease at LT >23, time to recurrence, >3 recurren

99 , which, in turn, exacerbate ethanol-induced liver disease both in mice and humans.

100 itlists to evaluate changes in the burden of liver disease in the United States.

101 Liver disease is a major cause of non-AIDS-related death

102 Hepatitis C virus (HCV)-mediated chronic liver disease is a serious health problem around the wor

103 cardiovascular disease risk is elevated and liver disease is common.

104 Liver disease mortality increased by 400% in the UK betw

105 nicotine may act as a mitogen in cholestatic liver disease processes, thereby facilitating malignant

106 A liver disease progression Markov model, which used a lif

107 er fibrosis is a critical step for end-stage liver disease progression.

108 nodeficiency virus (HIV) are at high risk of liver disease progression.

109 ge D ( P < .001), higher Model for End-Stage Liver Disease Sodium scores ( P < .001), higher Child-Tu

110 ion Anxiety Stress Scales (DASS-21), (3) the Liver Disease Symptom Index-2.0 (LDSI-2.0) for testing d

111 is the direct cause (eg, nonalcoholic fatty liver disease) or is a significant risk factor, such as

112 ual cytokine levels in patients with chronic liver disease, but comprehensive cytokine profiling data

113 Ascites, liver disease, diabetes, obesity, and primary suture rep

114 n pneumonitis, and radioembolization-induced liver disease, which may occur despite careful pretreatm

115 ccumulation, a hallmark feature of alcoholic liver disease.

116 t Africa, and from patients with established liver disease.

117 n pediatric patients with nonalcoholic fatty liver disease.

118 clinical development for inborn and acquired liver diseases and could represent a curative treatment

119 Prevalence of fatty liver diseases and iron overload was calculated (weighte

120 pharmaceuticals to treat heritable metabolic liver diseases have been hampered by the lack of models.

121 Toxin-induced liver diseases lack effective therapies despite increase

122 tients with colorectal liver metastases with liver-dominant disease after chemotherapy.

123 ression of Amigo2 in QRsP-11 cells increased liver endothelial cell adhesion and liver metastasis.

124 Results Liver endothelial cells were successfully isolated, cult

125 g protein, hepatocyte specific (CREBH), is a liver-enriched, endoplasmic reticulum-tethered transcrip

126 nisms might be involved in the regulation of liver enzyme level.

127 Additionally, assay of liver enzymes and histology analysis of local tissues id

128 Consistently, liver enzymes were significantly increased in cholestati

129 Together, M2-like macrophages in fibrotic liver exert the protective effects against lethal insult

130 une 2013 to June 2015, we identified 1768 DD livers exported to regional candidates with MELD scores

131 2(+) non-NK innate-like cells present in the liver expresses IFN-gamma and can confer protection agai

132 ve therapy for toxic ingestion or idiopathic liver failure (DT) in a level 1 trauma center and large

133 Liver failure (LF) is associated with prolonged hospital

134 ith multiple organ failure (acute-on-chronic liver failure grade 2-3).

135 ry and it is the second most common cause of liver failure.

136 Baseline liver fat (AUROC 0.84; 95%CI: 0.76-0.92) predicted liver

137 Baseline liver fat (OR 2.17; 95%CI: 1.05-4.46) was an independent

138 lic abnormalities as the predictor of future liver fat and fibrosis.

139 fat (AUROC 0.84; 95%CI: 0.76-0.92) predicted liver fat at 11.3 years more accurately than routinely a

140 These data show that liver fat is more important than the associated metaboli

141 We examined levels of liver fat, lipogenic indices, markers of inflammation, s

142 iciently depicts the presence of significant liver fibrosis and, less accurately, mild liver fibrosis

143 use of cost, treatment is often denied until liver fibrosis has progressed to at least moderate fibro

144 r communication in the activation of HSC for liver fibrosis in HCV infection.IMPORTANCE HCV-associate

145 nt liver fibrosis and, less accurately, mild liver fibrosis in pediatric patients with nonalcoholic f

146 s in HCV infection.IMPORTANCE HCV-associated liver fibrosis is a critical step for end-stage liver di

147 Our findings demonstrated that liver fibrosis manifested a beneficial role for host sur

148 ecreased HBV DNA, HBV RNA, HBsAg, HBeAg, and liver fibrosis markers in serum and tissues, and improve

149 Purpose To determine the relationship of liver fibrosis, inflammation, and steatosis with the mag

150 n our efforts to generate a new medicine for liver fibrosis, we sought to identify improved small mol

151 involve in the hepatoprotection conferred by liver fibrosis.

152 be developed for treatment of patients with liver fibrosis.

153 ccuracy of the imaging parameters in staging liver fibrosis.

154 stellate cells to promote the resolution of liver fibrosis.

155 Before birth, B cells develop in the fetal liver (FL).

156 eef cattle, but it is unclear at what levels liver fluke burdens cause production losses.

157 l estimated that cattle classified as having liver fluke damage had on average 10 days greater slaugh

158 ulted in 49 organ transplants (31 kidney, 14 liver, four heart), with only one case of TMAT, which oc

159 rther be used to differentiate between fatty liver from healthy liver in an experimentally arrived mo

160 Livers from Alb/SND1 mice exhibited a relative increase

161 Oxidative damage was observed in livers from Ppargc1a(f/+)Alb-cre(+/0) mice of each sex,

162 a cell-autonomous manner, but was greater in livers from the female mice.

163 ntigen-positive viremic patients with normal liver function and the incorporation of new biomarkers t

164 sistance, serum ferritin, lipid profile, and liver function tests improved irrespective of bloodletti

165 Greatest impact on liver function was found in animals with polymicrobial s

166 is contraindicated in patients with impaired liver function, and activated partial thromboplastin tim

167 recurrence were compared with demographics, liver function, basic immune markers, treatment dose, an

168 ncers in highly expressed genes critical for liver function.

169 already in an active chromatin state in male liver generally showed early cGH responses; genes in an

170 MAIT cells from the liver had higher levels of activation and cytotoxicity t

171 Assessing liver health may be important for reducing the risk of f

172 Solitary kidney, liver, heart, and lung transplants performed between Jan

173 -tissue organ-on-a-chip system, comprised of liver, heart, and lung, and highlight examples of inter-

174 ent expression of hundreds of genes in mouse liver, imparting sex differences in hepatic drug/lipid m

175 fferentiate between fatty liver from healthy liver in an experimentally arrived mouse model using non

176 titis B virus (HBV) causes acute and chronic liver infection, which may lead to liver cirrhosis and h

177 ere excluded if they had HDV superinfection, liver infections other than HBV and HDV, or liver cirrho

178 entecavir reduced viral loads and decreased liver inflammation.

179 Its overuse provokes liver injury and it is the second most common cause of l

180 All cases of drug-induced liver injury enrolled into a prospective database over a

181 ms to impair hepatocyte proliferation during liver injury to evaluate the contribution of non-hepatoc

182 s NR may be therapeutic in settings of acute liver injury.

183 d indicate 20% as a threshold of more severe liver injury.

184 the transfer of lipids onto CD1d, regulates liver iNKT cell homeostasis in a manner dependent on hep

185 ditions (hemodynamic, biological, renal, and liver insults) than donors without extracorporeal membra

186 The liver integrates multiple metabolic pathways to warrant

187 on 10-fold, and causes a complete absence of liver invasion as mutants fail to attach to host cells.

188 The liver is a major factor VIII (FVIII) synthesis site, and

189 The liver is frequently affected in patients with active bru

190 The liver is the only organ in mammals that fully regenerate

191 and tested as inhibitors against muscle and liver isoforms of glycogen phosphorylase (GP).

192 Barcelona Clinic Liver Cancer, Cancer of the Liver Italian Program, and tumor-node-metastasis staging

193 Patients with liver LELC display distinctive demographics and tumor ch

194 etion of the Lipa gene in mice decreased the liver levels of RE, most likely as the result of a gradu

195 imaging tiny (<1 mm) micrometastases in the liver, lung, pancreas, kidneys, and bone, that have diss

196 to adult baseline values to detect pediatric liver mechanical abnormalities may not allow detection o

197 in a further breakdown of amino acids in the liver, mediated by increased glucagon, without preventin

198 clinical benefit in patients with colorectal liver metastases with liver-dominant disease after chemo

199 on of prior systemic therapy and presence of liver metastases.

200 ic lineages of two CRC patients with matched liver metastases.

201 alterations in pancreatic primary tumors and liver metastases.

202 ritical for the formation and maintenance of liver metastasis derived from colorectal cancers.

203 ncreased liver endothelial cell adhesion and liver metastasis.

204 in hepatocytes through IL-6 produced in the liver microenvironment.

205 detection ability, particularly of bone and liver micrometastases.

206 s markers in serum and tissues, and improved liver morphology more effectively than single treatments

207 re rescued by re-expression of Ptprg only in liver of mice lacking Ptprg globally.

208 The virus replicates to high titers in the liver of these animals after intravenous infection, whil

209 Nrf2 recruitment to the Srebp-1c promoter in livers of BPA-exposed mice was observed.

210 result of a gradual disappearance of HSCs in livers of Lipa(-/-) mice.

211 th H3K4me2 were significantly reduced in the livers of Nr2e3(rd7) (Rd7) mice that express low NR2E3 r

212 mice that express low NR2E3 relative to the livers of wild-type mice.

213 were delisted received a median 1 pediatric liver offer and waited a median of 33 days.

214 Of 11,328 donor livers offered to children, 2533 (12%) were transplanted

215 the HCV present at baseline persisted in the liver or another compartment and reemerged in the blood

216 and FGF21 and UCP1 mRNAs were not induced in liver or brown adipose tissue (BAT).

217 Fatty liver, oxidative stress, and mitochondrial dysfunction a

218 rge region of interest, inclusive of as much liver parenchyma as possible in the right lobe while avo

219 Biopsies were independently scored by six liver pathologists for interobserver agreement.

220 a large scale to monitor the progression of liver pathology in schistosomiasis japonica endemic area

221 A program of normothermic ex situ liver perfusion (NESLiP) was developed to facilitate bet

222 Normothermic ex situ liver perfusion has the potential to increase liver util

223 e.g., higher in NASH than nonalcoholic fatty liver, positive correlation with fibrosis score and live

224 The liver provides a tolerogenic immune niche exploited by s

225 In quiescent liver, PTEN causes pathological steatosis when lost, whe

226 s illuminate a previously unknown program of liver regeneration after acute injury and allow for expl

227 Various mouse models of liver regeneration after extended partial hepatectomy an

228 EDHB selectively augmented liver regeneration after partial hepatectomy and portal

229 ibitor ethyl-3,4-dihydroxybenzoate (EDHB) on liver regeneration and metastatic tumor growth.

230 -scale proteomics to identify key players in liver regeneration and the importance of posttranslation

231 l killer T cells is markedly elevated during liver regeneration and their activation under different

232 ose of APAP, resulted in early initiation of liver regeneration in a dose-dependent manner, without m

233 fully reduced HMGB1 orchestrates muscle and liver regeneration via CXCR4, whereas disulfide HMGB1 an

234 eased immediately after PH (priming phase of liver regeneration) in control mice, but this effect was

235 NAD availability is limiting during liver regeneration, and supplementation with precursors

236 rograms with potential applications to adult liver regeneration.

237 e role of natural killer T cells in impaired liver regeneration.

238 H) has become a major cause of cirrhosis and liver-related deaths worldwide.

239 dy is the overall shift toward excitation in liver-related hypothalamic neurons in the diabetic condi

240 We assessed non-liver-related non-acquired immunodeficiency syndrome (AI

241 when lost, whereas its role in regenerating liver remains unknown.

242 We suggest that AhR may serve to adjust liver repair and to block tumorigenesis by modulating st

243 Proteomic analysis of the liver reveals global differences in hepatic proteins whe

244 also given SAMe (30 mg/kg/day for 8 weeks); liver samples were collected and analyzed histologically

245 ion by stellate cells and CD34 expression by liver sinusoidal endothelial cells remained stable, cons

246 ttenuates insulin's metabolic actions in the liver, skeletal muscle and adipose tissue.

247 igated whether inhibiting cytokinesis in the liver slows tumor growth without compromising the health

248 Interestingly, liver specific Ant2 knockout mice are leaner and resista

249 egradation of CUGBP1, we generated mice with liver-specific deletion of Gank.

250 Liver-specific knockout or adenovirus-mediated overexpre

251 circulation stimulated glucose uptake by the liver spheroids, while the latter, in the absence of ins

252 aginase is rapidly cleared from the serum by liver-, spleen-, and bone marrow-resident phagocytic cel

253 During the liver stage of a malaria infection, Plasmodium parasites

254 At 56 and 84 Hz, liver stiffness increased with age (Spearman correlation

255 Comparing pediatric liver stiffness to adult baseline values to detect pedia

256 positive correlation with fibrosis score and liver stiffness) and correlated with hemoglobin A1C.

257 6) was an independent predictor of increased liver stiffness.

258 rm long-term expanding organoids that retain liver tissue function and genetic stability.

259 periostin and VCAM-1 was the inflamed sheep liver tissue.

260 2013 through May 2017, along with tumor-free liver tissues (control tissues) and peripheral blood sam

261 We find the HCV-infected liver to have a pattern of acquisition of DNA methylatio

262 sulin action in lean mice but sensitizes the liver to insulin during the challenge of HF feeding.

263 LV12 cells reduced attachment/metastasis to liver to the same level as that observed with QRsP-11 ce

264 btained from Alb-R26(Met) HCC versus control livers to design an "educated guess" drug screen, which

265 Obesity increases risk for liver toxicity by the anti-leukemic agent asparaginase,

266 g that patients who are urgently requiring a liver transplant are prioritized.

267 Among pediatric liver transplant candidates in the US, children who died

268 ith DCDD from the Improving DCDD Outcomes in Liver Transplant consortium demonstrates significant dif

269 dict graft failure or primary nonfunction at liver transplant decision time assists utilization of sc

270 h only one case of TMAT, which occurred in a liver transplant recipient and resulted in death from bl

271 th a short course (in hospital only) HBIG in liver transplant recipients with HBV DNA less than 100 I

272 d 2 generics in individuals with a kidney or liver transplant.

273 C) may be at higher risk of malignancy after liver transplantation (LT) compared to other LT recipien

274 ta that are associated with survival without liver transplantation at 90 and 180 days after initiatio

275 e originally defined in the context of adult liver transplantation for patients with hepatocellular c

276 prevalence in the population with data from liver transplantation waitlists to evaluate changes in t

277 rapidly becoming the leading indication for liver transplantation.

278 ARS was used to support patients with severe liver trauma (SLT), in ALF patients as a bridge to trans

279 and decreased the alcohol-induced increased liver triglyceride and fat droplet accumulation.

280 function is most visible after fasting, when liver triglyceride increases manyfold but circulating se

281 two independent clones seeded the metastatic liver tumor after having diverged at different time poin

282 nodular hyperplasia (FNH) is a common benign liver tumor for which conservative management is indicat

283 transgenic zebrafish resulted in accelerated liver tumor progression in males.

284 e review hypotheses of the cell of origin of liver tumorigenesis and clarify the classes of liver can

285 dy shows that lipogenesis is dispensable for liver tumorigenesis in mice treated with DEN, and identi

286 ced diethylnitrosamine-induced (DEN-induced) liver tumorigenesis that correlated with increased DEN-i

287 who had SVR to interferon-free therapy at 6 Liver Units in Spain.

288 s showed shorter blood half-times and higher liver uptake than the radiolabeled counterparts.

289 iver perfusion has the potential to increase liver utilization, but more work is required to define f

290 some HCC tissues and their absence in normal liver was established by immunohistochemistry staining a

291 In the PA mouse liver we identified 14 significantly dysregulated miRNAs

292 ng senescence in single cells in vivo in the liver, we demonstrate that this activates tissue-specifi

293 Although unique sequences in plasma or liver were observed, in the majority of cases the most d

294 ce were given injections of thiostrepton and livers were collected and analyzed by immunoblotting, im

295 Five discarded high-risk human livers were perfused with HBOC-based perfusion fluid and

296 G') comprised <63% of total miR-122 in human liver, whereas other variants (23-3A, 23-3U, 21-3U) repr

297 ists utilization of scarce resource of donor livers, while ensuring that patients who are urgently re

298 litate better assessment and use of marginal livers, while minimizing cold ischemia.

299 deregulation of the miR-155 target gene the liver X receptor (LXR)alpha in lung fibroblasts and macr

300 n inflammatory signaling and derepression of liver X receptor activity.