ライフサイエンスコーパス: ALD

1 ALD and NAFLD account for nearly 30% of liver transplant

2 ALD growth of Ni, Co, Fe, and Cr films is demonstrated.

3 ALD is seen commonly in patients with a long-standing hi

4 ALD of Pt on the NW surface led to a highly conformal co

5 ALD prevalence patterns were complex and were modified b

6 ALD progression is marked by fatty liver and hepatocyte

7 ALD was found to be successfully conjugated to the GNPs

8 ALD was measured over the period of 6 months before to 3

9 CV (OR = 1.45; 95% CI: 1.35-1.55; P < .001), ALD (OR = 1.15; 95% CI: 1.06-1.24; P < .001), or HCV and

10 erating nodules, fibrosis, and cirrhosis.(1) ALD develops via a complex process involving parenchymal

11 25 ALD cycles of TiO2 growth are found to be the optimized

12 .003) for eyes of children with age-adjusted ALD < -1 mm (myopic).

13 mer's, Parkinson's and adrenoleukodystrophy (ALD).

14 X-linked adrenoleukodystrophy (ALD) is a devastating inherited neurodegenerative diseas

15 X-linked adrenoleukodystrophy (ALD) may switch phenotype to the fatal cerebral form (ie

16 atively activated M2 KCs may protect against ALD and NAFLD.

17 its that fructose-1,6-bisphosphate aldolase (ALD) provides a critical link between the cytoplasmic ta

18 uding zoledronic acid (ZOL) and alendronate (ALD), have been proposed as sensitisers in gammadelta T

19 tionalized GNPs conjugated with alendronate (ALD), of the bisphosphonate group.

20 Although ALD and NAFLD recur frequently after liver transplantati

21 Finally, TgALD knockout parasites and an ALD mutant that specifically disrupts adhesin binding in

22 PBC samples (1.13 +/- 0.17, P < 0.0001) and ALD samples (0.62 +/- 0.10, P < 0.0001).

23 of 0.77% seen within the PBC (P = 0.024) and ALD groups (0.40%, P < 0.0001).

24 T cells from PSC (n = 20), PBC (n = 10), and ALD (n = 10) patients, alongside genomic human leukocyte

25 ry; however, a link between this alarmin and ALD has not been established.

26 mediates intestinal barrier dysfunction and ALD, we used TNFRI mutant mice carrying a conditional ga

27 cted from intestinal barrier dysfunction and ALD.

28 sed on lattice mismatch between the GaAs and ALD-deposited aluminum oxide due to their different coef

29 Subsequently, the ALD, GNPs, and ALD conjugated GNPs (GNPs-ALD) were analyzed by ultravio

30 15; 95% CI: 1.06-1.24; P < .001), or HCV and ALD (OR = 1.29; 95% CI: 1.18-1.42; P < .001) had higher

31 from 2887 to 3291); registrants with HCV and ALD decreased by 9% (from 880 to 803).

32 001); patients with HCV infection or HCV and ALD had similar odds for 90-day survival compared with N

33 list than patients with HCV, ALD, or HCV and ALD.

34 (ALD), or a combination of HCV infection and ALD.

35 /65 were found between the matched NAFLD and ALD cohort.

36 NAFLD and ALD each are associated with significant morbidity, impa

37 icrobial therapy for patients with NAFLD and ALD.

38 Systematic variations in shell thickness and ALD overlayer lead to photocurrent densities as high as

39 leptic Ca(II) amidinates suitable for use as ALD precursors.

40 ntioxidant capacity and SOD activity between ALD phenotypes in patients with cALD or adrenomyeloneuro

41 lammasomes mediate different aspects of both ALD and nonalcoholic fatty liver disease.

42 Key to enabling metalation by ALD In MOFs (AIM) was the synthesis of NU-1000, a new, t

43 articles (Pt-NP) decoration was performed by ALD onto TiO2 coated PAN nanofibers.

44 reactive metal reagents in the gas phase by ALD to form an outer metal ion bridging group, which can

45 In CaS ALD with 1 and H2 S, the ALD window was approximately tw

46 ype to the fatal cerebral form (ie, cerebral ALD [cALD]), the cause of which is unknown.

47 ed layer for gate oxide or contact conductor ALD has been deposited via two separate self-limiting an

48 inhibits type I NKT cells and, consequently, ALD.

49 hode backbone using Atomic Layer Deposition (ALD) and thermal treatment.

50 atinum deposited by atomic layer deposition (ALD) as a HER cocatalyst.

51 by low-temperature atomic layer deposition (ALD) as the transparent conductive oxide (TCO) layer on

52 siloxane (PDMS) via atomic layer deposition (ALD) assisted sacrificial etching.

53 Atomic layer deposition (ALD) has evolved as an important technique to coat confo

54 ed as Ni-AIM) using atomic layer deposition (ALD) in a MOF (AIM).

55 Notably, atomic layer deposition (ALD) in MOFs has recently emerged as a versatile approac

56 of the chemistry of atomic layer deposition (ALD) is presented for technologically important material

57 materials; however, atomic layer deposition (ALD) is uniquely suited to control composition and struc

58 ed precisely by the atomic layer deposition (ALD) method, whereas the terrace sites remain as active

59 Subsequent atomic layer deposition (ALD) of Al2O3 or TiO2 along with ALD-Pt deposition resul

60 Atomic layer deposition (ALD) of an alumina overcoat can stabilize a base metal c

61 d on the surface by atomic layer deposition (ALD) of either Al2O3 or TiO2 overlayers.

62 e precursor for the atomic layer deposition (ALD) of MoS2 thin films.

63 ethod that includes atomic layer deposition (ALD) of TiO2 followed by post-annealing treatment on spi

64 eport, we show that atomic layer deposition (ALD) of titania (TiO2) and alumina (Al2O3) on Ni-rich FC

65 face species during atomic layer deposition (ALD) on a silver surface.

66 tings deposited via atomic layer deposition (ALD) onto polyamide-6 nanofibers enable the formation of

67 ity and have useful atomic layer deposition (ALD) precursor properties.

68 oduce a new, robust atomic layer deposition (ALD) procedure for the preparation of molecular chromoph

69 photoelectrodes via atomic layer deposition (ALD) to examine their influence upon electron transfer (

70 The application of atomic layer deposition (ALD) to metal-organic frameworks (MOFs) offers a promisi

71 ssfully prepared by atomic layer deposition (ALD) with controlled oxidization states and tunable magn

72 e film deposited by atomic layer deposition (ALD) with optically pumped NMR (OPNMR).

73 r (LbL) deposition, Atomic Layer Deposition (ALD), and porous silicon (porSi) engineering.

74 ing followed by the atomic layer deposition (ALD), here we presented a high surface area platform as

75 n films prepared by atomic layer deposition (ALD), that require substrates to have a two-dimensional

76 yer of FeO(x) using atomic layer deposition (ALD).

77 ere synthesized via atomic layer deposition (ALD).

78 photoelectrode via atomic layer deposition (ALD).

79 from the gas phase: atomic layer deposition (ALD).

80 (ZnO) deposited by atomic layer deposition (ALD).

81 RMS) and chemical (atomic layer deposition, ALD) vapour deposition methods as a functional coating f

82 ned as age-adjusted axial length difference (ALD) (minus and plus denotes myopia and hypermetropia, r

83 oholic and nonalcoholic fatty liver disease (ALD and NAFLD) are the predominant causes of liver-relat

84 a common feature in alcoholic liver disease (ALD) and in mouse models of ethanol loading.

85 the development of alcoholic liver disease (ALD) and methionine and choline-deficient (MCD) diet-ind

86 the pathogenesis of alcoholic liver disease (ALD) and NAFLD, although studies of ALD have focused on

87 Alcoholic fatty liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are co

88 Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are si

89 Both alcoholic liver disease (ALD) and nonalcoholic fatty liver disease are characteri

90 ul for the study of alcoholic liver disease (ALD) and of other organs damaged by alcohol consumption.

91 ate immunity drives alcoholic liver disease (ALD) and that the interferon regulatory factor 3 (IRF3),

92 disease (NAFLD) and alcoholic liver disease (ALD) are common causes of chronic liver disease.

93 tics associated with advanced liver disease (ALD) at hepatitis C virus (HCV) diagnosis were examined

94 onsumption leads to alcoholic liver disease (ALD) characterized by steatosis, inflammation, and event

95 Alcoholic liver disease (ALD) develops in approximately 20% of alcoholic patients

96 Alcoholic liver disease (ALD) has been among the leading causes of cirrhosis and

97 Patients with alcohol-related liver disease (ALD) have antibodies directed to alcohol dehydrogenase (

98 The spectrum of alcoholic liver disease (ALD) is a major cause of mortality with limited therapie

99 Alcoholic liver disease (ALD) is associated with intestinal dysbiosis, increased

100 The pathogenesis of alcoholic liver disease (ALD) is not well established.

101 disease (NAFLD) and alcoholic liver disease (ALD) is still unsettled, but essential for the evaluatio

102 pathophysiology of alcoholic liver disease (ALD) remains unclear.

103 istinct spectrum of alcoholic liver disease (ALD) with intense neutrophilic (polymorphonuclear; PMN)

104 itis B virus (HBV), alcoholic liver disease (ALD), and other liver disease using International Classi

105 rus (HCV) compared to alcohol liver disease (ALD), and this reduction correlated with viral load in t

106 V) infection, NASH, alcoholic liver disease (ALD), or a combination of HCV infection and ALD.

107 the pathogenesis of alcoholic liver disease (ALD).

108 y events leading to alcoholic liver disease (ALD).

109 tant contributor to alcoholic liver disease (ALD).

110 patitis C (CHC) and alcoholic liver disease (ALD).

111 tion contributes to alcoholic liver disease (ALD).

112 diseases including alcoholic liver disease (ALD).

113 the pathogenesis of alcoholic liver disease (ALD).

114 ALOX15) in treating alcoholic liver disease (ALD).

115 ells contributes to alcoholic liver disease (ALD).

116 tis associated with alcoholic liver disease (ALD).

117 langitis (PSC), and alcoholic liver disease (ALD).

118 sed on the admixture linkage disequilibrium (ALD) is to remove the effect of source LD (SLD), which i

119 AMA1 cytoplasmic tail mutations that disrupt ALD binding in vitro showed no correlation with host-cel

120 these studies, the approximate lethal dose (ALD) exceeds 800 mug/dose and the NOAEL was 800 mug/dose

121 de (DMACl) surface species were found during ALD.

122 lized and redistribute within the MOF during ALD.

123 ional modeling to compare each subset during ALD and HCV.

124 n to have protective effects on experimental ALD.

125 to infer multiple-wave admixture by fitting ALD using a p-spectrum.

126 R antagonists may provide a new approach for ALD therapy.

127 latile and are thus promising precursors for ALD (= atomic layer deposition) and MOCVD (= metal-organ

128 Histological scoring systems for ALD and NAFLD have been proposed to monitor efficacy in

129 Patients receiving liver transplants for ALD or NAFLD have similar survival times as patients rec

130 Furthermore, ALD-depleted parasites were impaired when grown in gluco

131 The in-vitro study indicated that the GNPs, ALD and GNPs-ALD suppressed osteoclast formation in a do

132 study indicated that the GNPs, ALD and GNPs-ALD suppressed osteoclast formation in a dose-dependent

133 the ALD, GNPs, and ALD conjugated GNPs (GNPs-ALD) were analyzed by ultraviolet-visible absorbance (UV

134 The prepared GNPs-ALD were used to investigate their inhibitory effects on

135 results from these tests indicated that GNPs-ALD can be useful agents for preventing and treating ost

136 Additionally, the GNPs-ALD were applied to ovariectomy (OVX)-induced osteoporot

137 n the OVX mouse model, the mice treated GNPs-ALD had higher bone density as compared to other OVX mic

138 days on the waitlist than patients with HCV, ALD, or HCV and ALD.

139 e in the elderly, but associated with higher ALD risk among the disabled born 1945-1965.

140 1.41; P = 0.010) were associated with higher ALD risk.

141 t various phases in the progression of human ALD, we found that alcohol, in all of these models, indu

142 Indeed, bacterial decontamination improves ALD both in human and animal models.

143 In ALD, chronic ethanol exposure sensitizes Kupffer cells t

144 contribute to the abnormal gut-liver axis in ALD.

145 y specific marker of liver apoptosis both in ALD and NAFLD.

146 ssessed lipin-1 function in myeloid cells in ALD using a myeloid cell-specific lipin-1 knockout (mLip

147 potential biomarker for cerebral disease in ALD following future prospective studies.

148 reasingly is recognized as a major factor in ALD.

149 y signal that contributes to inflammation in ALD through activation of the Toll-like receptor 4.

150 eas type II NKT cells protect from injury in ALD.

151 ed for potential therapeutic intervention in ALD.

152 structure of the surface species involved in ALD and, ultimately, catalytic reactions on these suppor

153 The pathogenic role of IRF3 in ALD was independent of inflammation or Type-I interferon

154 ovel mechanism for altered beta-oxidation in ALD, and these data demonstrate for the first time that

155 on between rs738409 and HCC, particularly in ALD and CHC.

156 This association was more pronounced in ALD (OR=2.20; 95% CI: 1.80-2.67; P=4.71 x 10(-15) ) than

157 isease indicated that their up-regulation in ALD is dependent upon type I NKT cells.

158 d for understanding their pathogenic role in ALD and developing effective therapeutic approaches usin

159 ne (GSH) are known to play a central role in ALD.

160 ew targets for immunoregulatory therapies in ALD patients for halting detrimental effector T-cell res

161 suggesting a role for gut-derived toxins in ALD.

162 Liposomal ALD (L-ALD) has been suggested as a suitable alternative to lip

163 n vivo studies that liposomal alendronate (L-ALD) can sensitise cancer cells to destruction by Vgamma

164 wth was observed after treatment with both L-ALD and gammadelta T cells in pseudo-metastatic lung mel

165 Moreover, both L-ALD and t-L-ALD led to significant reductions in tumour

166 ntravenous injection of gammadelta T cell, L-ALD or the combination.

167 peptide A20FMDV2 as a targeting moiety for L-ALD, the therapeutic efficacy of this therapy can be inc

168 Higher concentrations of L-ALD (40-60muM) than L-ZOL (3-10muM) were required to pro

169 therapeutically relevant concentrations of L-ALD and gammadelta T cell could be achieved in the tumou

170 dy aims to assess the in vitro efficacy of L-ALD, in combination with gammadelta T cell immunotherapy

171 far has proven the therapeutic efficacy of L-ALD, in combination with gammadelta T cell immunotherapy

172 lung tumours were treated with L-ALD or t-L-ALD as monotherapies or in combination with ex vivo-expa

173 pendant uptake of t-L was observed, with t-L-ALD being more effective than L-ALD at sensitising A375P

174 Moreover, both L-ALD and t-L-ALD led to significant reductions in tumour growth when

175 Interestingly, t-L-ALD led to slightly higher but not significant reduction

176 tion with gammadelta T cells in vivo but t-L-ALD offered no added advantage compared to L-ALD.

177 ed, with t-L-ALD being more effective than L-ALD at sensitising A375Pbeta6 to gammadelta T cells.

178 ant reduction in tumour growth compared to L-ALD, when used as monotherapy in vivo.

179 ALD offered no added advantage compared to L-ALD.

180 metastatic lung tumours were treated with L-ALD or t-L-ALD as monotherapies or in combination with e

181 Liposomal ALD (L-ALD) has been suggested as a suitable alternative

182 Importantly, the low ALD growth temperature is compatible with photolithograp

183 -1.01; P = 0.081) were associated with lower ALD risk.

184 Measurable ALD protein was observed in all the patients.

185 Here we report that IRF3 mediates ALD via linking endoplasmic reticulum (ER) stress with a

186 y increased in patients with ambulatory mild ALD as compared to nonalcoholics.

187 es were unable to be measured after multiple ALD cycles as a result of a loss in SERS enhancement and

188 I) amidinates, which comprise a new class of ALD precursors.

189 One consequence of ALD is increased oxidative stress and altered beta-oxida

190 In X-ALD, mutation/deletion of ALD gene (ABCD1) and the resultant very long chain fatty

191 Depletion of ALD in the presence of glucose led to accumulation of fr

192 Thus, STING and IRF3 are key determinants of ALD, linking ER stress signaling with the mitochondrial

193 ses, is indispensable for the development of ALD.

194 tinal barrier dysfunction and development of ALD.

195 evel of MIR122 contributes to development of ALD.

196 ncluded patients who received a diagnosis of ALD and heterozygote female carriers, both of which grou

197 to CD34+CD146- cells, and minimal effects of ALD and HCV diseases on gene expression were observed.

198 w linear cycle-by-cycle growth emblematic of ALD.

199 Any form of ALD can lead to end-stage liver disease, according to lo

200 The main challenges for the future of ALD modeling are outlined.

201 ectrodes modified with an ultrathin layer of ALD Al2O3 and an overlayer of Pt dendrimer-encapsulated

202 e, intestinal TNFRI is a crucial mediator of ALD.

203 after oral immunization, in a mouse model of ALD and in human liver samples.

204 ry, we have established a zebrafish model of ALD that recapitulates key features of human disease pat

205 In a mouse model of ALD, ethanol feeding decreased miR181b-3p in liver and i

206 were fed ethanol for 8 weeks, as a model of ALD, or a control diet.

207 onic plus binge ethanol to create a model of ALD.

208 esponses were also evaluated in our model of ALD.

209 Experiments in mouse models of ALD or NAFLD further showed that BALB/c or resveratrol-t

210 tly prevent liver injury in murine models of ALD.

211 in SER signal as a function of the number of ALD cycles.

212 e (LPS) from the gut is key for the onset of ALD because it promotes macrophage infiltration and acti

213 te HMGB1 participates in the pathogenesis of ALD and undergoes post-translational modifications (PTMs

214 how recent insights into the pathogenesis of ALD will affect the treatment and management of patients

215 her HMGB1 contributes to the pathogenesis of ALD.

216 cuit critically mediates the pathogenesis of ALD.

217 g pathways involved in the pathomechanism of ALD.

218 ontribution of ASS to the pathophysiology of ALD, wildtype (WT) and Ass(+/-) mice (Ass(-/-) are letha

219 ologists to identify lesions and patterns of ALD and NAFLD; we review these lesions and propose metho

220 n contextual characteristics and presence of ALD at HCV diagnosis.

221 h alcohol abstinence can cause regression of ALD, and weight loss can cause regression of NAFLD, many

222 ght be manipulated to reduce the severity of ALD in patients.

223 death, and steatosis at different stages of ALD.

224 disease (ALD) and NAFLD, although studies of ALD have focused on pathological alcohol intake and few

225 novel therapeutic agent in the treatment of ALD.

226 potential molecular target for treatment of ALD.

227 The use of ALD for creating complex insulators, semiconductors, and

228 nts with nonalcoholic fatty liver disease or ALD.

229 ection, nonalcoholic fatty liver disease, or ALD did not change between 2003 and 2015.

230 percentages of patients with HCC from HCV or ALD and a small increase in HCC among persons with NASH)

231 tages of patients with cirrhosis from HCV or ALD, but increase in percentages of patients with cirrho

232 percentages of patients with CLF from HCV or ALD, with an almost 3-fold increase in percentage of pat

233 t or receiving liver transplants for NASH or ALD are increasing, despite different relative burdens o

234 nt a new therapeutic strategy for preventing ALD.

235 cells by retinoids or by sulfatide prevents ALD.

236 as measured using as little as 1 cycle of Pt ALD, which corresponded to a surface mass loading of app

237 l inflammation and permeability, and reduced ALD in mice.

238 The findings demonstrate that ALD is a remarkably uniform and precise method for modif

239 Taken together, these results suggest that ALD is primarily important for energy metabolism rather

240 The ALD deposition of iron oxide with well-controlled phase

241 The ALD technique can tune the selectivity of furfural hydro

242 Additionally, the ALD post-treatment renders the otherwise hydrophobic dye

243 by FTIR, TEM, and Mass Spectrometry, and the ALD process has been extended to polyvaline.

244 nto the lattice structure of LMNO during the ALD process.

245 ntent of oxygen with lower Ti content in the ALD films leads to the formation of layers with higher r

246 The power density of the ALD modified and inherently functional commercial cells

247 ons in ABCD1 lead to loss of function of the ALD protein.

248 to the nature of atom-by-atom growth of the ALD technique.

249 Increasing the thickness of the ALD-generated overcoats restricts the adsorption of furf

250 conventional solution-based procedures, the ALD approach offers significant advantages in scope and

251 In CaS ALD with 1 and H2 S, the ALD window was approximately two times wider and lower i

252 Here, we show the ALD of titanium dioxide (TiO2) protective nanolayer onto

253 Subsequently, the ALD, GNPs, and ALD conjugated GNPs (GNPs-ALD) were analy

254 We demonstrate that the ALD is regioselective, with preferential deposition of o

255 With the ALD procedure, assemblies bridged by Al(III), Sn(IV), Ti

256 species deposited in the MOF NU-1000 through ALD.

257 C cases, 54.9% were related to HCV, 16.4% to ALD, 14.1% to NAFLD, and 9.5% to HBV.

258 y formation, and diversification compared to ALD and NASH when cultured identically.

259 establish that PXR signaling contributes to ALD development and suggest that PXR antagonists may pro

260 ing trends in the gut-liver axis relevant to ALD.

261 ling microscopy studies of trimethylaluminum ALD on copper show that the remarkable stability imparte

262 -scale surface structural modification using ALD and post-treatment, which is of great importance for

263 with obesity and metabolic syndrome whereas ALD is associated with excessive alcohol consumption.

264 While ALD on flat substrates is well established, the complexi

265 H increased by 170% (from 804 to 2174), with ALD increased by 45% (from 1400 to 2024), and with HCV i

266 deposition (ALD) of Al2O3 or TiO2 along with ALD-Pt deposition results in to our knowledge the first

267 in liver tissues from patients and mice with ALD, compared with controls.

268 HMGB1 were detected in humans and mice with ALD.

269 obtained liver samples from 12 patients with ALD and cirrhosis and 9 healthy individuals (controls) a

270 ecreased in liver samples from patients with ALD and mice on the Lieber-DeCarli diet, compared with c

271 MIR122 decrease in livers from patients with ALD and mice with ethanol-induced liver disease, compare

272 whereas a higher proportion of patients with ALD die from liver disease.

273 Patients with ALD had a significantly higher mean Model for End-Stage

274 entified 1,746, 3,351, and 592 patients with ALD prevalence of 28.0%, 23.0%, and 15.0% for birth coho

275 Liver biopsies from patients with ALD showed a robust increase in HMGB1 expression and tra

276 after multivariate adjustment, patients with ALD were less likely to die within 90 days when compared

277 ncreased in liver tissues from patients with ALD, compared with controls; increases correlated with d

278 from ethanol-fed mice and from patients with ALD, there was disulfide-bonded hyperacetylated HMGB1, d

279 cardiovascular disorders than patients with ALD, whereas a higher proportion of patients with ALD di

280 Similar to patients with ALD, zebrafish abcd1 mutants have elevated VLCFA levels.

281 estimated role of apoptosis in patients with ALD.

282 ncreased in livers of mice and patients with ALD.

283 ral blood mononuclear cells of patients with ALD/alcoholic hepatitis compared to controls.

284 ortality in liver transplant recipients with ALD or NAFLD.

285 ildren with X-linked adrenoleukodystrophy (X-ALD) before and after haematopoietic stem cell transplan

286 X-linked adrenoleukodystrophy (X-ALD), an inherited peroxisomal disorder, is caused by mu

287 efective in X-linked adrenoleukodystrophy (X-ALD).

288 lination in X-linked adrenoleukodystrophy (X-ALD).

289 Biochemically, X-ALD is characterized by an accumulation of very long-cha

290 SAHA may have a therapeutic potential for X-ALD.

291 dy, we used primary human fibroblasts from X-ALD and Zellweger syndrome patients to investigate the p

292 nesterified very long-chain fatty acids in X-ALD and is abolished in Zellweger syndrome.

293 eta-oxidation activity toward C26:0-CoA in X-ALD fibroblasts is mediated by ABCD3, although the effic

294 duced beta-oxidation to levels observed in X-ALD fibroblasts.

295 we show that the beta-oxidation defect in X-ALD is directly caused by ABCD1 dysfunction as blocking

296 In X-ALD, mutation/deletion of ALD gene (ABCD1) and the resul

297 ay a prominent role in oligodendrocytes in X-ALD.

298 Children at an early stage of X-ALD (below 8 points in MRI severity scale) are more like

299 aging methods to assess the progression of X-ALD.

300 mean 8.14 years) with biochemically proved X-ALD, underwent plain MR imaging with a 1.5 T unit before