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 decreased by 1.7 g/L (95% confidence interval [CI]:

3 ALD stems from the production of toxic-reactive metaboli

4 ALD was found to be successfully conjugated to the GNPs

5 ALD-401 is an enriched population of aldehyde dehydrogen

6 cted to occur on other surfaces where TiO(2) ALD is feasible.

7 From 2007 to 2016, ALD accounted for 20.4% (18 399) of all CLD WL additions

8 25 ALD cycles of TiO2 growth are found to be the optimized

9 ted to HBV [39% and 29%], HCV [29% and 26%], ALD [16% and 25%], and NAFLD [8% and 9%]).

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

11 Adrenoleukodystrophy (ALD) is caused by mutations within the X-linked ABCD1 ge

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

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

14 Young adult ALD WL additions presented with a higher severity of liv

15 ient in cGAS and IRF3 were protected against ALD.

16 een developed for the detection of aldicarb (ALD) based on inner filter effect (IFE) of gold nanopart

17 ng-term systemic treatment with aldosterone (ALD) can enhance NKCC1 protein expression and activity i

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

19 Although ALD and NAFLD recur frequently after liver transplantati

20 y made possible by patterning and etching an ALD WO(3) thin film before conversion, second, an analog

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

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

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

24 /65 were found between the matched NAFLD and ALD cohort.

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

26 ASDR for LC-NAFLD and ALD increased annually by 1.42% (1.00%-1.83%) and 0.53%

27 icrobial therapy for patients with NAFLD and ALD.

28 The number of annual ALD WL deaths readily rose from 2014 to 2016, despite an

29 cule organic compounds in CB could attenuate ALD.

30 hibitor, cenicriviroc (CVC), would attenuate ALD.

31 ncrease in newly diagnosed patients with AUD/ALD post-COVID-19 pandemic.

32 especially detrimental to patients with AUD/ALD, and actions need to be taken now to limit the scope

33 bility of precursor classes for well-behaved ALD in MOFs (AIM) and identify challenges and solutions

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

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

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

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

38 general colloidal atomic layer deposition (c-ALD) synthesis to grow an alumina shell with tunable thi

39 rategy, colloidal atomic layer deposition (c-ALD) with stationary reactant phases, which largely circ

40 To demonstrate the power of the new c-ALD method, we synthesize a library of complex II-VI sem

41 mize and to elucidate the chemistry of the c-ALD process.

42 gressive demyelinating form of ALD, cerebral ALD, resulting in regions of demyelination observed on b

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

44 lcohol relapse, admissions for decompensated ALD, and an increase in newly diagnosed patients with AU

45 s quantified by using adjusted lung density (ALD).

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

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

48 We show that a few atomic layer deposition (ALD) cycles of zinc oxide onto suspended diamond nanomem

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

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

51 Here, atomic layer deposition (ALD) is employed to synthesize films down to 2 nm thickn

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

53 are synthesized by atomic layer deposition (ALD) of a few-nanometer amorphous Al(2) O(3) layers onto

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

55 Atomic layer deposition (ALD) of TiO(2) was performed in tandem with in situ surf

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

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

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

59 ating, deposited by Atomic Layer Deposition (ALD) on the tip of a single-mode fiber.

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

61 eening a library of atomic layer deposition (ALD) precursors, which span metals across the periodic t

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

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

64 films grown by the atomic layer deposition (ALD) with slightly different growth process parameters.

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

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

67 (3) synthesized via atomic layer deposition (ALD).

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

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

70 lly delivered autologous bone marrow-derived ALD-401 in patients with disabling middle cerebral arter

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

72 Alcoholic liver disease (ALD) accounts for 15%-30% of transplants performed in th

73 Alcohol-related liver disease (ALD) accounts for the majority of cirrhosis and liver-re

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

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

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

77 AFLD), and alcohol-associated liver disease (ALD) are main causes of chronic liver disease.

78 Alcoholic liver disease (ALD) causes significant morbidity and mortality, and pha

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

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

81 the United States, alcoholic liver disease (ALD) has recently become the leading indication for live

82 the development of alcoholic liver disease (ALD) in alcoholics by releasing free fatty acids and inf

83 Alcohol-associated liver disease (ALD) is a common chronic liver disease worldwide with hi

84 Alcoholic liver disease (ALD) is a major cause of liver-related mortality.

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

86 Alcoholic liver disease (ALD) is a significant health hazard and economic burden

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

88 n (LT) for alcohol-associated liver disease (ALD) is covered by Medicaid only with documentation of a

89 Alcohol-related liver disease (ALD) is highly prevalent and appears to be increasingly

90 ortality from alcohol-related liver disease (ALD) is increasing in the United States.

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

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

93 nfection, and alcohol-related liver disease (ALD) listed for LT during 2004-2017.

94 (AUD) and alcohol-associated liver disease (ALD) may be among the populations that are the most seve

95 5hmC formation and alcoholic liver disease (ALD) progression.

96 Alcoholic liver disease (ALD) samples were used to confirm relevance of our findi

97 performed using the alcoholic liver disease (ALD) transcriptomic public dataset.

98 Alcohol-related liver disease (ALD) was estimated to have a prevalence of 2% among the

99 station of alcohol-associated liver disease (ALD) with high mortality.

100 of viral hepatitis, alcoholic liver disease (ALD), and nonalcoholic fatty liver disease in the United

101 phenotypes of alcohol-related liver disease (ALD), we show that development of AH is characterized by

102 eases, particularly alcoholic liver disease (ALD).

103 tis associated with alcoholic liver disease (ALD).

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

105 ells contributes to alcoholic liver disease (ALD).

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

107 the pathogenesis of alcoholic liver disease (ALD).

108 lopment of alcohol-associated liver disease (ALD).

109 on, and fibrosis in alcoholic liver disease (ALD).

110 gy, is disrupted in alcoholic liver disease (ALD).

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

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

113 secondary inflammatory response that drives ALD.

114 er in both (absolute) Average Look Duration (ALD) and RALD to stimuli during an EEG experiment, with

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

116 ited: the diffusion through the oxide during ALD is utilized to passivate the interfacial defects by

117 at resonant tunneling enables cost-effective ALD coatings that lower the effective work function and

118 ess, the interface evolves during the entire ALD oxide deposition due to diffusion of reactant specie

119 cohol-induced hepatic injury in experimental ALD.

120 ontrolling the oxidant dose in the first few ALD cycles of the oxide deposition on SiGe.

121 t precursor and the SER spectra of the first ALD cycle of TiO(2) reveal typical ligand exchange chemi

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

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

124 APC = 0.29% [0.01%-0.59%]) but decreased for ALD (APC = -0.44% [-0.78% to -0.40%]), HCV (APC = -0.50%

125 LDLT for ALD results in excellent 1-, 5-, and 10-year graft and p

126 s to examine the outcomes following LDLT for ALD using data from the adult-to-adult living donor live

127 iving donor liver transplantation (LDLT) for ALD remain sparse.

128 licies may affect the distribution of LT for ALD, particularly post-2011, as centers have adopted ear

129 associated with lower proportions of LTs for ALD paid by Medicaid post-2011 compared to states with u

130 bsolute lower adjusted proportion of LTs for ALD paid by Medicaid post-2011.

131 and Drug Administration-approved therapy for ALD, and therefore, identifying therapeutic targets is n

132 paring patients who underwent transplant for ALD with those who were transplanted for other etiologie

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

134 ing PDE4 might be an effective treatment for ALD.

135 need for effective and novel treatments for ALD, anti-PCSK9 treatment with the monoclonal antibody t

136 Although liver-related mortality from ALD continued to increase, mortality from extrahepatic c

137 Further, ALD membranes are utilized to design micrometer-scale me

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

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

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

141 Human ALD liver samples were also used to validate these findi

142 liver injury in both experimental and human ALD.

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

144 In an ideal ALD process in which oxide is grown layer by layer, the

145 5hmC is involved in hepatocyte apoptosis in ALD progression.

146 more, we established a causal role for AR in ALD by showing that the genetic deficiency of AR (knocko

147 We found impaired autophagy both in ALD and alcoholic hepatitis (AH) mouse models and human

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

149 Disruption of Cx32 in ALD impaired IRF3-stimulated gene expression, resulting

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

151 lts identify cGAS and Cx32 as key factors in ALD pathogenesis and as potential therapeutic targets fo

152 ed in phagophore-autophagosome formation, in ALD.

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

154 Several cell types are involved in ALD progression, including hepatic macrophages.

155 irs autophagic flux at the lysosome level in ALD.

156 r the correct use of liver stiffness (LS) in ALD.

157 owever, the role of AR or its metabolites in ALD remains understudied and was examined using human sp

158 eded to elucidate the exact role of PCSK9 in ALD and alcohol use disorder (AUD) and to evaluate effic

159 thways regulating macrophage polarization in ALD.

160 hesized that increased exosome production in ALD may be linked to disruption of autophagic function.

161 LAMP1 and LAMP2 promotes exosome release in ALD.

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

163 athways that amplify inflammatory signals in ALD remains unknown.

164 This work showcases how seemingly innocuous ALD can evolve into a CVD process when the products can

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

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

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

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

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

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

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

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

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

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

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

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

179 In this thickness limit, ALD films of these materials behave elastically and can

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

181 e the current state of treating and managing ALD, the heterogeneity in definitions, and the significa

182 Measurable ALD protein was observed in all the patients.

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

184 he transient surface species across multiple ALD cycles.

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

186 his work, this diffusion process in nonideal ALD is investigated and exploited: the diffusion through

187 le diffusion of reactant species in nonideal ALD.

188 With addition of ALD into AuNPs, an intercalated layer was formed between

189 to demonstrate that in vitro application of ALD increased outward voltage-gated potassium currents s

190 mortality from extrahepatic complications of ALD did not change significantly during the 11-year stud

191 e machinery to counteract the development of ALD, implying a therapeutic potential of BAT activity mo

192 "treatment" started after the development of ALD.

193 evel of MIR122 contributes to development of ALD.

194 lays a pathogenic role in the development of ALD; hence, directed interventions aimed at inhibiting P

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

196 (15.8%) were transplanted for a diagnosis of ALD.

197 p a severe progressive demyelinating form of ALD, cerebral ALD, resulting in regions of demyelination

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

199 Intracarotid infusion of ALD-401 does not lead to clinical adverse events in pati

200 wed 2 days later by intracarotid infusion of ALD-401 versus sham harvest and then sham infusion in th

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

202 Given that the majority of ALD studies rely on clinical diagnosis and lack patholog

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

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

205 In a mouse model of ALD, liver injury (alanine aminotransferase [ALT]) and s

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

207 ver injury in in vivo and in vitro models of ALD.

208 tly prevent liver injury in murine models of ALD.

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

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

211 cuit critically mediates the pathogenesis of ALD.

212 g pathways involved in the pathomechanism of ALD.

213 ide evidence of the therapeutic potential of ALD for the prevention/treatment of inner ear disorders

214 account for any difference by prevalence of ALD among restrictive versus unrestrictive states.

215 of the liver involved in the progression of ALD by activating pathways that lead to the production o

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

217 e must also acknowledge the full spectrum of ALD clinically and histologically.

218 analysis of patients with a wide spectrum of ALD revealed that expression of the cGAS-IRF3 pathway co

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

220 in cholesterol (LDL-C), for the treatment of ALD using a rat model of chronic alcohol exposure.

221 BAT activity modulation for the treatment of ALD.

222 novel therapeutic agent in the treatment of ALD.

223 potential molecular target for treatment of ALD.

224 nts with nonalcoholic fatty liver disease or ALD.

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

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

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

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

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

230 Periodic ozone exposure during gate oxide ALD on SiGe is shown to reduce the integrated trap densi

231 s show no significant oxidation caused by PE-ALD of Al(2)O(3).

232 plasma enhanced atomic layer deposition (PE-ALD) of Al(2)O(3) on graphene for top gated field effect

233 The reactive nature of PE-ALD enables deposition of thin (2 nm) dielectrics direct

234 yers on top of graphene channels prior to PE-ALD, the graphene is protected from oxidation enabling B

235 Compared to gas-phase ALD, this newly developed synthesis has the advantage of

236 nt a new therapeutic strategy for preventing ALD.

237 A rat ALD model was used to study 5hmC in relationship to hepa

238 ignificantly reduced 5hmC formation in a rat ALD model.

239 However, in a real ALD process, the interface evolves during the entire ALD

240 ls, mediated by a mineralocorticoid receptor-ALD complex.

241 d in hepatic tissues of patients with severe ALD.

242 The age-standardized ALD WL addition rate was 0.459 per 100 000 US population

243 Our results provide supporting evidence that ALD was profoundly influenced by host-gut microbiota met

244 mRNA levels remained stable, indicating that ALD modulates NKCC1 protein expression via the activatio

245 % confidence interval, 30.33% to 64.72%).The ALD WL addition rate increased over twofold among young

246 re was no significant difference between the ALD-401 and placebo groups on the modified Rankin scale

247 rom the SiGe with ozone insertion during the ALD growth process is confirmed by electron energy loss

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

249 h is engineering of diffusion species in the ALD process due to facile diffusion of reactant species

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

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

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

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

254 dation of proposed method indicates that the ALD sensor is promising and adaptable for everyday on sp

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

256 These subpopulations within the ALD cohort need to be evaluated in future studies to imp

257 These ALD-induced changes were blocked by applying the mineral

258 These results establish thin ALD films as a scalable basis for micrometer-scale actua

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

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

261 ents with chronic liver disease (CLD) due to ALD from 2007 to 2016.

262 Novel strategies to treat ALD aim at targeting Kupffer cells.

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

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

265 data on LT recipients from 2002 to 2017 with ALD as the primary listing diagnosis.

266 ence, CQDs FL intensity recovered along with ALD concentration varying between 3.8 and 76 ug L(-1) wi

267 g the hepatitis and fibrosis associated with ALD pathogenesis.

268 sidering leniency to some LT candidates with ALD who cannot access appropriate alcohol treatment due

269 in vitro electrophysiology experiments, with ALD in the presence of NKCC1, K(+) channel and mineraloc

270 milar to patients of the same age group with ALD or HCV.

271 itis (AH) mouse models and human livers with ALD as indicated by increased hepatic p62 and LC3-II lev

272 ed membrane protein 2 (LAMP2) in livers with ALD.

273 Men with ALD were 95% more likely to be listed and 105% more like

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

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

276 Patients with ALD and impaired renal function have a higher risk of gr

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

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

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

280 retrospective review of adult patients with ALD evaluated for LT at a single transplant center from

281 Among the 949 patients with ALD evaluated, mean age was 53 years, 84% were Caucasian

282 Patients with ALD have reduced MATalpha1 levels and a decrease in meth

283 and early clinical studies in patients with ALD injury supports the notion that pathogenic macrophag

284 the notion that early LDLT for patients with ALD may help optimize outcomes.

285 hough outcomes were similar to patients with ALD or HCV of corresponding age.

286 of LTs paid by Medicaid among patients with ALD post-2011.

287 type 5 (Ccr5) in the livers of patients with ALD, and increased circulating chemokines, C-C chemokine

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

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

290 iversity in fecal samples from patients with ALD, with the most significant changes in samples from p

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

292 estimated role of apoptosis in patients with ALD.

293 ncreased in livers of mice and patients with ALD.

294 e viral microbiome (virome) in patients with ALD.

295 liver transplantation (LT) in patients with ALD.

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

297 PCSK9 treatment in clinical populations with ALD/AUD.

298 ic and substance use disorders in women with ALD may improve their transplant eligibility.

299 416 days (range: 0-2784), listed women with ALD were less likely to undergo transplantation (42% ver

300 ly to be transplanted compared to women with ALD.