ライフサイエンスコーパス: ALT

1 ALT elevations > 5 times the ULN occurred in eight (29%)

2 ALT telomeres exhibit a unique chromatin environment and

3 ALT tumor cells often contain abundant DNA damage foci a

4 ALT was identified in 23.4% of high-risk neuroblastoma t

5 ]=8.49 and OR=16.54, respectively, P=.0004), ALT (OR=3.13 per doubling, P=.003), hypertension (OR=10.

6 rotein[a] (39.59%) and varied between 0.09% (ALT) and 18.49% (LDL [low-density lipoprotein]) for the

7 ographic and clinical factors and grades 1-4 ALT on the selected models.

8 L 4.3%) and peak hospitalization (AST 83.4%, ALT 61.6%, ALP 22.7%, and TBIL 16.1%).

9 x the upper limit of normal (ULN; AST 63.7%, ALT 63.5%, ALP 80.0%, and TBIL 75.7%).

10 Among 86 ALT-associated genes, only MND1 showed consistent down-r

11 l liver tests prehospitalization (AST 25.9%, ALT 38.0%, ALP 56.8%, and TBIL 44.4%).

12 with COVID-19, both at admission (AST 66.9%, ALT 41.6%, ALP 13.5%, and TBIL 4.3%) and peak hospitaliz

13 uction in alanine aminotransferase activity [ALT, weighted mean difference (WMD): -11.23 IU/L; 95% CI

14 ysaccharide-induced liver injury (TNF-alpha, ALT, and lactate dehydrogenase release).

15 L, with or without alanine aminotransferase (ALT) >=2-fold the upper limit of normal, and hepatitis B

16 egative women with alanine aminotransferase (ALT) >=40 IU/L as a predictor of high HBV DNA level.

17 > 10(7) IU/mL and alanine aminotransferase (ALT) <= 1.5 times the upper limit of normal (ULN) (male:

18 (-30%; P < 0.001), alanine aminotransferase (ALT) (-49%; P = 0.009), and aspartate aminotransferase (

19 cT1; -8% and -9%), alanine aminotransferase (ALT) (-67% and -60%), aspartate aminotransferase (-57% a

20 ch may result from alanine aminotransferase (ALT) and branched-chain amino acid aminotransferase (BcA

21 T) was higher than alanine aminotransferase (ALT) at admission (46 vs. 30 U/L) and during the hospita

22 tment, and reduced alanine aminotransferase (ALT) by 92% and 77% at 5 weeks and by 80% and 64% at 10

23 BsAg, HBV DNA, and alanine aminotransferase (ALT) concentrations in addition to standard safety asses

24 nsferase (AST) and alanine aminotransferase (ALT) decreased significantly in the entire group and in

25 of peak values of alanine aminotransferase (ALT) during COVID-19 showed moderate liver injury (ALT 2

26 ed blood levels of alanine aminotransferase (ALT) for drug-induced liver injury often assume that the

27 viral load and/or alanine aminotransferase (ALT) in the relation of smoking with HBV-associated HCC

28 increase in plasma alanine aminotransferase (ALT) level of 26% in those with score 5 or 6 versus 0.

29 d 35% had elevated alanine aminotransferase (ALT) levels on admission.

30 relationship with alanine aminotransferase (ALT) overtime were examined in HIV-HBV coinfection.

31 r initial and peak alanine aminotransferase (ALT) than those who tested negative.

32 the time for serum alanine aminotransferase (ALT) to fall below 100 U/L.

33 al or had elevated alanine aminotransferase (ALT) were higher than among those who were lean patients

34 ntifying levels of alanine aminotransferase (ALT), a primary biomarker associated with liver function

35 in, triglycerides, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) using a gener

36 nsferase (GGT) and alanine aminotransferase (ALT), and higher number of heavy drinking days (all ps <

37 ced blood glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phospha

38 line and change in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutam

39 y, blood levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, total c

40 of total protein, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrog

41 h steatosis/normal alanine aminotransferase (ALT), steatosis/elevated ALT, and no steatosis/normal AL

42 elevated levels of alanine aminotransferase (ALT).

43 ibited lower serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST) levels and less he

44 ALD, liver injury (alanine aminotransferase [ALT]) and steatosis were prevented by CVC whether admini

45 nsferase [AST] and alanine aminotransferase [ALT]), alkaline phosphastase, and creatine kinase.

46 transferase [AST], alanine aminotransferase [ALT], alkaline phosphatase [ALP], total bilirubin [TBIL]

47 of less than 2000 IU/mL and one (14%) had an ALT less than the ULN at week 24.

48 , while in development, limit the cost of an ALT screening test to $1.60 per test.

49 4.568; 95% CI 1.458-14.312; P = 0.009), and ALT-positivity (OR 3.486; 95% CI 1.093-11.115; P = 0.035

50 MDA, uric acid and ALT levels also increased, whereas GSH and HDL levels sh

51 (rho = 0.375, p = 0.001), as well as AST and ALT (rho = 0.43, p = 0.0004, and rho = 0.27, p = 0.03, r

52 Elevations of both AST and ALT are mostly below 5 times the upper reference limit a

53 gnificant differences at 12 weeks in AST and ALT between the simvastatin 20 mg/day plus rifaximin and

54 oup showed a significant increase in AST and ALT compared with the placebo group (mean differences be

55 AST and ALT elevations are more frequent in US patients compared

56 hallenge, and display elevated serum AST and ALT levels, hyperactivation of NKT cells, and enhanced I

57 esterol, tryacylglicerol); (4) blood AST and ALT; (5) liver histology (histopathology, hemosiderin de

58 gher systolic blood pressure, serum AST, and ALT at 72 weeks, compared with baseline (p = 0.03, p = 0

59 Besides BMI and ALT, integrase inhibitor exposure was associated with hi

60 s components and impact on weight change and ALT values in the 12 months following referral.

61 MA-IR, triglycerides, total cholesterol, and ALT.

62 Weight, creatinine and ALT did not differ between groups.

63 ch as DAXX mutations, chromosomal gains, and ALT, are associated with an increased risk of metastasis

64 An algorithm using HBeAg and ALT level could be an effective strategy to identify HBV

65 ncluding the participant who lost HBeAg, and ALT values returned to near baseline levels in all but f

66 ate patterns of simulated hepatic injury and ALT release that scale (or not) to be quantitatively sim

67 cts with repeated measures of viral load and ALT over periods of up to 16 years, we further observed

68 cant mediation effect by both viral load and ALT was also evidenced.

69 A concentrations of less than 2000 IU/mL and ALT concentrations less than the ULN at TFFU week 24.

70 baseline HBV DNA was 8.2 log(10) IU/mL, and ALT was 0.9 times the ULN.

71 romosomal gains, CN-LOH, DAXX mutations, and ALT-positivity.

72 tion of acetylcysteine treatment, defined as ALT doubling and peak ALT greater than 100 IU/L, indicat

73 promote homologous recombination-associated ALT pathways.

74 livary concentrations of total protein, AST, ALT, and LDH than the CN group.

75 livary concentrations of total protein, AST, ALT, and LDH, decreased salivary flow rate and a signifi

76 inotransferase/alanine aminotransferase (AST/ALT).

77 patients, and populations with elevated AST/ALT.

78 is likely, and concomitant decreases in AST/ALT suggest an intrahepatic anti-inflammatory effect.

79 vents replisomes from stalling/collapsing at ALT telomeres by disrupting TERRA R-loops.

80 by ATRX loss, leaving telomere repair-based ALT as the only viable mechanism for telomere maintenanc

81 2C2 nuclear foci varies considerably between ALT+ cell lines and does not correlate with the level of

82 We suggest that RNF8 mediates both ALT-EJ and HDR, but via distinct mechanisms, since only

83 nce of specialized PML nuclear bodies called ALT-associated PML bodies (APBs).

84 ly 19 (10.1%) patients developed concomitant ALT flare with oral HBV antiviral therapy; the risk was

85 suring mucosal ulcer area, serum creatinine, ALT, and body weight at day 4.

86 nt effects were observed for TG, HbA1c, CRP, ALT, and AST.

87 enrollment in WM, weight loss, and decreased ALT.

88 s accumulate at telomeres in FANCM deficient ALT cells and downregulation of which attenuates the ALT

89 down-regulation across three NR2F2-depleted ALT+ cell lines.

90 s (MiDAS) specifically at telomeres to drive ALT activity.

91 antagonizing promiscuous BLM activity during ALT recombination.

92 Conversely, RNF8 promotes alternative EJ (ALT-EJ) events involving microhomology that is embedded

93 , hyperglycemia (n = 3 [4.6%]), and elevated ALT (n = 3 [4.6%]).

94 ompared to those with steatosis and elevated ALT and not different from the risk in a clinical cohort

95 ased atherogenic lipid profile, and elevated ALT overtime.

96 lder patients with dyslipidemia and elevated ALT, even if normoweight.

97 ed in five (4%) patients, including elevated ALT concentrations in two patients, hepatic flare in two

98 wer than in patients with steatosis/elevated ALT (cirrhosis: 3.85; 95% CI: 3.50-4.23, and HCC: 0.37;

99 Patients with steatosis/elevated ALT had a higher risk of developing cirrhosis (adjusted

100 is/normal ALT, those with steatosis/elevated ALT were younger and more likely to be obese (both P < 0

101 ALT, 15,419 patients with steatosis/elevated ALT, and 9,267 patients with no steatosis/normal ALT.

102 e aminotransferase (ALT), steatosis/elevated ALT, and no steatosis/normal ALT.

103 , or >=20 Gray were associated with elevated ALT.

104 PML bodies, and thus artificially engineered ALT-associated PML body (APB)-like condensates in vivo.

105 ignificant increases of trait levels (except ALT) and increased risks for overweight/obesity (odds ra

106 In addition, four of five ALT+ cell lines lack (TCAGGG)(n) repeats in some telomer

107 ween the 2 groups (3.16 for SLT and 2.83 for ALT) and was not statistically significant (P = 0.71) Fu

108 or AST -14 IU/L [-91 to 64; p=0.728] and for ALT -8 IU/L [-49 to 33; p=0.698]).

109 30 IU/L [95% CI 54 to 205; p=0.0009] and for ALT 61 IU/L [22 to 100; p=0.0025].

110 er ATRX, pointing to an epigenetic basis for ALT.

111 Except for ALT (alanine transaminase), all GRSs were significantly

112 serve as an immediate repressive switch for ALT.

113 of four potentially explanatory theories for ALT release.

114 ing to this finding was the strong trend for ALT to fail more quickly than SLT.

115 R/Cas9 to delete PML and APB components from ALT-positive cells to cleanly define the function of APB

116 y comparing the hepatic parameters ALP, GGT, ALT, AST and total bilirubin, also considering the adver

117 A total of 1,137 (41.3%) CSS had ALT > upper limit of normal (Common Terminology Criteria

118 ein and albumin concentrations) and hepatic (ALT, AST) parameters.

119 tcomes included incidence of hepatotoxicity (ALT > 1,000 IU/L), peak international normalized ratio (

120 des (aOR, 1.34; 95% CI, 1.11-1.63), and high ALT (aOR, 1.15; 95% CI, 1.05-1.26), while a high level o

121 classified into three subgroups (TERT-high, ALT(+), and TERT-low/non-ALT) based on presence of C-cir

122 t-free survival was similar among TERT-high, ALT(+), or TERT-low/non-ALT patients.

123 on might not cause adiposity; instead higher ALT might reduce BMI, raising the question as to the rol

124 ne (versus none) were associated with higher ALT overtime (1.93 and 1.34 times higher, respectively;

125 It explains how ALT externalization is the combined consequence of lobul

126 ent susceptibility to RS, we show that human ALT telomeres are highly enriched for macroH2A1.2.

127 ALI was categorized as mild if ALT was greater than the upper limit of normal (ULN) but

128 f normal (ULN) but <2 times ULN, moderate if ALT was between 2 and 5 times the ULN, and severe if ALT

129 between 2 and 5 times the ULN, and severe if ALT was >5 times the ULN.

130 nalogous to Saccharomyces cerevisiae type II ALT survivors.

131 Together, these findings implicate ALT activation as an adaptive response to ATRX/DAXX loss

132 f the FANCM complex (FANCM-FAAP24-MHF1&2) in ALT cells induced pronounced replication stress, which p

133 ls to cleanly define the function of APBs in ALT.

134 of sister telomeres and that loss of ATRX in ALT cells results in diminished telomere cohesion.

135 (P < 0.001) retained baseline and change in ALT (AUROC, 0.80; 95% CI, 0.67-0.93).

136 (P = 0.0004) retained baseline and change in ALT (AUROC, 0.80; 95% CI, 0.67-0.93).

137 rticipation, change in weight, and change in ALT were evaluated in the 12-months following referral a

138 Here, we characterized the changes in ALT associated phenotypes in cells deficient of the FANC

139 tly, RAD51AP1 protein levels are elevated in ALT+ cells due to MMS21 associated SUMOylation.

140 nitiation and maintenance of CC formation in ALT cells is still largely unknown.

141 lating the chromatin-assembly factor HIRA in ALT cancer cells.

142 l features of NASH along with improvement in ALT and dyslipidemia in the DIAMOND mice.

143 a protein that is frequently inactivated in ALT tumors.

144 at this facilitates telomere interactions in ALT+ cells.

145 chanism critical for telomere maintenance in ALT cancer cells.

146 of RAD51-associated protein 1 (RAD51AP1) in ALT+ cancer cells leads to generational telomere shorten

147 st that NR2F2 does not play a direct role in ALT and we speculate about an alternative role for this

148 at direct NR binding does not play a role in ALT at these telomeres.

149 Telomeres in ALT cancer cells exhibit a distinctive nucleoprotein arc

150 and is particularly enriched on telomeres in ALT cells.

151 ) and induced ALT-like phenotypes, including ALT-associated promyelocytic leukemia (PML) bodies (APBs

152 dium-risk intensification, 50% had increased ALT and 3% hyperbilirubinemia (both grade 3/4 and correl

153 results indicated a causal role of increased ALT (alanine aminotransferase) in the development of typ

154 Loss of SLX4IP increases ALT-related phenotypes, which is incompatible with cell

155 eric double-strand breaks (DSBs) and induced ALT-like phenotypes, including ALT-associated promyelocy

156 and represents a novel target for inhibiting ALT cancer cells.

157 PPARalpha and CPT1)), hepatocellular injury (ALT), hepatic inflammation (mRNA expression of pro-infla

158 ) in 22.2% (n = 18) and severe liver injury (ALT > 5x ULN) in 12.3% (n = 10).

159 uring COVID-19 showed moderate liver injury (ALT 2-5x upper limit of normal [ULN]) in 22.2% (n = 18)

160 T tumors lacked genomic alterations in known ALT-associated genes.

161 RAD51AP1 KO ALT+ cells exhibit telomere dysfunction and cytosolic te

162 ith severe AFOCHB with bilirubin >50 umol/l, ALT >10x upper limit of normal, and INR >1.5 were includ

163 le was associated with only marginally lower ALT in lean nondrinkers with low genetic risk of hepatic

164 plicative DNA repair processes that maintain ALT telomere stability and cancer cell viability.

165 Mean ALT change was - 15.2 (SD 38.5) U/L without WM and - 28.

166 y between pre-DAA and DAA, whereas only mean ALT continued to decrease until post-SVR.

167 The mean ALT and AST normalized rapidly between pre-DAA and DAA,

168 hile SLX4 was dispensable for RAD52-mediated ALT telomere synthesis in G2, combined SLX4 and RAD52 lo

169 Using MR, ALT was inversely associated with BMI (-0.14 standard de

170 ability occurred in low TERT-expressing, non-ALT patient-derived high-risk neuroblastoma cell lines.

171 nt OS: a previously undescribed TERT-low/non-ALT cohort with superior OS (even after relapse) and two

172 ever, overall survival (OS) for TERT-low/non-ALT patients was significantly higher relative to TERT-h

173 lar among TERT-high, ALT(+), or TERT-low/non-ALT patients.

174 rved higher OS in patients with TERT-low/non-ALT tumors, continuous shortening of telomeres and decre

175 bgroups (TERT-high, ALT(+), and TERT-low/non-ALT) based on presence of C-circles and TERT mRNA expres

176 h hepatic steatosis with persistently normal ALT are at lower risk for cirrhosis compared to those wi

177 is and HCC in patients with steatosis/normal ALT and those without steatosis was not significantly di

178 ntified 3,522 patients with steatosis/normal ALT, 15,419 patients with steatosis/elevated ALT, and 9,

179 In patients with steatosis/normal ALT, the incidence rates of cirrhosis and HCC were 1.22

180 ed to patients with hepatic steatosis/normal ALT, those with steatosis/elevated ALT were younger and

181 and 9,267 patients with no steatosis/normal ALT.

182 atosis/elevated ALT, and no steatosis/normal ALT.

183 < 0.01) than patients with steatosis/normal ALT; they also had a higher risk of HCC, although it did

184 SLX4 reduced the proliferation of RAD52-null ALT cells.

185 Observationally, ALT was positively associated with BMI (0.10 kg/m(2) per

186 X were detected in 60% of ALT tumors; 40% of ALT tumors lacked genomic alterations in known ALT-assoc

187 alterations in ATRX were detected in 60% of ALT tumors; 40% of ALT tumors lacked genomic alterations

188 most specific and quantifiable biomarker of ALT.

189 and telomere clustering, a characteristic of ALT telomeres, catalyzes RAD52-dependent mitotic DNA syn

190 Depletion of HIRA elicits systemic death of ALT cancer cells that is mitigated by re-expression of A

191 nerabilities for the targeted elimination of ALT cancer cells that infiltrate tissues and organs to b

192 Among the many prominent features of ALT cells, C-circles (CC) formation is considered to be

193 One of the hallmarks of ALT cancer is the excessively clustered telomeres in pro

194 ion led to preferential growth inhibition of ALT cells, which was accompanied by telomere chromatin d

195 -) mice displayed increased plasma levels of ALT, ALP, and bilirubin as well as a significantly highe

196 otoxicity grade, and increased likelihood of ALT >=80 U/L (odds ratio, 3.14; 95% confidence interval,

197 r increased viral load and the likelihood of ALT >=80 U/L.

198 X mutations in potentiating the mechanism of ALT remains incompletely understood.

199 suppression associated with normalization of ALT is considered an intermediate goal.

200 Using MR, genetic predictors of ALT, ALP and gamma glutamyltransferase (GGT), were appli

201 telomere length and ensure proliferation of ALT+ cancer cells.

202 BMI, raising the question as to the role of ALT in body composition.

203 ow that SLX4IP is inactivated in a subset of ALT-positive osteosarcomas.

204 telomere length maintenance and survival of ALT cancer cells.

205 eterminants of the emergence and survival of ALT cancer cells.

206 The usefulness of ALT and related biomarkers will improve by developing me

207 g of telomeres (ALT) pathway that depends on ALT-associated promyelocytic leukemia nuclear bodies (AP

208 Therefore, targeted sequencing and/or ALT analysis may help in the clinical decisions for thes

209 ignificantly higher relative to TERT-high or ALT patients (log-rank test; P < 0.01) independent of cu

210 ontent, 7alpha-hydroxy-4-cholesten-3-one, or ALT, were observed in histological responders than in no

211 One setting of 180 degrees of either SLT or ALT was assigned randomly and applied to each participan

212 r cells are maintained without telomerase or ALT.

213 he time-to-failure analyses favored SLT over ALT.

214 In multivariable analysis, peak ALT was significantly associated with death or discharge

215 , peak AST (364 vs. 77; P = 0.003), and peak ALT (220 vs. 52; P = 0.002) were higher in intubated pat

216 treatment, defined as ALT doubling and peak ALT greater than 100 IU/L, indicating the need for furth

217 ve response to ATRX deficiency that pervades ALT cancers.

218 vement in fibrosis, inflammation, and plasma ALT.

219 alidation targets, which are elevated plasma ALT values following acetaminophen (APAP) exposure in mi

220 A/TA homozygotes had 12% to 18% lower plasma ALT among the most obese, in heavy drinkers, and in indi

221 ociated with stepwise lower levels of plasma ALT of up to 1.3 U/L in TA/TA homozygotes versus T/T hom

222 ts in virtual mice directly to target plasma ALT values in individual mice.

223 ounts of telomeres in human cancers promotes ALT that is mediated by MiDAS, analogous to Saccharomyce

224 eased presence of C-circles, more pronounced ALT-associated phenotypes and elongated telomeres.

225 We can quantify ALT with increased sensitivity (1.53 nA/(U/L*mm(2)) and

226 d histologic evidence of injury, and reduced ALT by 58%, which is comparable to control rats sustaini

227 The results showed that BPF99 reduced ALT (mean 71.6 vs 44.6 IU/l, p < 0.01), triglycerides (3

228 ter ischemia, in the 5-week HFHF rat reduced ALT by 71% and reduced necrosis.

229 onitoring during PrEP should include regular ALT and HCV testing.

230 We scale ALT amounts in virtual mice directly to target plasma AL

231 Serum ALT level was graded using the Common Terminology Criter

232 a concerning for iDILI were defined as serum ALT > 5x or serum bilirubin > 1.5x upper limit of normal

233 In the remaining children, serum ALT and HBV DNA levels at week 96 were similar to baseli

234 uced liver inflammation, and decreased serum ALT/AST levels.

235 by H&E staining and little increase in serum ALT and AST after treatment with JQ1 loaded ApoE-NPs.

236 hildren with NAFLD, dynamic changes in serum ALT and GGT are associated with change in liver histolog

237 Median serum ALT and total bilirubin at presentation were 462 U/L (IQ

238 These markers were predictors of severe ALT flares, after treatment withdrawal, and HBV DNA reac

239 cruitment of BLM to the replication stressed ALT telomeres.

240 zation to telomeres is sufficient to sustain ALT activity.

241 he three model mechanisms matched all target ALT values quantitatively.

242 )-based Alternative Lengthening of Telomere (ALT) pathway.

243 ed for alternative lengthening of telomeres (ALT) by Fluorescence In Situ Hybridization.

244 and in alternative lengthening of telomeres (ALT) cells, which have spontaneous telomeric damage.

245 The alternative lengthening of telomeres (ALT) facilitates telomere lengthening by a DNA strand in

246 employ alternative lengthening of telomeres (ALT) for chromosomal end protection, yet the underlying

247 Alternative lengthening of telomeres (ALT) is a homology-directed repair (HDR) mechanism of te

248 Alternative lengthening of telomeres (ALT) is a mechanism of telomere maintenance that is obse

249 Alternative lengthening of telomeres (ALT) is a telomerase-independent telomere maintenance me

250 on the alternative lengthening of telomeres (ALT) mechanism to maintain their telomeres.

251 -based alternative lengthening of telomeres (ALT) pathway that depends on ALT-associated promyelocyti

252 ng the alternative lengthening of telomeres (ALT) pathway, but it is not known how ATRX loss leads to

253 on the alternative lengthening of telomeres (ALT), a homology-directed telomere-maintenance pathway.

254 ducing alternative lengthening of telomeres (ALT), which relies on telomere recombination.

255 termed alternative lengthening of telomeres (ALT).

256 called alternative lengthening of telomeres (ALT).

257 or by alternative lengthening of telomeres (ALT).

258 derpin alternative lengthening of telomeres (ALT).

259 on for alternative lengthening of telomeres (ALT).

260 er for alternative lengthening of telomeres (ALT)], TERT mRNA expression by RNA-sequencing, whole-gen

261 ed rapidly following DAXX induction and that ALT is again restored following withdrawal of DAXX.

262 Using an inducible system, we show that ALT-associated PML bodies are disrupted rapidly followin

263 The ALT-lowering effect of rs72613567:TA was amplified by in

264 gh risk of fatty liver disease amplifies the ALT-lowering effect of HSD17B13 rs72613567:TA in the Dan

265 aintenance mechanisms with TERT mRNA and the ALT DNA biomarker C-circles to stratify neuroblastoma in

266 of RNF8 on EJ is distinct from 53BP1 and the ALT-EJ factor, POLQ.

267 s and downregulation of which attenuates the ALT-associated PML bodies (APBs), replication stress and

268 We found that PML is required for the ALT mechanism, and that this necessity stems from APBs'

269 necessity of APBs and their function in the ALT pathway has remained unclear.

270 dent manner bypasses the need for PML in the ALT pathway, suggesting that BTR localization to telomer

271 me analysis following NR2F2-depletion in the ALT+ cell lines revealed different very responses.

272 hat RAD51AP1 is an essential mediator of the ALT mechanism and is co-opted by post-translational mech

273 ntroduction of wild type DAXX suppresses the ALT phenotype and restores the localization of ATRX/DAXX

274 These ALT-EJ events likely require limited end resection, wher

275 the response was inconsistent between three ALT+ cell lines.

276 nt with the cell cycle arrest and changes to ALT markers, but these features were not shared by the o

277 ocalizing the BLM-TOP3A-RMI (BTR) complex to ALT telomere ends.

278 position of APBs independently contribute to ALT, suggesting a general framework for how chromatin co

279 , but it is not known how ATRX loss leads to ALT.

280 NAC did not shorten time to ALT&100 U/L in participants with AT-DILI, but significan

281 Median time to ALT&100 U/L was 7.5 days (IQR 6 -11) in the NAC arm and

282 s compared with argon laser trabeculoplasty (ALT) in a randomized clinical trial for patients with me

283 per 1 kg/m2; P < .01), alanine transaminase (ALT) (aOR, 1.76 per 10 U/L; P < .01), and exposure to in

284 ss the associations of alanine transaminase (ALT) and alkaline phosphatase (ALP) at ~17.5 years with

285 with plasma levels of alanine transaminase (ALT) and clinical liver disease and mortality in 111,612

286 dose with normal serum alanine transaminase (ALT) and creatinine on presentation and at 12 hours, and

287 c, detected by routine alanine transaminase (ALT) or HCV monitoring.

288 minotransferase (AST), alanine transaminase (ALT), and mitochondrial aspartate transaminase (m-AST).

289 eactive protein (CRP), alanine transaminase (ALT), aspartate transaminase (AST), and liver fat conten

290 se features were not shared by the other two ALT+ cell lines.

291 In a subset of patients with two ALT measurements over a 6-month period (n=89), the AUROC

292 Cells that use ALT are characterized, in part, by the presence of speci

293 1 year in comparison to baseline for SLT vs. ALT was found to be different by 0.33 mmHg between the 2

294 ry abnormalities, the majority of which were ALT elevations (36 patients).

295 that these bodies act as a platform on which ALT can occur.

296 While ALT occurs in only a subset of tumors, it is strongly as

297 AST highly correlated with ALT throughout the illness course (r = 0.97; P < 0.0001)

298 positive, 47 (9.1%) were HBeAg negative with ALT >=40 IU/L, and 144 (28.0%) had an HBV DNA >5.3 log10

299 t HO-1 expression correlated negatively with ALT levels (P = .0178).

300 was observed for 4 criteria: age >=52 years, ALT >217 U/L, platelets <127, and abnormal baseline imag