ライフサイエンスコーパス: transaminase

1 lutarate transaminase and alanine-glyoxylate transaminase.

2 nduce splenomegaly or increase serum alanine transaminase.

3 des the mitochondrial glutamate oxaloacetate transaminase.

4 are accompanied by significant increases in transaminases.

5 immunostaining, and less elevation of serum transaminases.

6 curring via glutamate dehydrogenase (GDH) or transaminases.

7 often with normal or only slightly abnormal transaminases.

8 is and five instances of slight increases in transaminases.

9 , in response to ER stress, elevating plasma transaminases.

10 ated with transient but marked elevations of transaminases.

11 included lymphopenia, diarrhea, and elevated transaminases.

12 2; P = 1.4 x 10(-6)) and with higher alanine transaminase (0.02 [0.01, 0.03]; P = 0.002) and gamma-gl

13 e polymorphisms in branched-chain amino-acid transaminase 1 (BCAT1) and phenylalanine hydroxylase (PA

14 ed activity of the branched-chain amino acid transaminase 1 (BCAT1) enzyme.

15 ess high levels of branched-chain amino acid transaminase 1 (BCAT1), the enzyme that initiates the ca

16 gene encoding glutamine-fructose-6-phosphate transaminase 1 (GFPT1) cause the neuromuscular disorder

17 Glutamine-fructose-6-phosphate transaminase 1 (GFPT1) is a key rate-limiting enzyme in

18 tamate metabolism and glutamate oxaloacetate transaminase 1 (GOT1)-dependent redox balance in PCa, wh

19 from aspartate through glutamic-oxaloacetic transaminase 1 (GOT1).

20 ehydrogenase ([1-(13)C]lactate), and alanine transaminase ([1-(13)C]alanine) was assessed.

21 nase 15.0% (95% CI, 13.6%-16.5%) and alanine transaminase 15.0% (95% CI, 13.6%-16.4%).

22 ver abnormalities were as follows: aspartate transaminase 15.0% (95% CI, 13.6%-16.5%) and alanine tra

23 GPT2 [also known as alanine transaminase 2 (ALT2)] is one of two related transaminas

24 er expression levels of glutamic-oxaloacetic transaminase 2 (GOT2) messenger RNA (Spearman R = 0.42,

25 etabolism by upregulating glutamate pyruvate transaminase 2 (GPT2) in colorectal cancer (CRC) cells,

26 e mutations in the enzyme glutamate pyruvate transaminase 2 (GPT2) in large kindreds initially ascert

27 ncluding the BCAT2 branched-chain amino acid transaminase 2) gene.

28 ngin vs 9 fluconazole), and elevated alanine transaminase (4 caspofungin vs 8 fluconazole).

29 acteria that we termed PtaA for "periplasmic transaminase A" An in-frame-deleted ptaA mutant selectiv

30 ed with higher circulating levels of alanine transaminase, a marker of liver injury, and with lower l

31 a chiral center, both (R)- and (S)-selective transaminases accepting glyoxylate as amino acceptor are

32 Functional biomarkers include erythrocyte transaminase activities and, more recently, plasma level

33 C282Y homozygotes if they have normal liver transaminase activities.

34 In this HEIRS substudy, serum hepatic transaminases activities (e.g., alanine aminotransferase

35 ds decreased triglyceride levels and alanine transaminase activity and caused an increase in antiradi

36 Transaminase activity is detected upon transfer of an am

37 Knockdown of glutamate-oxaloacetate transaminase activity significantly reduced the lipotoxi

38 te dehydrogenase activity, but not aspartate transaminase activity, in HFD-fed mice.

39 HDV-specific CD8(+) T cells correlated with transaminase activity.

40 Assays of PatA (putrescine transaminase) activity and beta-galactosidase from cells

41 However, whether transaminases-adapted cut-off values should be used for

42 Median peak aspartate transaminase after transplantation was 925 (interquartil

43 reduction by approximately 50% in peak serum transaminases after transplantation compared to untreate

44 oprotective effect of glutamate oxaloacetate transaminase against stroke.

45 transaminase (GABA-T) and alanine-glyoxylate transaminase (AGXT2), to the homeostasis of carnosine an

46 y score, steatosis, triglycerides, aspartate transaminase, alanine transaminase, and stellate cell pr

47 Except for ALT (alanine transaminase), all GRSs were significantly associated wi

48 I) (aOR, 1.58 per 1 kg/m2; P < .01), alanine transaminase (ALT) (aOR, 1.76 per 10 U/L; P < .01), and

49 ession to assess the associations of alanine transaminase (ALT) and alkaline phosphatase (ALP) at ~17

50 of rs72613567 with plasma levels of alanine transaminase (ALT) and clinical liver disease and mortal

51 aminophen overdose with normal serum alanine transaminase (ALT) and creatinine on presentation and at

52 tivity to report liver injury versus alanine transaminase (ALT) and International Normalized Ratio (I

53 steatosis, slight elevation of serum alanine transaminase (ALT) and little or no inflammation.

54 e of evidence of increased levels of alanine transaminase (ALT) in patients receiving the high-dose m

55 d females versus males with elevated alanine transaminase (ALT) levels in the chronic HCV patient gro

56 ted aspartate transaminase (AST) and alanine transaminase (ALT) levels, indicative of severe liver da

57 The liver enzymes, alanine transaminase (ALT) or aspartate transaminase (AST), are

58 re asymptomatic, detected by routine alanine transaminase (ALT) or HCV monitoring.

59 in (LDL) cholesterol, triglycerides, alanine transaminase (ALT), and aspartate transaminase (AST) wer

60 for whom levels of plasma fetuin-A, alanine transaminase (ALT), and gamma-glutamyltranspeptidase (GG

61 of aspartate aminotransferase (AST), alanine transaminase (ALT), and mitochondrial aspartate transami

62 uric acid, C-reactive protein (CRP), alanine transaminase (ALT), aspartate transaminase (AST), and li

63 Monitoring of alanine transaminase (ALT), creatinine, and full blood count rev

64 by gamma-glutamyltransferase (GGT), alanine transaminase (ALT), fetuin-A, and the algorithm-based fa

65 tural log (ln)-transformed values of alanine transaminase (ALT), gamma-glutamyltransferase (GGT), and

66 age by alcohol was worse with higher alanine transaminase (ALT), more immune cell infiltration and in

67 ic assay targets alanine and employs alanine transaminase (ALT), pyruvate oxidase (POx), and horserad

68 (-10)) was associated with levels of alanine transaminase, an indicator of liver damage.

69 midazolam clearance with increase in alanine transaminase and a lower clearance of the glucuronide me

70 Majority preferred aspartate transaminase and alanine transaminase less than 50 IU/mL

71 nine and cystatin-C), and hepatic (aspartate transaminase and alanine transaminase) damage and of dec

72 ating enzymes 4-aminobutyrate-2-oxoglutarate transaminase and alanine-glyoxylate transaminase.

73 tandard deviation (SD) decreases for alanine transaminase and aspartate aminotransferase at week 12 c

74 duced changes in the serum levels of alanine transaminase and aspartate transaminase (p<0.05).

75 Asymptomatic transient increases in alanine transaminase and aspartate transaminase were observed at

76 The transaminase and bilirubin levels remained comparable du

77 Laboratory tests revealed elevated liver transaminase and bilirubin levels that were attributed t

78 n who received GO showed modest elevation of transaminase and bilirubin without signs of veno-occlusi

79 ctivity, but also by reductions in aspartate transaminase and glutamate dehydrogenase activities, sug

80 Higher levels of alanine transaminase and interleukin 10 were also associated wit

81 ctly by the PLP-dependent enzymes kynurenine transaminase and kynureninase contributed to the explana

82 h are substrate-product pairs for kynurenine transaminase and kynureninase, respectively, may reflect

83 odenal ulcers and elevated levels of alanine transaminase and total bilirubin in patients receiving T

84 liver biopsy, commonly for steatosis, raised transaminases and 1 or more features of metabolic syndro

85 Elevations in transaminases and liver fat also occurred in some patien

86 ic regression model, adjusted for sex, liver transaminase, and alcohol consumption, the independent p

87 renal injury markers (creatinine, aspartate transaminase, and heart-type fatty acid binding protein)

88 els of gamma-glutamyl transferase, aspartate transaminase, and soluble tumor necrosis factor alpha re

89 iglycerides, aspartate transaminase, alanine transaminase, and stellate cell proliferation by up to 5

90 nd platelet count, as well as the bilirubin, transaminases, and alkaline phosphatase, after 12 months

91 ting features include dyslipidemia, elevated transaminases, and hepatomegaly.

92 D is well tolerated, rapidly decreases serum transaminases, and that these improvements are sustained

93 Herein transaminases are shown to react with aromatic beta-fluo

94 Transaminases are valuable enzymes for industrial biocat

95 e of exploiting the catalytic promiscuity of transaminases as a tool for novel transformations.

96 The widespread application of omega-transaminases as biocatalysts for chiral amine synthesis

97 he screening effort in directed evolution of transaminases, as only active variants are selected for

98 ver toxicity (proportion of patients alanine transaminase, aspartate aminotransferase and AlkPhos >5x

99 al leucocyte count, urea, bilirubin, alanine transaminase, aspartate transaminase, international norm

100 Elevated alanine transaminase/aspartate transaminase was seen in 67% of p

101 manifested as profoundly elevated aspartate transaminase (AST) and alanine transaminase (ALT) levels

102 ing a model enzyme pair comprising aspartate transaminase (AST) and malic dehydrogenase.

103 s, alanine transaminase (ALT), and aspartate transaminase (AST) were measured.

104 olic and lipidomic data with aspartate amino transaminase (AST), a hepatic leakage enzyme to assess o

105 (CRP), alanine transaminase (ALT), aspartate transaminase (AST), and liver fat content.

106 mes, alanine transaminase (ALT) or aspartate transaminase (AST), are commonly used in clinical practi

107 ymes (alanine transferase, ALT and aspartate transaminase, AST) were only significantly observed in t

108 ing glycerate kinase (glxK), valine-pyruvate transaminase (avtA), superoxide dismutase (sodB), and 2

109 r destruction as indicated by elevated liver transaminases, azotemia, and hypoalbuminemia.

110 eta = 0.021; P = 3 x 10(-4)), higher alanine transaminase (beta = 0.002; P = 3 x 10(-5)), lower sex-h

111 Elevations of serum transaminases, bilirubin, and creatine kinase were infre

112 ll transplanted livers functioned, and serum transaminases, bilirubin, international normalized ratio

113 d resulted in significant reduction of serum transaminases, bilirubin, triphosphate nick-end labeling

114 The pyridoxal 5'-phosphate (PLP)-dependent transaminase BioA catalyzes the second step in the biosy

115 The PLP-dependent transaminase (BioA) of Mycobacterium tuberculosis and ot

116 ray findings, PaO2/FiO2, creatinine, alanine transaminase, cancer, cardiac arrest, chronic heart dise

117 significantly higher serum triglycerides and transaminases compared to mice on HFD alone.

118 rum alkaline phosphatase but increased serum transaminases compared with KO alone.

119 ne participant in each treatment group had a transaminase concentration of more than 3 x the upper li

120 rsensitivity [n=2], asymptomatic increase in transaminase concentrations [n=1]) and none of the parti

121 inued because of grade 3 or 4 raised alanine transaminase concentrations in 19 of 662 individuals in

122 y due to asymptomatic transient increases in transaminase concentrations in some idalopirdine-treated

123 It also normalized plasma transaminase concentrations, ameliorated liver fibrosis,

124 The duration of follow-up and serum alanine transaminase correlated with liver stiffness, and short

125 hepatic (aspartate transaminase and alanine transaminase) damage and of decongestion (N-terminal pro

126 teatosis, cold ischemic time, peak aspartate transaminase, day 5 bilirubin or international normalize

127 Transaminases decreased in patients in LAL-CL01 and incr

128 (56.4% vs. 24.4%, P=0.0009) and episodes of transaminase elevation (38.5% vs. 7.3%, P=0.0003) and wo

129 n = 6), nausea (n = 5), fatigue (n = 5), and transaminase elevation (n = 4).

130 vestigator-reported liver disease or >2-fold transaminase elevation at randomization.

131 nsient events were tachycardia in 1, alanine transaminase elevation in 1, and hyperglycemia in 2 part

132 grade 3 or higher laboratory AEs (1 with DR transaminase elevation); 14 subjects with serious clinic

133 reactions: 1 (4.8%) herpes zoster, 3 (14.3%) transaminase elevation, and 1 (4.8%) ischemic optic neur

134 events were reversible weight gain, hepatic transaminase elevation, and hypoalbuminemia.

135 e associated with peak hospitalization liver transaminase elevations >5x ULN.

136 (31/5), thrombocytopenia (25/11), and serum transaminase elevations (48/25).

137 3/10), and alanine transaminase or aspartate transaminase elevations (60/20).

138 .09; 95% confidence interval, 1.02-1.16) and transaminase elevations (odds ratio, 1.51; 95% confidenc

139 No patient developed transaminase elevations greater than twice baseline or g

140 Aspartate and alanine transaminase elevations occurring before treatment disco

141 ir participants led to study withdrawal; all transaminase elevations resolved on restarting lopinavir

142 A dose relationship to the transaminase elevations was not identified; all normaliz

143 Methotrexate-associated hepatic transaminase elevations were associated with obesity (35

144 Transaminase elevations were not observed in the RPT/INH

145 pletion, monthly follow-up visit compliance, transaminase elevations, and adverse reactions leading t

146 er treatment completion rate and causes less transaminase elevations, and weekly reminders may be an

147 attenuated the alcohol feeding-induced serum transaminase elevations, hepatic inflammation (mRNA expr

148 vastatin were associated with higher odds of transaminase elevations.

149 patients experienced transient grade 3 and 4 transaminase elevations.

150 ecific T-cell responses were detected during transaminase elevations.

151 Glutamate oxaloacetate transaminase enables anaplerotic refilling of TCA cycle

152 endpoints as opposed to ultrasonographic and transaminase endpoints.

153 We found increased levels of blood transaminases, enhanced liver necrosis, and more pronoun

154 and decarboxylases and combine these with a transaminase enzyme and norcoclaurine synthase for the e

155 extended to monitor the activity of alanine transaminase enzyme, a key biomarker for the detection o

156 aminopolyols, biocatalytic aminations using transaminase enzymes (TAms) have been investigated as a

157 Appropriate selection of the carboligase and transaminase enzymes enabled the biocatalytic formation

158 utility by sorting 25 nL droplets containing transaminase expressed in vitro.

159 nflammatory cell infiltration, serum alanine transaminase, expression of hepatic inflammatory markers

160 Group A donors had higher body mass index, transaminases, fasting blood sugar, triglyceride, low de

161 he Pi*MZ genotype have lower levels of serum transaminases, fewer AAT inclusions in liver, and lower

162 se markers were predictors of severe alanine transaminase flares, after treatment withdrawal, and HBV

163 In order to enable substrate profiling of transaminases for acceptance of different amines, a glyc

164 protein, a cytosolic enzyme acetylornithine transaminase, for which we now identified a moonlighting

165 zymes, namely 4-aminobutyrate-2-oxoglutarate transaminase (GABA-T) and alanine-glyoxylate transaminas

166 nin exhibited higher gamma-aminobutyric acid transaminase (GABA-T) enzyme activity which ensured suff

167 ein, a mitochondrial gamma-aminobutyric acid transaminase (GABAT), and reduces GABA in fly brains.

168 the specific enzyme that degrades GABA, GABA transaminase (GABAT), increases sleep, and we show here

169 se (PatD/YdcW and PuuC), gamma-aminobutyrate transaminase (GabT and PuuE), and succinic semialdehyde

170 Cytosolic GABA is degraded by the GABA transaminase, GabT, in the mitochondria.

171 kaline phosphatase (ALP), and gamma-glutamyl transaminase (GGT) were measured.

172 tively metabolized by glutamate oxaloacetate transaminase (GOT) to maintain cellular energetics and p

173 trated the ability of glutamate oxaloacetate transaminase (GOT) to metabolize neurotoxic glutamate in

174 ondria and cytoplasm, glutamate oxaloacetate transaminases (GOT), and malate dehydrogenases (MDH).

175 be converted into oxaloacetate by aspartate transaminase (GOT1).

176 The mitochondrial alanine transaminase GPT2 was found to be necessary and sufficie

177 hepatic safety event (an increase in alanine transaminase >3 times the upper limit of normal or an in

178 Plasma transaminases, hepatic histopathological and transmissio

179 Serum transaminases, histological changes, and animal survival

180 ll mice exhibited significantly higher serum transaminases, histological signs of necrosis, neutrophi

181 arsenic trioxide group, raised liver alanine transaminase in 11 (10%) of 108 versus 27 (25%) of 109,

182 In silico analyses indicated a periplasmic transaminase in fluorescent pseudomonads and other prote

183 Elevated liver transaminase in three (1%; one symptomatic) darunavir pa

184 was associated with risk of mildly elevated transaminases in GD independent of a lifestyle intervent

185 myelosuppression and transient elevation of transaminases in the trabectedin arm.

186 anine transaminase increase (20%), aspartate transaminase increase (15%), anemia and thrombocytopenia

187 ccurred in 84% of neutropenia (32%), alanine transaminase increase (20%), aspartate transaminase incr

188 ncrease (30 [12%] vs one [<1%]), and alanine transaminase increase (28 [11%] vs 15 [6%]).

189 jects with serious laboratory AEs (1 with DR transaminase increased).

190 y observed grade 3 and 4 adverse events were transaminase increases (40% alanine aminotransferase, 17

191 cells co-treated with palmitate and the pan-transaminase inhibitor aminooxyacetic acid confirmed tha

192 on of endogenous GHB formation with the GABA transaminase inhibitor vigabatrin also failed to influen

193 Moreover, aminooxyacetic acid, a transaminase inhibitor, was able to potently suppress PG

194 , bilirubin, alanine transaminase, aspartate transaminase, international normalized ratio, acute kidn

195 diatric Acute Liver Failure criteria (raised transaminases, International Normal Ratio >=2.0, no hist

196 at the stereogenic center established by the transaminase is not affected by the monoamine oxidase, a

197 ability and with downward trend in the donor transaminases) is not associated with higher post-liver

198 a neuromodulator, are identical to glutamine transaminase K (GTK), alpha-aminoadipate aminotransferas

199 sent studies show that KAT III and glutamine transaminase L are identical enzymes.

200 ant to ethanol-induced hepatic steatosis and transaminase leakage than the wild-type mice, suggesting

201 preferred aspartate transaminase and alanine transaminase less than 50 IU/mL.

202 .08-0.67 mukat/L]), a serum glutamic-pyruvic transaminase level of 34 U/L [0.57 mukat/L] (normal rang

203 on and revealed a serum glutamic-oxaloacetic transaminase level of 9 U/L [0.15 mukat/L] (normal range

204 ignificant (>/=grade 3) increases in alanine transaminase level or decreases in neutrophil count.

205 ignificant fibrosis (defined as an aspartate transaminase level to platelet count ratio index [APRI]

206 perfusion, at which point perfusate alanine transaminase level was 1152 IU/L and urea concentration

207 hospitalized for 9 days; predonation alanine transaminase level was 63 IU/L, and the period from with

208 Endpoints included peak serum aspartate transaminase level, postoperative complications, and hos

209 Secondly, clinicians should check liver transaminases level, and if AST are above 100 IU/L, they

210 lity (19%), thrombocytopenia (15%), elevated transaminase levels (7%), and fatigue (7%).

211 ere bilirubin levels (p<0.001), pretreatment transaminase levels (AST) (p=0.022), Child-Pugh subclass

212 s (p = 0.01), and greater reduction of liver transaminase levels (p < 0.03) than controls.

213 Transaminase levels and adiponectin were inversely assoc

214 e associated with a >40-fold increase in his transaminase levels and elevated INR and alkaline phosph

215 Only one patient had high transaminase levels and liver biopsy showed cystine crys

216 o AILI, as indicated by higher serum alanine transaminase levels and mortality.

217 y, which were most commonly fever, increased transaminase levels and rash.

218 High hepatic tumor burden and liver transaminase levels at baseline indicate poor outcome.

219 Comparison of transaminase levels between patients with normal liver a

220 er injury as assessed by histology and serum transaminase levels compared with C57Bl/6 AOM-treated mi

221 sease, which is defined by a rise in alanine transaminase levels during ART.

222 vated case fatality rates and elevated liver transaminase levels in subjects whose samples were RDT p

223 Persistent elevations in serum transaminase levels may serve as important noninvasive m

224 Transient increases in transaminase levels were noted in the MK-5172 groups giv

225 Transaminase levels within normal ranges were closely as

226 eurologic problems, unexplained elevation of transaminase levels, and female infertility.

227 ers of liver injury, including serum alanine transaminase levels, apoptosis, hepatic fat loading, and

228 fragments throughout the sinusoids, elevated transaminase levels, increased hepatic CD8+ and F4/80+ c

229 an 8-y-old male with intermittently elevated transaminase levels, liver fibrosis, mild ataxia, and co

230 The serum alanine transaminase levels, terminal deoxynucleotidyl transfera

231 dicated by apoptosis, fibrosis and increased transaminase levels.

232 esterol and serum bile salts, bilirubin, and transaminase levels.

233 anine aminotransferase levels, and aspartate transaminase levels.

234 d higher pre-ART triglycerides and aspartate transaminase levels.

235 (P = 0.015) significantly reduced aspartate transaminase levels.

236 formin preconditioning significantly reduced transaminase levels.

237 -groups showed significantly lower aspartate transaminase-levels compared with the SCS-groups 3 hours

238 nsaminase (ALT), and mitochondrial aspartate transaminase (m-AST).

239 ogically relevant variables identified serum transaminases--markers of tissue breakdown--as predictor

240 rat hepatocytes, causing a shift to aberrant transaminase metabolism that fuels CAC dysregulation and

241 Increases in plasma and tissue transaminases might represent a normal response to stres

242 drug-related adverse events: elevated liver transaminases, n = 1; rash, n = 1).

243 age < 40 years, single vasopressor or less, transaminases no greater than 3 times the normal limit,

244 ignificantly affected; elevations in alanine transaminase occurred in combination with atazanavir/rit

245 the use of imine reductase (IRED) and omega-transaminase (omega-TA) biocatalysts to establish the ke

246 omega-Transaminase (omega-TA) is an ideal catalyst for asymmet

247 ction (20/0), pneumonia (13/10), and alanine transaminase or aspartate transaminase elevations (60/20

248 n incidence rates for an increase in alanine transaminase or total bilirubin between both CSL112 arms

249 C increase (p = 0.005)], increased aspartate transaminase [OR, 2.47 (p = 0.019)], and decreased total

250 e aminotransferase (P = .024), and aspartate transaminase (P = .0040); elevated lactate dehydrogenase

251 e higher body mass index (P = 0.04), alanine transaminase (P = 0.0001), alkaline phosphatase (P = 0.0

252 levels of alanine transaminase and aspartate transaminase (p<0.05).

253 ver reperfusion (P<0.05), and reduced plasma transaminases (P<0.05) and ultrastructural markers of in

254 acid by the sequential activities of a C4''-transaminase (Pam), a 4-N-acetyltransferase (Pdi), a UDP

255 The GABAA receptor, GABA transporter, GABA transaminase, parvalbumin, and reelin were all highly ex

256 alate dehydrogenase and glutamic-oxaloacetic transaminase, predominantly in DCD tissue.

257 glycemic profiles, C-reactive protein, liver transaminases, prevalence of hypertension, and metabolic

258 with excellent enantioselectivity through a transaminase process.

259 hed methods including H&E-staining and serum transaminase profile failed.

260 is correlated with peak-postoperative serum-transaminases (PSTs) and whether PST is predictive of ou

261 ion was aspartate, which is generated from a transaminase reaction whereby Q-derived glutamate is con

262 d from unlabeled glutamate via the aspartate transaminase reaction.

263 ment of Mdr2KO mice with Ghr improved plasma transaminases, reduced biliary and fibrosis markers.

264 Subjects with HIV had smaller transaminase reductions after SVR.

265 ainst MDA-adducts positively correlated with transaminase release and hepatic tumor necrosis factor a

266 From postoperative days 1-4, serum transaminase release was significantly lower in the cDCD

267 control mice livers, but further stimulated transaminase release, lobular inflammation, and the hepa

268 Transaminases represent one of the most important enzyme

269 approaches based on the use of a lipase and transaminase, respectively, the combination of a chemica

270 Three participants developed a transaminase rise (alanine aminotransferase 4.5-5.9 time

271 inal symptoms, and increased levels of liver transaminases, serum creatinine, and pancreatic enzymes.

272 ant increase in serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transamina

273 ransaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) and lactate dehydrogenase (LDH) leve

274 igh selectivity (91-99% ee) depending on the transaminase source.

275 Herein, a novel one-pot omega-transaminase (TA)/monoamine oxidase (MAO-N) cascade proc

276 HMD by carboxylic acid reductases (CARs) and transaminases (TAs), which involves two rounds (cascades

277 transaminase 2 (ALT2)] is one of two related transaminases that catalyze the reversible addition of a

278 with signs of liver disease (e.g., elevated transaminases, thrombocytopenia), human immunodeficiency

279 either end-stage liver disease or aspartate transaminase to platelet ratio index (APRI) of >1.5, wer

280 50 while the fourth is a gamma-aminobutyrate transaminase; together they produce verazine from choles

281 ; 95% confidence interval, 2.41-13.34) and a transaminase toxicity grade of 2 or more (P= 0.009; haza

282 kogram, and dosages of aspartate and alanine transaminases, urea, and creatinine.

283 rrelated with waist-to-height ratio, alanine transaminase, uric acid, serum triglycerides, and blood

284 The median posttransplant peak in alanine transaminase was 1136 U/L (220-6683 U/L).

285 ls per mm(3), and serum glutamic oxaloacetic transaminase was 234 U/l.

286 Postoperative peak of aspartate transaminase was defined as primary endpoint, secondary

287 Elevated alanine transaminase/aspartate transaminase was seen in 67% of patients (23% grade >/=3

288 atment-related adverse event; elevated serum transaminases was the most frequently reported (7%), fol

289 us adverse events; a raised concentration of transaminases was the only serious adverse event regarde

290 reases in alanine transaminase and aspartate transaminase were observed at Day 7, resolving by Day 28

291 rial (GOT2) isoforms of glutamic-oxaloacetic transaminase were repressed in HCU animals by 86 and 30%

292 In the UK biobank database, levels of serum transaminases were increased in subjects with the Pi*MZ

293 TGF-beta1, IL-6, TNF-alpha and liver transaminases were measured in serum at two-months inter

294 However, plasma transaminases were not significantly different in the OD

295 Levels of serum transaminases were retrieved from 444,642 participants,

296 Increases in levels of transaminases were significantly more frequent (P < .001

297 Notably, immune cell infiltrates and liver transaminases were unchanged.

298 Sinusoidal perfusion and liver transaminases were used as markers of I/R injury.

299 aist circumference, waist-hip ratio, alanine transaminase, white blood cell count and lower high-dens

300 l infiltration as well as elevation of serum transaminases without affecting ethanol-induced steatosi