ライフサイエンスコーパス: transaminase

1 nduce splenomegaly or increase serum alanine transaminase.

2 lutarate transaminase and alanine-glyoxylate transaminase.

3 immunostaining, and less elevation of serum transaminases.

4 curring via glutamate dehydrogenase (GDH) or transaminases.

5 is and five instances of slight increases in transaminases.

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

7 ated with transient but marked elevations of transaminases.

8 e harbors three genes annotated as gabT GABA transaminases.

9 are accompanied by significant increases in transaminases.

10 n GABA suggested the importance of these two transaminases.

11 2; P = 1.4 x 10(-6)) and with higher alanine transaminase (0.02 [0.01, 0.03]; P = 0.002) and gamma-gl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 tinine levels, creatinine clearance), liver (transaminase activities, bilirubin levels), and cardioci

27 C282Y homozygotes if they have normal liver transaminase activities.

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

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

30 Transaminase activity is detected upon transfer of an am

31 Abdominal pain and increased transaminase activity were more frequent following chemo

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

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

34 Median peak aspartate transaminase after transplantation was 925 (interquartil

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

36 oprotective effect of glutamate oxaloacetate transaminase against stroke.

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

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

39 blood urea nitrogen) and hepatic (aspartate transaminase, alanine transaminase, and total bilirubin)

40 tory disease; statin use; and LFTs (albumin, transaminase, alkaline phosphatase, bilirubin, and gamma

41 Plasma alanine transaminase (ALT) activity, liver histology, and collag

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

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

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

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

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

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

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

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

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

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

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

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

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

55 ckade of HMGB1 significantly decreased serum transaminases (ALT and AST), markedly reduced the number

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

57 There were decreases in aspartate transaminase and alanine transaminase in the above-norma

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

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

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

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

62 The transaminase and bilirubin levels remained comparable du

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

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

65 cells depend on both glutamate-oxaloacetate transaminase and glutamate dehydrogenase to maintain Gln

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

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

68 dadRAX locus encoding the regulator alanine transaminase and racemase coupled with SpuC, the major p

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

70 A transient elevation in liver transaminases and dose-dependent QTc prolongation withou

71 rculating liver mRNAs with traditional serum transaminases and histopathology indicated that the circ

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

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

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

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

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

77 and hepatic (aspartate transaminase, alanine transaminase, and total bilirubin) function in 309 (235

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

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

80 xia, pain, rash, allergic reaction, elevated transaminases, and hyperbilirubinemia.

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

82 were hyperglycemia, hyperlipidemia, elevated transaminases, anemia, leucopenia, neutropenia, and muco

83 han pyruvate, the major alanine-synthesizing transaminases are AvtA, YfbQ (AlaA), and YfdZ (which we

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

85 Transaminases are valuable enzymes for industrial biocat

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

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

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

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

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

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

92 injury, which was assessed by histology and transaminase assays.

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

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

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

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

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

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

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

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

101 n pyruvate is a consequence of the decreased transaminase B (IlvE) activity that has previously been

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

103 substantial improvements in serum levels of transaminases, bilirubin, and amino acids.

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

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

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

107 inued lenalidomide because of rash, elevated transaminases/bilirubin, and cytopenias.

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

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

110 icopy suppression suggest that several other transaminases can contribute to alanine synthesis.

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

112 arrhea, urticaria, mild elevation of hepatic transaminases, capillary leak syndrome, and hypotension.

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

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

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

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

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

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

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

120 Transaminases decreased in patients in LAL-CL01 and incr

121 and strongly reduced in the Ler pop2-1 GABA transaminase-deficient mutant that accumulates higher le

122 rescine catabolic pathway that starts with a transaminase-dependent deamination.

123 is closely related to glutamate-oxaloacetate transaminase, EC 2.6.1.1.

124 antiepileptic drug designed to inhibit GABA-transaminase, effectively halting seizures.

125 (56.4% vs. 24.4%, P=0.0009) and episodes of transaminase elevation (38.5% vs. 7.3%, P=0.0003) and wo

126 [12.3%] versus clopidogrel 8/208 [3.8%]) and transaminase elevation (alanine transferase/aspartate tr

127 Grade 4 toxicities were a transaminase elevation (DL2) as a result of biliary sten

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

129 Transient dose-dependent transaminase elevation and relative QTc prolongation wer

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

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

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

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

134 (31/5), thrombocytopenia (25/11), and serum transaminase elevations (48/25).

135 3/10), and alanine transaminase or aspartate transaminase elevations (60/20).

136 .09; 95% confidence interval, 1.02-1.16) and transaminase elevations (odds ratio, 1.51; 95% confidenc

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

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

139 Grade 3 to 4 transaminase elevations were also more common with the c

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

141 Transaminase elevations were not observed in the RPT/INH

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

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

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

145 patients experienced transient grade 3 and 4 transaminase elevations.

146 vastatin were associated with higher odds of transaminase elevations.

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

148 Glutamate oxaloacetate transaminase enables anaplerotic refilling of TCA cycle

149 endpoints as opposed to ultrasonographic and transaminase endpoints.

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

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

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

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

154 ed grade < or = 2 thrombocytopenia, elevated transaminases, fatigue, nausea, and anemia.

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

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

157 xal 5'-phosphate (PLP)-dependent S-selective transaminase from Mesorhizobium sp. strain LUK (MesAT) i

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

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

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

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

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

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

164 We then transferred mutations in several transaminase genes into a yfbQ mutant and isolated a mut

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

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

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

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

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

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

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

172 Transient and reversible elevations in liver transaminases >3 times the upper limit of normal were ob

173 LEF, the incidence of infection and elevated transaminases have been comparable.

174 Plasma transaminases, hepatic histopathological and transmissio

175 Serum transaminases, histological changes, and animal survival

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

177 Compared to transaminase IlvE and NADH-dependent valine dehydrogenas

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

179 ifested by increased blood levels of alanine transaminase in common for most of the eight compounds.

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

181 nt on L-lysine suggests a minor role of this transaminase in L-lysine catabolism.

182 reases in aspartate transaminase and alanine transaminase in the above-normal groups from 121+/-206 a

183 Sitagliptin (Januvia(R)) uses a transaminase in the final chemical step.

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 TG2 and the transaminase-inactive mutant C277S-TG2 inhibited a HIF-d

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

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

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

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

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

192 The significance of hepatic fat and transaminase increases remains uncertain at this time.

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

194 ly improved body weight, liver weight, serum transaminases, insulin resistance, hyperglycemia, hyperc

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

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 1, diminished the elevation of serum alanine transaminase level after I/R injury (174.0+/-28.3 U/L fo

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

210 Cr) concentration, BUN:Cr ratio, and hepatic transaminase levels (P </= .05 for toxin effect or time

211 secreting and which correlated with alanine transaminase levels (r2 = 0.45; P = .001), were found be

212 Transaminase levels and adiponectin were inversely assoc

213 (P = 0.0002), correlating with reduced serum transaminase levels and E1A expression.

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

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

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

217 Comparison of transaminase levels between patients with normal liver a

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

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

220 Transaminase levels remained unchanged, or were reduced,

221 t-treated animals and a 10-fold elevation in transaminase levels that correlated with increases in ce

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

223 ituximab on HCV plasma viremia or on hepatic transaminase levels were observed.

224 Transaminase levels within normal ranges were closely as

225 sity, diabetes mellitus, and increased serum transaminase levels, an evidence-based approach to diagn

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 P attenuated the I/R-induced increased serum transaminase levels, histologic damage, increased induci

229 Sporadic increases in transaminase levels, increases in cholesterol and serum

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

231 The serum alanine transaminase levels, terminal deoxynucleotidyl transfera

232 anine aminotransferase levels, and aspartate transaminase levels.

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

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

235 (median 11-25 IU/ml) and have normal alanine transaminase levels.

236 low density lipoprotein, insulin, and liver transaminase levels.

237 dicated by apoptosis, fibrosis and increased transaminase levels.

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

239 Eq/L (LR, 18; 95% CI, 11-30), elevated liver transaminases (LR range, 2.5-5.2), hematuria (LR range,

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

241 hepatic oxidative insult, nor plasma alanine transaminase marking hepatocyte damage.

242 d serial assessment of liver injury by serum transaminase measurements, and histologic analysis was p

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

244 (n = 6; 15%), diarrhea (n = 4; 10%) elevated transaminases (n = 4; 10%), gastrointestinal hemorrhage

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

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

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 er limit of normal were reported for hepatic transaminases or creatinine kinase.

250 was associated with LIC (P = .006), alanine transaminase (P = .025), and weight (P = .026).

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 Blocks in both the GP and transaminase pathways were required to prevent growth wi

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

258 with excellent enantioselectivity through a transaminase process.

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

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

261 d from unlabeled glutamate via the aspartate transaminase reaction.

262 Subjects with HIV had smaller transaminase reductions after SVR.

263 d with WT, JNK2 KO mice had 38% less alanine transaminase release and 39% less necrosis by histology.

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

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

266 Transaminases represent one of the most important enzyme

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

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

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

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

271 , PUGNAc: 126 +/- 21 IU, p < .05), aspartate transaminase (sham surgery: 536 +/- 110, control: 1661 +

272 , PUGNAc: 42 +/- 22 pg/mL, p < .05), alanine transaminase (sham surgery: 95 +/- 14, control: 297 +/-

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

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

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

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

277 50 while the fourth is a gamma-aminobutyrate transaminase; together they produce verazine from choles

278 ; 95% confidence interval, 2.41-13.34) and a transaminase toxicity grade of 2 or more (P= 0.009; haza

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

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

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

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

283 uH gene encoding an arginine/lysine:pyruvate transaminase was expressed constitutively from plasmids;

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

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

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

287 Transaminases wer increased in 8 (16%), three of whom ac

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

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

290 Although mean serum transaminases were normal in TASH, total cytokeratin 18,

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

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

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

294 led with SpuC, the major putrescine-pyruvate transaminase, were key components to maintaining alanine

295 as also established that SpnR functions as a transaminase which converts the SpnQ product, TDP-4-keto

296 Third, glutamate pyruvate transaminase, which degrades ambient but not synaptic gl

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

298 ) plant proteins: a putative acetylornithine transaminase (WIN1), a protein phosphatase (WIN2) and a

299 modeling, and mutation approach to create a transaminase with marginal activity for the synthesis of

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