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1 scores) and hepatocellular injury (levels of aminotransferases).
2 between chorismate mutase and phenylpyruvate aminotransferase.
3 ls of alanine aminotransferase and aspartate aminotransferase.
4 oA, a pyridoxal 5'-phosphate (PLP)-dependent aminotransferase.
5 nsferase, and diaminobutyrate-2-oxoglutarate aminotransferase.
6 advanced fibrosis and 54% had normal alanine aminotransferase.
7 as associated with elevated plasma levels of aminotransferases.
8 t increase the incidence of elevated hepatic aminotransferases.
9 along with excellent selectivity over other aminotransferases.
10 e < 100 U/L, below analyzer range; aspartate aminotransferase 0 hour, 15.6 +/- 9.3 U/L vs 7 hours, 24
11 ly assayed in clinical laboratories (alanine aminotransferase 1, C-reactive protein, and myoglobin).
12 lycerate dehydrogenase, Phgdh; phosphoserine aminotransferase-1, Psat1) following treatment from days
13 8 who received placebo), increased aspartate aminotransferase (11 [8%] vs two [3%]), anaemia (seven [
14 ting (125 [66%]), and an increase in alanine aminotransferase (114 [60%]) in the ceritinib group and
16 e 3-4 adverse events were elevated aspartate aminotransferase (14 of 44, 32%), elevated gamma-glutamy
17 ng >/=2% of patients) were increased alanine aminotransferase (17 [3%] of 573 vs one [<1%] of 570) an
19 nts were transaminase increases (40% alanine aminotransferase, 17% aspartate aminotransferase), macul
21 sed amylase (31 [6%]), and increased alanine aminotransferase (28 [5%]), whereas in the sunitinib gro
22 induced significant improvement in aspartate aminotransferase (32.4 +/- 17.4 vs 21.5 +/- 6.9U/L), ala
23 (32.4 +/- 17.4 vs 21.5 +/- 6.9U/L), alanine aminotransferase (39.9 +/- 28.6U/L vs 23.8 +/- 14.1U/L),
24 pants developed a transaminase rise (alanine aminotransferase 4.5-5.9 times the upper limit of normal
25 aminotransferase (7 [11.3%] SAD), aspartate aminotransferase (4 [6.5%] SAD), and creatinine phosphok
27 transferase (ALT) (-67% and -60%), aspartate aminotransferase (-57% and -52%), and fibrogenesis bioma
28 alanine aminotransferase (64%) and aspartate aminotransferase (60%), hypoalbuminemia (55%), periphera
29 Mean postoperative day (POD) 7, aspartate aminotransferase (61.13 + 24.77 vs 73.17 + 53.71 IU/L; P
30 erse events were increased levels of alanine aminotransferase (64%) and aspartate aminotransferase (6
32 ated with a significant reduction in alanine aminotransferase activity [ALT, weighted mean difference
34 gical staining, measurement of serum alanine aminotransferase activity, and expression analyses of pr
37 sis (Arabidopsis thaliana), the lysine (Lys) aminotransferase AGD2-LIKE DEFENSE RESPONSE PROTEIN1 (AL
38 including nitrate reductase (NR) and alanine aminotransferase (AlaAT), were induced during secretion
39 ailable perfusate parameters (PP) (aspartate aminotransferase, alanine aminotransferase, lactate dehy
41 spartate aminotransferase (ASAT) and alanine aminotransferase (ALAT); oxidative stress (malondialdehy
42 the median age at onset was higher, alanine aminotransferase, albumin, and International Normal Rati
43 ence for alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma-glutam
44 BV DNA >=2000 IU/mL, with or without alanine aminotransferase (ALT) >=2-fold the upper limit of norma
45 women and HBeAg-negative women with alanine aminotransferase (ALT) >=40 IU/L as a predictor of high
46 dults with HBV DNA > 10(7) IU/mL and alanine aminotransferase (ALT) <= 1.5 times the upper limit of n
47 tamyl transferase (-30%; P < 0.001), alanine aminotransferase (ALT) (-49%; P = 0.009), and aspartate
48 y), corrected T1 (cT1; -8% and -9%), alanine aminotransferase (ALT) (-67% and -60%), aspartate aminot
49 tor-1 (markers for fibrinolysis) and alanine aminotransferase (ALT) (marker of ischemia-reperfusion [
50 ased contents, which may result from alanine aminotransferase (ALT) and branched-chain amino acid ami
51 inotransferase (AST) was higher than alanine aminotransferase (ALT) at admission (46 vs. 30 U/L) and
52 ed BM sproc recruitment, and reduced alanine aminotransferase (ALT) by 92% and 77% at 5 weeks and by
53 ualitative serum HBsAg, HBV DNA, and alanine aminotransferase (ALT) concentrations in addition to sta
54 Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) decreased significantly in the en
56 aspartate aminotransferase (AST) or alanine aminotransferase (ALT) elevation with fevers, and grade
57 etations of elevated blood levels of alanine aminotransferase (ALT) for drug-induced liver injury oft
58 mediating role of viral load and/or alanine aminotransferase (ALT) in the relation of smoking with H
59 and risk factors for elevated serum alanine aminotransferase (ALT) level among adult childhood cance
60 ssociated with an increase in plasma alanine aminotransferase (ALT) level of 26% in those with score
61 as viral DNA levels >2000 IU/mL and alanine aminotransferase (ALT) levels >80 U/mL, respectively.
63 tional studies of the association of alanine aminotransferase (ALT) levels with ischaemic heart disea
64 tes of FLD and its relationship with alanine aminotransferase (ALT) overtime were examined in HIV-HBV
65 tive and had higher initial and peak alanine aminotransferase (ALT) than those who tested negative.
67 tabolically abnormal or had elevated alanine aminotransferase (ALT) were higher than among those who
68 say capable of quantifying levels of alanine aminotransferase (ALT), a primary biomarker associated w
69 ng gamma-glutamyl transferase (GGT), alanine aminotransferase (ALT), and aspartate aminotransferase (
70 -density lipoprotein, triglycerides, alanine aminotransferase (ALT), and aspartate aminotransferase (
71 gamma-glutamyl transferase (GGT) and alanine aminotransferase (ALT), and higher number of heavy drink
72 ary concentrations of total protein, alanine aminotransferase (ALT), aspartate aminotransferase (AST)
74 and flavones reduced blood glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST)
75 tructed using baseline and change in alanine aminotransferase (ALT), aspartate aminotransferase (AST)
76 oups: patients with steatosis/normal alanine aminotransferase (ALT), steatosis/elevated ALT, and no s
78 ice fed an HFD exhibited lower serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST)
79 e classified as presumed NAFLD (pNF; alanine aminotransferase [ALT] level >/= 20 for women or >/= 31
80 a mouse model of ALD, liver injury (alanine aminotransferase [ALT]) and steatosis were prevented by
81 aspartate aminotransferase [AST] and alanine aminotransferase [ALT]), alkaline phosphastase, and crea
82 s (aspartate aminotransferase [AST], alanine aminotransferase [ALT], alkaline phosphatase [ALP], tota
83 nsistent pattern of rapid-onset elevation of aminotransferases, altered mentation, and disturbed coag
84 ession tree models based on level of alanine aminotransferase and abundance of genes encoding flagell
85 isplayed significantly higher mean aspartate aminotransferase and alanine aminotransferase levels thr
86 s accompanied by decreased levels of alanine aminotransferase and aspartate aminotransferase in the p
87 vo and correspondingly reduced serum alanine aminotransferase and aspartate aminotransferase levels a
90 kidneys showed significantly lower aspartate aminotransferase and lactate dehydrogenase levels compar
91 NEL) staining, circulating levels of alanine aminotransferase and lactate dehydrogenase, and inflamma
92 and alanine aminotransferase; POD3 aspartate aminotransferase and prothrombin time-international norm
93 regression tree model with level of alanine aminotransferase and relative abundance of the lipopolys
96 sedimentation rate, and creatinine, alanine aminotransferase, and aspartate aminotransferase levels
98 tions of alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferase in child
99 ey injury (P = 0.01), lower plasma aspartate aminotransferase, and reduced rate of troponin rise (P =
100 ten-3-one, bile acids, alanine and aspartate aminotransferases, and neoepitope-specific N-terminal pr
101 ve clinical variables and revealed aspartate aminotransferase as an important, albeit previously unde
102 lume (BV/TV) by micro-CT analysis; aspartate aminotransferase (ASAT) and alanine aminotransferase (AL
103 cle toxicity, as defined by changes in liver aminotransferases (aspartate aminotransferase [AST] and
104 n control group (mean difference for alanine aminotransferase, aspartate aminotransferase, alkaline p
105 01) serum total lipids, cholesterol, alanine aminotransferase, aspartate aminotransferase, and creati
107 ALP had greater reductions in serum alanine aminotransferase, aspartate aminotransferase, gamma-glut
108 r than 50 years; increased levels of alanine aminotransferase, aspartate aminotransferase, or gamma-g
109 with significant elevation of serum alanine aminotransferase, aspartate aminotransferase, total bili
110 th lower serum alkaline phosphatase; alanine aminotransferase; aspartate aminotransferase; gamma-glut
111 ID-19 patients had elevated plasma aspartate aminotransferase (AST) and 35% had elevated alanine amin
113 They found that an increase in aspartate aminotransferase (AST) and its dynamicity correlated wit
114 ating characteristics curve showed aspartate aminotransferase (AST) had highest area under the curve
115 ng, lower platelet count, elevated aspartate aminotransferase (AST) level, positivity in the nonstruc
116 rum alanine aminotransferase (ALT)/aspartate aminotransferase (AST) levels and less hepatic inflammat
117 ts showed significantly lower peak aspartate aminotransferase (AST) levels than those receiving CS gr
118 h grade 3 rash and fevers, grade 4 aspartate aminotransferase (AST) or alanine aminotransferase (ALT)
119 lanine aminotransferase (ALT), and aspartate aminotransferase (AST) using a general linear model for
120 lder patient's age, abnormal serum aspartate aminotransferase (AST) value, Hepatitis C virus (HCV) in
122 ng to reported data, patients with aspartate aminotransferase (AST)>100 IU/L and 50 IU/L showed signi
124 city with improved blood levels of aspartate aminotransferase (AST), alanine transaminase (ALT), and
125 e, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, creatinine
126 lanine aminotransferase (ALT), and aspartate aminotransferase (AST), among a discovery set of 731 par
127 in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (
129 of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, total cholesterol, chol
130 limit of normal (ULN), platelets, aspartate aminotransferase (AST), hemoglobin, sodium, patient age,
131 g for the total enzyme activity of aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and
132 n, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and
133 inoma (HCC) and the performance of aspartate aminotransferase (AST)-platelet ratio index (APRI) and a
135 hanges in liver aminotransferases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT
136 ical characteristics, liver tests (aspartate aminotransferase [AST], alanine aminotransferase [ALT],
137 t-generation gamma-amino butyric acid (GABA)-aminotransferase (AT) inhibitor, shows comparable pharma
138 ssential E. coli enzymes: the branched-chain aminotransferase BCAT and the DNA replication initiator
139 rresponding to leucine, can assess both BCAA aminotransferase (BCAT) and branched-chain alpha-keto ac
140 nsferase (ALT) and branched-chain amino acid aminotransferase (BcAT)'s high expression levels, respec
141 supported by elevations in plasma aspartate aminotransferase, blood urea nitrogen, and creatinine, 8
142 he kynurenine-3-monooxygenase and kynurenine aminotransferase branches of the kynurenine pathway are
144 fection, with normal or only slightly raised aminotransferases; cirrhosis and hepatocellular carcinom
145 s, inflammation, and serum levels of alanine aminotransferase compared with mice given a control vect
147 ons (two [7%] patients), increased aspartate aminotransferase concentration (two [7%] patients), and
148 s (36 [9%] vs 12 [3%]) and increased alanine aminotransferase concentrations (34 [9%] vs 28 [7%]).
150 ents were rash (89 [56%]), increased alanine aminotransferase concentrations (74 [46%]), and increase
152 (15 [50%] of 30 patients), increased alanine aminotransferase concentrations (two [7%] patients), inc
153 (3) IU/mL (HBeAg-negative) and serum alanine aminotransferase concentrations less than seven times th
158 who achieved SVR12 (n = 14), serum levels of aminotransferases did not normalize during or after DAA
159 elated adverse events were increased alanine aminotransferase (eight [3%] of 260 patients), anaemia (
160 grade 3 dermatitis (five patients), grade 3 aminotransferase elevation (seven patients), grade 3 dia
162 lt in mild cholestasis, chronic elevation of aminotransferases, elevation of (low-density lipoprotein
163 vation in this cohort exhibited peak alanine aminotransferase elevations >2 times the upper limit of
164 lone, statin initiators had reduced risks of aminotransferase elevations (HR, 0.57 [95% CI, .45-.72])
166 Limited, asymptomatic, and transient alanine aminotransferase elevations in the low-dose (n = 1) and
169 mbocytopenia (five [28%]), increased alanine aminotransferase (five [28%]), and hypokalaemia (four [2
171 In Study 2, 16 g/d increased mean aspartate aminotransferase from baseline (19 U/L; 95% CI: 17, 22 U
172 features of liver damage and serum levels of aminotransferase, gamma-glutamyl transferase, and biliru
173 in serum alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, tissue inh
174 phatase; alanine aminotransferase; aspartate aminotransferase; gamma-glutamyltransferase; and, in wom
176 ymptomatic seroconversion illness or alanine aminotransferase > 10 x upper limit of normal) or anti-H
177 We determined development of (1) liver aminotransferases >200 U/L, (2) severe ALI (coagulopathy
178 ral load [IVL]) and normal levels of alanine aminotransferase, HBcrAg levels of 10 KU/mL or more iden
179 ow-up time, with increasing level of alanine aminotransferase, hemoglobin A1C (P<.05), gamma-glutamyl
181 both kynurenic acid synthesis and kynurenine aminotransferase II activity in cultured hepatocytes and
182 indings uncover a critical role for tyrosine aminotransferase in the oxidative stress response via m-
183 ls of alanine aminotransferase and aspartate aminotransferase in the plasma, indicating less liver da
184 HDV co-infection and normalisation of serum aminotransferases in a high proportion of patients 1 yea
186 ated a causal role of increased ALT (alanine aminotransferase) in the development of type 2 diabetes
187 nspired by the discovery of the nonselective aminotransferase inactivator (1R,3S,4S)-3-amino-4-fluoro
188 ble mechanisms, based on mechanisms of known aminotransferase inactivators: Michael addition, enamine
189 ferase increase (39%), nausea (38%), alanine aminotransferase increase (28%), and dysgeusia (25%) wer
190 lour changes (67%), fatigue (54%), aspartate aminotransferase increase (39%), nausea (38%), alanine a
191 25 patients in the sunitinib group), alanine aminotransferase increase (54 [13%] vs 11 [3%]), and dia
192 g in more than two patients included alanine aminotransferase increase (five [14%]), pyrexia (four [1
193 se events were pyrexia (four [11%]), alanine aminotransferase increase (four [11%]), hypertension (fo
194 fatigue (three [1%] vs seven [3%]), alanine aminotransferase increase (three [1%] vs four [2%]), and
195 five [14%]), pyrexia (four [11%]), aspartate aminotransferase increase (three [8%]), and ejection fra
196 oma, three [7%] for osteosarcoma), aspartate aminotransferase increase (two [4%] for Ewing sarcoma, t
197 vs 28.1%), pyrexia (38.7% vs 26.0%), alanine aminotransferase increased (33.9% vs 22.8%), and lipase
198 tients, statin initiators had lower risks of aminotransferase increases (HR, 0.52 [95% CI, .40-.66]),
199 oot or intrathecal infusion of aminobutyrate aminotransferase inhibitor attenuated the spontaneous ac
201 ulfoacetaldehyde by a known taurine:pyruvate aminotransferase is followed, unexpectedly, by reduction
202 alpha1 enhances the expression of kynurenine aminotransferases (Kats), which convert kynurenine into
203 of aspartate aminotransferase (AST), alanine aminotransferase, lactate dehydrogenase, and creatinine
204 rs (PP) (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, glucose, lactat
205 disease (hepatic steatosis >10% and alanine aminotransferase level >=45 U/L) randomized 1:1 to an in
206 al normalized ratio <= 1, baseline aspartate aminotransferase level <= 49 U/L, and a decrease in alan
207 (in 21% of the patients), increased alanine aminotransferase level (in 11%), increased aspartate ami
208 nsferase level (in 11%), increased aspartate aminotransferase level (in 9%), hyponatremia (in 8%), an
212 e level <= 49 U/L, and a decrease in alanine aminotransferase level at week 24 by 17 U/L or more, to
214 enzyme levels were elevated, with an alanine aminotransferase level of 48 U/L (0.80 ukat/L) (normal r
215 enzyme levels were elevated, with an alanine aminotransferase level of 48 U/L (0.80 ukat/L) (normal r
216 99 U/L [0.65-1.65 ukat/L]), and an aspartate aminotransferase level of 88 U/L (1.47 ukat/L) (normal r
217 nge, 0-29 U/L [0-0.48 ukat/L]), an aspartate aminotransferase level of 98 U/L (1.6 ukat/L) (normal ra
218 nge, 0-29 U/L [0-0.48 ukat/L]), an aspartate aminotransferase level of 98 U/L (1.6 ukat/L) (normal ra
219 iglyceride levels, and a decrease in alanine aminotransferase level) to significantly associate with
220 tients, statin initiators had lower risks of aminotransferase levels >200 U/L (HR, 0.66 [95% CI, .53-
221 ted by decreased serum alanine and aspartate aminotransferase levels and numbers of TUNEL-positive ce
222 serum alanine aminotransferase and aspartate aminotransferase levels as well as proinflammatory cytok
225 for viral load and for serum creatinine and aminotransferase levels each correlated with improved su
226 nd that plasma creatine kinase and aspartate aminotransferase levels in Acsl1(M) (-/-) mice are 3.4-
228 f the 6 patients (67%) had increased alanine aminotransferase levels of more than 1.5 times the upper
229 iation study combining cirrhosis and alanine aminotransferase levels performed in 5 discovery studies
230 of 22 patients (18%) with increased alanine aminotransferase levels showed positive reactivity on HE
231 mean aspartate aminotransferase and alanine aminotransferase levels throughout pregnancy, but this d
240 an excess of myalgias, elevation of hepatic aminotransferases levels in the plasma, incident diabete
241 ber of the MocR/GabR-type proteins that have aminotransferase-like, pyridoxal 5'-phosphate-binding do
242 kines and a marker of liver failure (alanine aminotransferase); liver tissues were collected and anal
243 (40% alanine aminotransferase, 17% aspartate aminotransferase), maculopapular rash (17%), and neutrop
245 cluding leg cramps (n = 2), elevated alanine aminotransferase (n = 2), diarrhea (n = 1), and nausea/a
246 s and improved liver markers such as alanine aminotransferase, NAFLD activity score, and fibrosis.
250 o show that Rv3722c is the primary aspartate aminotransferase of M. tuberculosis, and mediates an ess
252 5 [22%] patients), and elevations in alanine aminotransferase or aspartate aminotransferase (25 [12%]
253 NA below 2000 IU/mL, normal level of alanine aminotransferase) or functional cure (HBsAg below 0.05 I
254 evels of alanine aminotransferase, aspartate aminotransferase, or gamma-glutamyl transferase; and low
255 creased leukocyte count (P < .0001), alanine aminotransferase (P = .024), and aspartate transaminase
257 of ALDH2, and two traits including aspartate aminotransferase (P = 5.20 x 10(-13)) and alanine aminot
258 enylhydrazine, resulted in increased alanine aminotransferase plasma levels and NGAL expression.
259 age, using validated serum fibrosis markers, aminotransferase platelet ratio index (APRI) and fibrosi
260 ices for ruling out cirrhosis: the aspartate aminotransferase-platelet ratio index (APRI) and fibrosi
262 hosphatase (R = 0.543, P = 0.003), aspartate aminotransferase (R = 0.420, P = 0.029), and lactate (R
263 ienced hypotension, and 5 had elevated serum aminotransferases, reinforcing the need for vigilant mon
264 urface antigen (HBsAg), HBV DNA, and alanine aminotransferase results obtained while on DAA treatment
268 her populations were associated with alanine aminotransferase (rs200088103; p.Arg133Trp, P = 2.02 x 1
269 binemia (seven of 44, 16%), elevated alanine aminotransferase (seven of 44, 16%), and pain (seven of
270 ctate correlated with EAD, 90-minute alanine aminotransferase showing the highest area under the rece
271 g >/=2% of patients) were elevated aspartate aminotransferase (six [2%] vs none), dyspnoea (six [2%]
275 Caenorhabditis elegans ortholog of tyrosine aminotransferase (TATN-1)-the first enzyme involved in t
276 ated more closely with gold standard alanine aminotransferase than miR-122, and there was a surprisin
277 ted grade 4 increase in the level of alanine aminotransferase that led to treatment discontinuation.
279 e decline or increase of FIB-4 and aspartate aminotransferase to platelet ratio index (APRI) on HCC r
280 ASH clinical scoring system (NCS), aspartate aminotransferase to platelet ratio index (APRI), FIB-4 a
281 non-invasively via the serum tests Aspartate Aminotransferase to Platelet Ratio Index and HepaScore a
282 with biocatalysts such as ketoreductases and aminotransferases to realize stereoconvergent syntheses
283 d outperformed the Mayo Clinic and aspartate aminotransferase-to-platelet ratio index (APRI) scores (
285 for three noninvasive biomarkers (aspartate aminotransferase-to-platelet ratio index, Fibrosis-4 ind
286 ircumference, levels of alanine or aspartate aminotransferase, total and low-density lipoprotein chol
287 of serum alanine aminotransferase, aspartate aminotransferase, total bilirubin and direct bilirubin l
288 erious adverse events were increased alanine aminotransferase (two [<1%] of 260 patients), increased
289 [<1%] of 260 patients), increased aspartate aminotransferase (two [<1%]), and nausea (two [<1%]).
290 gait disturbance (one event), elevated liver aminotransferases (two events in two patients, one with
293 markers lactate dehydrogenase and aspartate aminotransferase were persistently low (lactate dehydrog
294 hyperkalaemia, and grade 4 increased alanine aminotransferase were reported in one patient each.
296 omiting and low-magnitude increases in liver aminotransferases were the most frequent treatment-emerg
297 rmalities, including elevated creatinine and aminotransferases, were mild and normalized after treatm
299 homodimeric PLP-dependent enzyme, aspartate aminotransferase, which was reacted in situ with alpha-m
300 ession of EPSPS, as well as genes coding for aminotransferases, zinc finger proteins, and several unc