ライフサイエンスコーパス: AST

1 AST was probably complexed with immunoglobulins possibly

2 ions remained (ALT beta = -0.11, p = 0.0037; AST beta = -0.05, p = 0.0330; NAFLD liver fat score beta

3 iations with ALT (beta = -0.08, p = 0.0111), AST (beta = -0.05, p = 0.0155) and NAFLD liver fat score

4 minotransferase (42 versus 28U/L, P = 0.02), AST (35 versus 25U/L, P = 0.02), AST-to-platelet ratio i

5 P = 0.02), AST (35 versus 25U/L, P = 0.02), AST-to-platelet ratio index (0.77 versus 0.25, P = 0.000

6 d significant (ALT beta = -0.08, p = 0.0400; AST beta = -0.03, p = 0.20; NAFLD liver fat score beta =

7 d the MIC results obtained using the Vitek 2 AST-GN69 and AST-XN06 cards to those obtained by CLSI br

8 The performances of Vitek 2 AST-GN69 and AST-XN06 cards were compared to Clinical an

9 ients had grade 3 rashes and one had grade 3 AST elevation.

10 elevated ALT (HR, 4.08; 95% CI: 1.99-8.33), AST (HR, 4.33; 95% CI: 2.18-8.59), and GGT (HR, 7.91; 95

11 atio index (APRI), fibrosis-4 index (FIB-4), AST/alanine aminotransferase (ALT) ratio (AAR), and age-

12 Of the investigated biomarkers, IL-6, AST, and GGT produced the highest change in the regressi

13 ernational normalized ratio (INR), and day-7 AST were independently associated with PNF on multivaria

14 (OR (>/= 2 vs 0 cup/d): 0.62 [0.41, 0.94]), AST (0.74 [0.49, 1.11]), and GGT (0.70 [0.49-1.00]).

15 AST]/platelet ratio, FIB-4, hyaluronic acid, AST/alanine aminotransferase ratio, and Mayo score) in d

16 can be suppressed by use of a gut adsorbent, AST-120.

17 the redox imbalance and functionally affect AST.

18 Age, AST, AST/ALT ratio, and total bilirubin were identified

19 s, WBC count, creatinine clearance, albumin, AST, number of study drugs, biologic study drug (yes v n

20 ere 1 to 2 log2 concentrations higher by all AST methods, except Etest, potentially impacting definit

21 ALT, AST, and GGT correlated with BMI, CRP and HbA1c and inve

22 Chronic ALT, AST and gamma-GT elevation was present in 29%, 20% and 5

23 The increased levels of ALT, AST and MDA along with decreased activities of SOD and C

24 .69 (0.57, 0.83) for abnormal levels of ALT, AST, ALP, and GGT, respectively.

25 <6 months by >/=1 additional NAT(s), or ALT, AST, and platelets <90 days, or any test ordered by an i

26 sma alanine/aspartate aminotransferases (ALT/AST) and hepatic triglycerides/free cholesterol.

27 DLTs were increased ALT/AST (n = 1), dizziness, confusion, and sensory disturban

28 sis markers (alanine aminotransferase [ALT], AST, and platelets plus patient age) to stage liver dise

29 erum aspartate and alanine aminotransferase (AST, ALT) (aOR AST: 3.34, ALT: 2.18 for >25% values >100

30 included higher aspartate aminotransferase (AST) (odds ratio [OR] = 1.12, P = 0.007) and lower plate

31 ferase (ALT) and aspartate aminotransferase (AST) (P < 0.0001, analysis of variance [ANOVA]).

32 , P < 0.001) and aspartate aminotransferase (AST) (r(2) = 0.15, P = 0.002).

33 associated with aspartate aminotransferase (AST) 14-day post-transplantation (q < 0.05) and were mor

34 Aspartate aminotransferase (AST) activity at LT (hazard ratio [HR] = 1.38 for doubli

35 ansferase (ALT), aspartate aminotransferase (AST) and fetuin-A were determined in fasting blood sampl

36 The increase of aspartate aminotransferase (AST) by >25% (hazard ratio [HR] 8.4; P < 0.001), an incr

37 es liver fat and aspartate aminotransferase (AST) concentrations in healthy men compared with the con

38 ics curve showed aspartate aminotransferase (AST) had highest area under the curve 0.761 (95% CI: 0.6

39 count, elevated aspartate aminotransferase (AST) level, positivity in the nonstructural protein 1 (N

40 ciations between aspartate aminotransferase (AST) levels and T2D risk, with a corresponding relative

41 re defined using aspartate aminotransferase (AST) levels, fibrosis-4 (FIB-4) index and AST-to-platele

42 y FibroSURE with aspartate aminotransferase (AST) measurements and HIV co-infection status, the discr

43 fevers, grade 4 aspartate aminotransferase (AST) or alanine aminotransferase (ALT) elevation with fe

44 as postoperative aspartate aminotransferase (AST) peak value; early graft dysfunction and histologica

45 superior to the aspartate aminotransferase (AST) to platelet ratio index (APRI) for all fibrosis sta

46 ferase (ALT) and aspartate aminotransferase (AST) were increased in wildtype, but not MIF-/-, mice.

47 levels of plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) and tissue necrosis

48 uses a patient's aspartate aminotransferase (AST), alanine aminotransferase (ALT), and international

49 serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total alkaline

50 ansferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and gamma-glutamytransf

51 ansferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and gamma-glutamyl tra

52 erase (ALT), and aspartate aminotransferase (AST), among a discovery set of 731 participants of the R

53 minotransferase, aspartate aminotransferase (AST), and bilirubin levels <1.5 times the upper limit of

54 ansferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase (GGT) elevation was

55 t albumin, day-1 aspartate aminotransferase (AST), day-1 lactate, day-3 bilirubin, day-3 internationa

56 minotransferase, aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), and total bilirub

57 triglyceridemia, aspartate aminotransferase (AST), platelets, and the homeostasis model assessment of

58 Aspartate aminotransferase (AST)-to-platelet ratio (APRI) was calculated as = 100*(a

59 stic accuracy of aspartate aminotransferase (AST)-to-platelet ratio index (APRI), fibrosis-4 index (F

60 a high ratio of aspartate aminotransferase (AST):ALT were independent risk factors for ALF.

61 27, P = 0.005), aspartate aminotransferase (AST; 26 versus 21, P = 0.01), direct bilirubin (0.13 ver

62 s and placebo in aspartate aminotransferase (AST; p<0.0001), alanine aminotransferase (ALT; p<0.0001)

63 LFTs, including aspartate-aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyltran

64 inotransferases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) are usually inc

65 ferase [ALT] and aspartate aminotransferase [AST]) were compared between 162 C282Y homozygotes and 1,

66 ansferase [ALT], aspartate aminotransferase [AST], gamma-glutamyl transpeptidase [GGT], alkaline phos

67 o validate APRI (aspartate aminotransferase [AST]-to-platelet ratio index) and FIB-4, an index from s

68 l markers (e.g., aspartate aminotransferase [AST]/platelet ratio, FIB-4, hyaluronic acid, AST/alanine

69 ulated as = 100*(aspartate aminotransferase [AST]/upper limit of AST)/platelet.

70 novo lipogenesis, alanine aminotransferase, AST, and gamma-glutamyl transpeptase) and fructose or su

71 hatase, ALP, and aspartate aminotransferase, AST) and total serum protein.

72 an increase in aspartate aminotransferase, (AST), alanine aminotransferase (ALT), alkaline phosphata

73 on univariate analysis, and acceptance of an AST intervention was associated with a trend toward redu

74 y required a 100 muL sample and relied on an AST-free calibration.

75 for doubling of creatinine, P = 0.0004), and AST at LT (HR = 1.36 for doubling of AST, P = 0.004) wer

76 significant increases in ALT (p < 0.001) and AST (p = 0.013) with increased fat content and evidence

77 mbin time (14.4 versus 12.4, P = 0.002), and AST-to-platelet ratio index (0.31 versus 0.23, P = 0.003

78 Expanded mutagenesis of the alphaN and AST allowed us to further assess the role of these two r

79 a C282Y homozygote increased as the ALT and AST activities decreased.

80 Mean ALT and AST activities were significantly lower in C282Y homozyg

81 ALT and AST tended to normalize in 81% of patients; CB2 mRNA lev

82 ALT and AST values were significantly higher in males than in fe

83 antly decreased serum transaminases (ALT and AST), markedly reduced the number of hepatic inflammator

84 294 and 292; and 366 and 321 U/L for ALT and AST, in Vit D, LE and LE + Vit D treated groups, respect

85 thrombocytopenia, and elevations of ALT and AST, resulting in 0.3 mug/kg per day being determined th

86 levating the levels of liver enzymes ALT and AST.

87 ts, both of whom experienced grade 3 ALT and AST.

88 manifested by a marked decrease in ALT, and AST serum levels (from 900 and 1021 U/L in the control g

89 receiving tenofovir disoproxil fumarate) and AST (20 [3%] of 577 patients receiving tenofovir alafena

90 ults obtained using the Vitek 2 AST-GN69 and AST-XN06 cards to those obtained by CLSI broth microdilu

91 The performances of Vitek 2 AST-GN69 and AST-XN06 cards were compared to Clinical and Laboratory

92 mproved overall TAT to ID (18 to 16.5 h) and AST (42.3 to 40.7 h) results compared to MALDI (P < 0.00

93 e (AST) levels, fibrosis-4 (FIB-4) index and AST-to-platelet ratio index (APRI) score.

94 aminotransferase-to-platelet ratio index and AST:alanine aminotransferase ratio were not different.

95 A, V7E, L8E, V11A, S12A, Y13A, and M17A) and AST (G475I, V477D, and I485A) regions impair or potentia

96 tar erythrodysesthesia (PPE), mucositis, and AST, ALT, and lipase elevations and grade 2 mucositis th

97 ion occurred between the preintervention and AST intervention groups (64.3% versus 72.6%, P = 0.173).

98 ation rate, albumin-to-creatinine ratio, and AST.

99 17.3 x ULN, TBL greater than 6.6 x ULN, and AST:ALT greater than 1.5 identified patients who develop

100 and alanine aminotransferase (AST, ALT) (aOR AST: 3.34, ALT: 2.18 for >25% values >100 U/L versus <25

101 HCV at 6 months posttransplant with ascites, AST 503 IU/mL, alkaline phosphatase of 298 IU/mL, HCV RN

102 rum markers of liver damage, high aspartate (AST, >49.9 IU/L) and alanine aminotransferase (ALT, >56.

103 Age, AST, AST/ALT ratio, and total bilirubin were identified as si

104 three patients (6.8%) and included asthenia, AST elevation, creatine phosphokinase elevation, and dec

105 flow of bacterial and yeast ID and bacterial AST using the Accelerate Pheno system in the clinical mi

106 h compared to days in standard culture-based AST techniques.

107 MIC determined using dielectrophoresis-based AST (d-AST) was consistent with the results of the broth

108 fication that agreed with cell culture-based ASTs, obtained by a quicker, more convenient procedure.

109 d the severity of IR injury as determined by AST and ALT levels, as well as immune cell infiltrates.

110 sistance pattern most frequently observed by AST devices was "cefoxitin resistance/oxacillin suscepti

111 foundation to develop a rapid, point-of-care AST and strengthen global antibiotic stewardship.

112 The applicability of single cell AST is demonstrated by the rapid determination of the an

113 To optimize the protocol for single cell AST, the bacterial growth rate of individual bacteria un

114 tracking of single Ag-specific CD4 T cells (ASTs) involved in these immune responses challenging.

115 fection with HCV (7.29, 1.95-27.34), chronic AST (6.58, 1.30-33.25) and gamma-GT (5.17, 1.56-17.08) e

116 stration (FDA) limitations on how commercial AST systems can be used for diagnostic testing, the abse

117 ia to defined locations in high-conductivity AST buffer.

118 This viewpoint will highlight contemporary AST challenges faced by the clinical laboratory, and pro

119 nsplantation compared to untreated controls (AST 563.5 vs. 1204 U/L, P = 0.023).

120 ncluded history of vomiting, platelet count, AST level.

121 model that included baseline platelet count, AST/ALT ratio, bilirubin, and severe worsening of platel

122 We describe the origins of current AST reference methodology, highlight the sources of AST

123 Current ASTs rely on time-consuming differentiation of resistanc

124 ermined using dielectrophoresis-based AST (d-AST) was consistent with the results of the broth diluti

125 that our mobile-reader meets the FDA-defined AST criteria, with a well-turbidity detection accuracy o

126 inical events committee-adjudicated definite AST (occurring </=24 hours after percutaneous coronary i

127 An increased risk of definite AST was associated with shorter than with longer procedu

128 site, recognized by the previously described AST-1 Ets domain factor, and two distinct types of homeo

129 This digital AST (dAST) determined susceptibility of clinical isolate

130 gainst Diploptera punctata allatostatin (Dip-AST), Manduca sexta allatotropin (Mas-AT), and serotonin

131 s per hemisphere: cluster 1 and 3 showed Dip-AST/5HT immunostaining, whereas cluster 2 showed Dip-AST

132 immunostaining, whereas cluster 2 showed Dip-AST/Mas-AT immunostaining.

133 = 2), thrombocytopenia (n = 2), and elevated AST/ALT (n = 1), were observed with schedule A; one dose

134 story of heavy alcohol consumption, elevated AST and/or ALT (<300 U/L), serum bilirubin >34 mumol/L,

135 ose-limiting toxicity was observed (elevated AST/ALT) was observed with schedule B.

136 into many small volumes during dPCR enabled AST results after short exposure times by 1) precise qua

137 els positively correlated with liver enzymes AST and ALT, and negatively correlated with white blood

138 For AST, test cells were treated with drugs before ferricyan

139 The AUROC for AST/ALT ratio, the NAFLD fibrosis score, and the BARD sc

140 being a C282Y homozygote was determined for AST and ALT ranges.

141 No probe was identified for AST levels.

142 Isolated or combined LFTs for AST, ALT, gammaGT, LDH, and PA are not helpful for detec

143 s proposed as a quality control organism for AST of Nocardia sp., and the use of a disk diffusion tes

144 Age, gender, AST, alanine aminotransferase, alkaline phosphatase, pla

145 cholesterol; triglycerides; fasting glucose; AST; and ALT levels were analyzed on a biochemistry anal

146 Similar to other AGC kinases, the GRK5 AST is an integral part of the nucleotide-binding pocket

147 t-TLA TATs to organism IDs (18.5 to 16.9 h), AST results (41.8 to 40.8 h), and preliminary results fo

148 High AST completely mediated the HBV infection-any cataract a

149 High AST significantly mediates the effects of HBV infections

150 osis severity and graft survival, and a high AST at LT may be an important predictor of fibrosis risk

151 r and any cataract were not mediated by high AST or ALT.

152 ct effects, not by mediation effects of high AST or ALT.

153 minants of advanced fibrosis included higher AST (OR = 1.08, P = 0.007), lower alanine aminotransfera

154 A significantly improved TAT to organism ID, AST report, and preliminary negative results.

155 ID/AST performance, the average times to results, and workf

156 Pheno system provides rapid and accurate ID/AST results for most of the organisms found routinely in

157 is easy to use, reduces hands on time for ID/AST of common blood pathogens, and enables clinically ac

158 ne susceptibility testing using the Vitek II AST-P620 card.

159 review, we discuss how and why PK-PD impacts AST and the way infectious diseases are being treated, w

160 variability, and propose ideas for improving AST predictive power.

161 (117 in the preintervention group and 129 in AST the intervention group), and 78 patients had bactere

162 Detection of these isolates in AST systems based on cefoxitin and/or oxacillin testing

163 pathologic features in the livers, including AST, ALT, and a panel of cytokines and chemokines, were

164 yme elevations (increased ALT: 9%; increased AST: 9%).

165 luded hyperbilirubinemia (25%) and increased AST (36%).

166 es of thrombocytopenia (11.9%) and increased AST serum concentration (4.3%).

167 tropenia (11% v 9%, respectively), increased AST (11% v 2%, respectively), and increased ALT (10% v 3

168 Using only initial AST, ALT, and INR measurements, the model accurately pre

169 were independent predictors of liver injury (AST >2 x ULN).

170 ficient 0.887), align with the international AST standard (ISO 200776-1; 2006) and could be used for

171 In isolated AST-elevation, macro-AST has to be considered in order t

172 rors of metabolism was worried that isolated AST-elevation indicated cell damage in MCAD-deficiency.

173 ency in whom at the age of 11 years isolated AST-elevation was found without any clinical or biochemi

174 lation (21 mono-N-acetylglucosamines) of its AST domain.

175 percent changes from baseline in ALT levels, AST levels, and caspase-3-cleaved cytokeratin (CK)-18 fr

176 Macro-AST formation is not a special feature of MCAD-deficienc

177 In isolated AST-elevation, macro-AST has to be considered in order to avoid unnecessary,

178 polyethylene glycol precipitation that macro-AST formation was responsible for this biochemical findi

179 sociated with increased liver injury markers AST and ALT and portal fibrosis.

180 es in levels of hepatobiliary injury markers AST, ALT, LDH, and gamma-GT after 6 hours of NMP.

181 In the 40-mg group, mean AST decreased by 13 U/L from baseline (not significant),

182 E1, required for bio-activation of CCl4, nor AST and ALT activity in the plasma were affected by etha

183 significant), and the proportion with normal AST increased from 20% at baseline to 48% at week 4.

184 m allowed for the selective determination of AST in the complex matrix of serum samples containing re

185 4), and AST at LT (HR = 1.36 for doubling of AST, P = 0.004) were associated with graft loss, but LDL

186 LT (hazard ratio [HR] = 1.38 for doubling of AST, P = 0.005) and biliary strictures (HR = 2.68, P = 0

187 HRs evaluating the impact of the duration of AST on the risk of PCSM were 0.67 (95% CI, 0.29 to 1.56;

188 T marrow exhibited only modest elevations of AST and ALT levels.

189 The "holy grail" of AST is a phenotype-based test that can be performed with

190 No differences were found in the levels of AST and ALT in any of the groups studied.

191 four liver enzymes and continuous levels of AST, ALP, and GGT.

192 artate aminotransferase [AST]/upper limit of AST)/platelet.

193 ime was associated with an increased risk of AST in patients treated with bivalirudin but not patient

194 erence methodology, highlight the sources of AST variability, and propose ideas for improving AST pre

195 t and albumin as well as severe worsening of AST/ALT ratio and albumin was the best predictor of live

196 th shallow, multiple identifier-based HTS of ASTs identified by activation marker upregulation after

197 ify rare TCRbeta-chain variable sequences of ASTs in large polyclonal populations.

198 An algorithm based on AST level greater than 17.3 x ULN, TBL greater than 6.6

199 the clinical effect of procedure duration on AST when either bivalirudin or heparin plus glycoprotein

200 s (79%) experienced either grade >/=1 ALT or AST elevation during the study, and 13 subjects (54%) ex

201 r greater, or a new ratio (nR) value (ALT or AST, whichever produced the highest xULN/ alkaline phosp

202 Other AST clonotypes share CDR3beta amino acid sequences throu

203 and/or PBP2a tests when requested to perform AST on atypical isolates of S. aureus.

204 e need for trained diagnosticians to perform AST, reduce the cost-barrier for routine testing, and as

205 in the United States to effectively perform ASTs is challenged by several factors.

206 er-plate (MTP) reader, capable of performing AST without the need for trained diagnosticians.

207 minotransferase (ALT), alkaline phosphatase (AST), total bilirubin (TBIL) and direct bilirubin (DBIL)

208 There was only a slight increase in plasma AST and ALT levels between diseased and healthy states (

209 (-/-) mice displayed higher levels of plasma AST, ALT, bile salts, and hepatic necrosis after 3 days

210 p showed a significant association of plasma AST, salivary AST, and salivary ALT with uric acid level

211 rapid diagnostic testing with MALDI-TOF plus AST review and intervention for adult hospitalized patie

212 It had a limit of detection equal to 5.0 pM AST (0.10 U L(-1)) with no need for the incubation perio

213 conditioning did not influence postoperative AST peak values or other liver function tests.

214 Median postoperative AST peak values was similar in both groups (426 vs 463 I

215 racking within an individual reveals private AST clonotypes resident in the memory population, as wou

216 PST-AST (336 IU/L; interquartile range: 204-573) and PST-ALT

217 eiver operating characteristic curve for PST-AST: 0.61, confidence interval: 0.56-0.66, P<0.01, and a

218 ise, potentially providing a basis for rapid AST.

219 urrent innovations and challenges with rapid AST, VISA/hVISA identification, and clinical bioinformat

220 Reference AST methods are based on bacterial growth in antibiotic

221 re current laboratory protocol for repeating AST every 5 days was inadequate to identify resistant or

222 d with the duration of inflow occlusion (rho-AST=0.20, P<0.01; rho-ALT=0.18, P<0.01).

223 licated, because many do not grow on routine AST media, including Mueller-Hinton agar (MHA) and catio

224 an a model without fS-pIGFBP-1 or S-ALT or S-AST alone.

225 nificant association of plasma AST, salivary AST, and salivary ALT with uric acid level.

226 However, salivary AST and ALT levels showed a approximately 6-fold rise in

227 cantly increased hepatic steatosis and serum AST level as well as hepatic cellular NF-kappaB activati

228 hepatocytes correlated with changes in serum AST (partial r(2) = 0.75, P < 0.0001), hepatocyte balloo

229 limbic striatum (LST), associative striatum (AST), and sensorimotor striatum (SMST).

230 S-based clonotyping will facilitate studying AST dynamics, epitope spreading, and repertoire changes

231 ation (ID) and antimicrobial susceptibility (AST) reports were calculated for 5,402 positive culture

232 DI-TOF) with antimicrobial stewardship team (AST) intervention has the potential for early organism i

233 th real-time antimicrobial stewardship team (AST) review and intervention on antimicrobial prescribin

234 ifting on the attentional set-shifting test (AST), whereas chronic unpredictable stress (CUS) impaire

235 rate a rapid antibiotic susceptibility test (AST) based on the changes in dielectrophoretic (DEP) beh

236 nd robust antimicrobial susceptibility test (AST) can be constructed by statistically characterizing

237 automated antimicrobial susceptibility test (AST) devices that use revised Clinical and Laboratory St

238 ents) show that active surveillance testing (AST) followed by contact precautions for positive patien

239 e cell antimicrobial susceptibility testing (AST) approach for rapid determination of the antibiotic

240 nce of antimicrobial susceptibility testing (AST) by the clinical laboratory is paramount to combatin

241 outine antimicrobial susceptibility testing (AST) can prevent deaths due to bacteria and reduce the s

242 ime in antimicrobial susceptibility testing (AST) endangers patients and encourages the administratio

243 Antimicrobial susceptibility testing (AST) is a fundamental mission of the clinical microbiolo

244 tional antimicrobial susceptibility testing (AST) is intrinsically limited by observation of cell col

245 ercial antimicrobial susceptibility testing (AST) methods were compared to broth microdilution for te

246 Antimicrobial susceptibility testing (AST) of clinical isolates of Nocardia is recommended to

247 Antimicrobial susceptibility testing (AST) of these isolates is complicated, because many do n

248 D) and antimicrobial susceptibility testing (AST) results for the most commonly identified organisms

249 omated antimicrobial susceptibility testing (AST) systems and five selective chromogenic agar plates.

250 faster antimicrobial susceptibility testing (AST) to guide antibiotic treatment.

251 repeat antimicrobial susceptibility testing (AST) when an organism is recurrently isolated from the s

252 Rapid antimicrobial susceptibility testing (AST) would decrease misuse and overuse of antibiotics.

253 curate antimicrobial susceptibility testing (AST) would rule out standard treatment with vancomycin.

254 (PD), antimicrobial susceptibility testing (AST), and how these concepts relate, is essential to thi

255 ectrum antimicrobial susceptibility testing (AST).

256 nase small lobe, and the active site tether (AST) of the AGC kinase domain have previously been impli

257 : the C-lobe tether, the active-site tether (AST), and the N-lobe tether (NLT).

258 ALT is more specific for liver injury than AST and has been shown to be a good predictor of liver r

259 The AST also mediates contact between the kinase N- and C-lo

260 The AST provided evidence-based antibiotic recommendations a

261 The AST systems showed false-negative results with varying n

262 s, and 30-day hospital readmissions, but the AST intervention group had a decreased duration of unnec

263 main to its substrate may be hindered by the AST domain where O-glycosylation changes its conformatio

264 significant difference between groups in the AST (F = 8.13, df = 2,31, p = .001), and at the SMST (F

265 Patients in the AST group with blood cultures contaminated with CoNS had

266 e initiated on optimal therapy sooner in the AST intervention group (58.7 versus 34.4 h, P = 0.030),

267 6 in the preintervention group and 32 in the AST intervention group).

268 nfirmed that HV displacement (-2.86%) in the AST was significantly different in CHR (6.97%) and SCZ (

269 results indicate that full engagement of the AST domain by SecA2 is modulated by one or more of the A

270 veal that the lack of O-glycosylation of the AST domain significantly increases Acm2 enzymatic activi

271 Cross-linking of the N-terminal end of the AST domain to SecA2 occurred regardless of whether Asp1-

272 termine the sequences of nine members of the AST-B family of peptides that were found in the stomatog

273 onally tested the diagnostic accuracy of the AST/ALT ratio, BARD score and the NAFLD fibrosis score i

274 acillin-tazobactam and imipenem found on the AST-GN69 card, with no very major or major errors noted

275 ession, then tested animals drug free on the AST.

276 tide and an adjacent 24-residue segment (the AST domain).

277 to the septum of dividing cells, whereas the AST domain and its O-glycosylation are not involved in t

278 to identify proteins that interact with the AST domain during transport.

279 the photo-cross-linker was placed within the AST domain, the preprotein was found to cross-link to Se

280 he duration of androgen suppression therapy (AST) had an impact on the risk of prostate cancer-specif

281 N-terminal region rich in Ala, Ser, and Thr (AST domain), which is of low complexity and unknown func

282 , increased rates of acute stent thrombosis (AST) have been noted when bivalirudin is discontinued at

283 dy treatment before trial termination due to AST increases between the upper limit of normal (ULN) an

284 omic data with aspartate amino transaminase (AST), a hepatic leakage enzyme to assess organ damage, a

285 profoundly elevated aspartate transaminase (AST) and alanine transaminase (ALT) levels, indicative o

286 zyme pair comprising aspartate transaminase (AST) and malic dehydrogenase.

287 nsaminase (ALT), and aspartate transaminase (AST) were measured.

288 ransaminase (ALT) or aspartate transaminase (AST), are commonly used in clinical practice as screenin

289 transferase, ALT and aspartate transaminase, AST) were only significantly observed in the GBR group.

290 an modulate ADC-to-SCC transdifferentiation (AST).

291 come was PST of aspartate-amino-transferase (AST) and alanine-amino-transferase (ALT).

292 Unfortunately, AST for vancomycin is relatively slow and standard metho

293 ical laboratory will be asked to select what AST method(s) to use and to provide data monitoring outc

294 FibroSURE in combination with AST levels has an excellent capacity to identify moderat

295 o evidence for an increased risk of T2D with AST.

296 MALDI-TOF with AST intervention decreased time to organism identificati

297 MALDI-TOF with AST intervention decreased time to organism identificati

298 e and after implementation of MALDI-TOF with AST intervention for patients with CoNS bacteremia and C

299 cted to analyze the impact of MALDI-TOF with AST intervention in patients with bloodstream infections

300 Fibrosis-4 (FIB-4) was calculated as (age x AST)/(platelet x radical alanine aminotransferase [ALT])