ライフサイエンスコーパス: AA

1 AA degradation rates ranged from 1.7 to 29.3% and from 2

2 AA patients had increased CLA(+) /CLA(-) Th2 (P < .007),

3 AA was associated with a reduced risk of asthma, aeroall

4 AAs are underrepresented in clinical trials in transplan

5 2%) contents, TPC (28.32+/-2.10mg GAE/100g), AA toward DPPH (57.85+/-1.36mg AAE/100g), and total redu

6 cell function in healthy individuals (n = 14 AA, n = 14 AG, n = 14 GG).

7 trahepatic insulin clearance in 29 EA and 18 AA healthy women.

8 The discovery cohort included 5,204 AA participants from Mount Sinai's BioMe biobank.

9 In a sample of 2382 AA individuals from 482 families drawn from the Collabor

10 pective analysis of data of a cohort of 2588 AA and 3566 WA women aged between 40 and 70 years with a

11 tial NMR assignments, and JM mutants (ST(296)AA or T(304)A) investigated, confirm that the backbone a

12 recombinant dentin matrix protein-1 (17-513 AA), this bioinspired approach provides compelling evide

13 An additional 820 EA and 57 AA participants in the Partners Biobank were genotyped a

14 Among the 66 AA patients who developed subsequent invasive breast can

15 tions.We used data and biospecimens from 909 AA and 847 EA healthy control subjects from the Carolina

16 isease (ESRD) due to reactive amyloidosis A (AA) are scarce and inconclusive.

17 Multiple amino acids (AA), AA metabolites, and bile acids were also significantly l

18 s in EAs were significant (P > 0.05) in AAs, AA women who carried the allele of a functional single n

19 ion of SES with epigenetic age acceleration (AA).

20 lm cadaverine, lysine, and other amino acid (AA) contents were determined by liquid chromatography.

21 We examined whether amino acid (AA) mismatches (MMs) at the antigen recognition site of

22 apentaenoic acid (EPA) and arachidonic acid (AA) concentrations increase with age.The aim of this stu

23 poxygenase (5-LOX)-related arachidonic acid (AA) derivatives in the peritoneal fluid.

24 a(2+)-activated release of arachidonic acid (AA) in mitochondria from non-failing hearts was calcium-

25 t hepoxilin A3 (HXA3) from arachidonic acid (AA), promotes acute pulmonary inflammation and systemic

26 d by addition of exogenous arachidonic acid (AA).

27 ioactive T. arjuna compound, arjunolic acid (AA), in ameliorating hemodynamic load-induced cardiac fi

28 e presence of uric acid (UA), ascorbic acid (AA) and glucose.

29 as photoactive nanomaterials, ascorbic acid (AA) as electron donor and ruthenium (III) hexaammine (Ru

30 ure (optical microscopy), and ascorbic acid (AA) degradation kinetics were performed.

31 shows high sensitivity toward ascorbic acid (AA).

32 n-propyl gallate (n-PG), and ascorbic acid (AA).

33 6 PUFAs (linoleic acid and arachidonic acid [AA]) in blood samples at age 8 years were measured for 9

34 Multiple amino acids (AA), AA metabolites, and bile acids were also significan

35 Plasma concentrations of amino acids (AAs), in particular, branched chain AAs (BCAAs), are oft

36 he fly" biodetection of D and L-amino acids (AAs), respectively.

37 h) in the presence of different amino acids (AAs; the basic units of protein matrix of teeth) as a si

38 henolic content (TPC), antioxidant activity (AA) of all formulations were measured, and sensory attri

39 nol content (TPC), and antioxidant activity (AA) of apple samples were measured at different times du

40 rms of the kinetics of antioxidant activity (AA), anthocyanins (A) and total phenolic compound conten

41 henolic content (TPC), antioxidant activity (AA), sensory, physicochemical, and textural properties o

42 Additionally, AA was associated with an increased probability of asthm

43 of rejection, graft loss, and death in adult AA KTX recipients, particularly in those who are sensiti

44 Twenty-five thousand eighty-four adult AAs receiving solitary KTX were included, 16,927 (67.5%)

45 Anthropogenic Aerosols (AA) have slowed down the warming rate.

46 y increased 5-LO metabolite production after AA stimulation.

47 All AAs were depleted in biofilm from smokers, but only lysi

48 Homozygotes for the PSC disease risk allele (AA) showed significantly lower CD28 mRNA expression ex-v

49 mmunohistochemistry in 163 African American (AA) and 144 White TNBC tissue microarrays (TMAs) pooled

50 withdrawal in a sample of African American (AA) and European American (EA) smokers.

51 ces in sleep between black/African American (AA) and white/European American (EA) adults explain raci

52 ction, particularly within African American (AA) kidney transplant recipients; little is known about

53 therapeutic resistance in African American (AA) men.

54 African American (AA) women (n = 312) had lower initial levels of 25(OH)D

55 white American (WA) women, African American (AA) women have a 2-fold higher incidence of breast cance

56 st cancer subtype or among African American (AA) women, who are disproportionately affected by T2D an

57 n, graft loss and death in African-American (AA) kidney transplant (KTX) recipients.

58 Caucasian Americans (CA), African Americans (AA), and Asian Americans (AS).

59 tion-related genes in 256 African Americans (AAs) (117 cases with AD-ND codependence and 139 controls

60 ntional CVD risk factors, African Americans (AAs) are less likely to develop CAC, and when they do, h

61 f vitamin D deficiency in African Americans (AAs) may be a contributing factor to the cancer health d

62 African Americans (AAs) tend to have higher plasma insulin concentrations t

63 6/LCT and SLC5A10 were also associated among AA.

64 European ancestry (EA) and African ancestry (AA).

65 he aim of this study was to evaluate EPA and AA metabolism in young and old men by using uniformly la

66 The kinetics of TPC and AA showed an initial and final period of degradation att

67 with increased risk of incident vitiligo and AA in adulthood.

68 GSLs, ITCs and AAs increased significantly after processing and during

69 ded thoracic aorta (TA) and abdominal aorta (AA) segments, 1-oleoyl-LPA and the LPA1-3 agonist VPC311

70 ed to determine the risk of alopecia areata (AA) and vitiligo associated with atopic dermatitis (AD)

71 Treatments for alopecia areata (AA) have evolved over the decades from broad and nonspec

72 acterizing blood profile of alopecia areata (AA) is important not only for treatment advancements, bu

73 ted with increased plasma BCAAs and aromatic AAs and were mildly associated with the GSG-index, while

74 mmendations on treatment of allergic asthma (AA) caused by HDM allergy, although some included AIT as

75 d States, the prevalence of allergic asthma (AA) is inexplicably rising and in utero exposure to ciga

76 derate-to-severe persistent allergic asthma (AA) that remains uncontrolled despite high-dose inhaled

77 frequently associated with allergic asthma (AA).

78 they carried the FTO risk allele (level 3 AT/AA carriers) than in the nonpersonalized group (level 0)

79 We did not find differences between AA and non-AA mothers in the effect of maternal vitamin

80 approach to explore the relationship between AA and outcomes.

81 IFN-gamma levels were mostly similar between AA, AD, and controls (P > .1).

82 dation related to ethnic differences between AAs and EAs.

83 tor to the cancer health disparities between AAs and European Americans (EAs).We compared concentrati

84 (13)C-AA metabolism was not different between young and old me

85 The (13)C-AA plasma half-life was approximately 4.4 d in both youn

86 icipants (P = 0.589).The metabolism of (13)C-AA was not modified by age, whereas (13)C-EPA metabolism

87 identified substantial differences among CA, AA, and AS populations in the expression of DXME genes a

88 icipants were stratified into risk carriers (AA/AT) and nonrisk carriers (TT) of the FTO gene for ana

89 05) with the exception of the branched chain AA valine, which was elevated in diabetic animals (P < 0

90 tes, bile acids, and elevated branched chain AA).

91 o acids (AAs), in particular, branched chain AAs (BCAAs), are often found increased in nonalcoholic f

92 arts, increased iPLA2gamma activity channels AA into toxic HETEs.

93 At Cl:AA = 2.8, the chlorine was found to first react quickly

94 ding on the chlorine to amino acid ratio (Cl:AA).

95 reactive secondary group can increase the Cl:AA ratio required for the formation of N,N-dichloramines

96 Ectopic overexpression of the newly cloned AA-enriched variant, PIK3CD-S, in EA PCa cell lines enha

97 Mental Disorders Alcohol Dependence in COGA AA families, and two (rs13093097, rs7428372) were replic

98 A combined AA and EA meta-analysis (n=8021) identified three highly

99 e and higher measured 25(OH)D concentrations.AA women have lower concentrations of total 25(OH)D than

100 For patients with PAR and concomitant AA, the median annual cost varied between 266euro and 37

101 ct cost for PAR, with or without concomitant AA, in France.

102 A-A, -B, and -DRB1 alleles and corresponding AA polymorphisms from antigenic specificity through the

103 gnitude lower than that of the corresponding AA.DD duplex.

104 that enrolled a total of 6,081 patients-COU-AA-301, AFFIRM, ELM-PC-5, ELM-PC-4, and COMET-1- Clinica

105 d-Amino acids (d-AAs) are endogenous molecules found throughout the metaz

106 Levels of these structurally similar d-AAs were significantly different in subpopulations of ce

107 s diagnosed with Phenylketonuria and total D-AAs in Vibrio cholera cultures are pioneer illustrated a

108 ding studies of the first double-H-bonded DD.AA-type complexes of a series of aromatic boronic acids

109 ng a newly synthesized library of deuterated AA isotopologues.

110 associated with increased risk of developing AA (OR 1.80, 95% CI 1.18-2.76) and vitiligo (OR 2.14, 95

111 nsplantation (hazard ratio, 1.30 per 15 DRB1 AA MM; P < 0.0001).

112 PPARalpha knockdown during AA treatment in hypertrophy samples, including angiotens

113 cant effects on AD-ND codependence in either AAs or EAs.

114 he physiological KIE (PKIE) during enzymatic AA oxygenation by living cells using a newly synthesized

115 y) MMs with kidney graft survival, estimated AA MMs at peptide-binding sites of the HLA-DRB1 molecule

116 We show that estimated AA MMs at particular positions in the peptide-binding po

117 rowth factor; platelet-derived growth factor AA and BB; placental growth factor; vascular endothelial

118 ensation between bisalkylsulfonyl fluorides (AA monomers) and bisphenol bis(t-butyldimethylsilyl) eth

119 formation of 2-furomethyl-amino acids (2-FM-AA) as indicators of Maillard reaction (MR) in black gar

120 ping TNBC was 0.56% (95% CI, 0.32%-1.0%) for AA patients and 0.25% (95% CI, 0.12%-0.53%) for WA patie

121 Both methods were also applied for AA quantification in industrialized orange and pineapple

122 d lung epithelial cells and was critical for AA release from membrane phospholipids.

123 le in the change in spatial distribution for AA-containing lipids.

124 osses of up to 74, 45 and 78% were found for AA, A and TPC, respectively.

125 some included AIT as a treatment option for AA in general.

126 s this evolution and how novel therapies for AA have changed over the decades, what we have in our cu

127 8 and CAC were detected in AAs with T2D from AA-DHS and replicated in the JHS.

128 Additionally, ERCC4 rs1799798 GA/AA genotypes were associated with poorer OS (HRadj = 1.3

129 Aloe vera gel (AV) and Aloe arborescens gel (AA) alone or in combination with rosehip oil (RO) at 2%

130 The gain-of-function variants, genotypes (AA/AG), were associated with lower FEV1 /FVC in subjects

131 Low SES was associated with greater AA (beta = 0.99 years; 95% CI 0.39,1.59; p = 0.002; comp

132 fluorescence and color characteristics of HA-AAs before and after bleaching treatment, we found that

133 "GG" and "GA" genpotypes than those having "AA" genotype (P = 0.04).

134 sociated with kidney disease in hypertensive AAs.

135 ma AAs compared to controls (CTs); and b) if AA concentrations are associated with IR and liver histo

136 decreased ATG16L1 stabilization in Ikkalpha(AA/AA) mice.

137 In AA individuals, PGS provided no improvement in variation

138 individuals and approximately 12% to 18% in AA individuals.

139 tify 58 distinct non-HLA regions in EA, 9 in AA and 16 in HA ( approximately 50% of these regions hav

140 erminants of low vitamin D concentrations in AA populations.

141 latory cells were significantly decreased in AA patients than controls (P < .01) and were correlated

142 cant explanatory variable for disparities in AA recipients.

143 and genotyped 67 vitamin D-related genes in AA women only.AA women had lower 25(OH)D concentrations

144 A-DR activation were significantly higher in AA than controls (P < .05).

145 CpG (HTR2B cg27531267) was hypomethylated in AA cases (P = 7.2 x 10(-5)), while 17 CpGs in 16 genes (

146 dy has investigated the role of microRNAs in AA.

147 nockdown more severely impaired migration in AA TNBC cells than White TNBC cells.

148 e to the necessity of KIFC1 for migration in AA TNBC cells.

149 respectively) in multivariable Cox models in AA TNBCs but not White TNBCs.

150 dies have implicated autoimmune processes in AA etiology, understanding of the etiopathogenesis is in

151 n independent biomarker of poor prognosis in AA TNBC patients, potentially due to the necessity of KI

152 The strongest result in AA-DHS alone was rs6491315 in the 13q32.1 region (parame

153 ) and CD8(+) and activated T-cell subsets in AA vs atopic dermatitis (AD) and control blood.

154 OH)D and vitamin D-binding protein (VDBP) in AA and EA women and investigated determinants of the vit

155 ations in EAs were significant (P > 0.05) in AAs, AA women who carried the allele of a functional sin

156 these chromosomes as contributors to CAC in AAs with T2D, as well as to variation in CAC between pop

157 are lower concentrations of free 25(OH)D in AAs.

158 sm underlying reduced insulin degradation in AAs remains to be clarified, as does the relative import

159 6, 7, 9, 16 and 18 and CAC were detected in AAs with T2D from AA-DHS and replicated in the JHS.

160 cant explanatory variable for disparities in AAs; the crude relative risk of acute rejection in AAs w

161 a insulin was approximately twice as high in AAs as in EAs.

162 ll, intrapatient tacrolimus CV was higher in AAs versus non-AAs (39.9 +/- 19.8 % vs 34.8 +/- 15.8% P

163 rahepatic insulin clearance was not lower in AAs than in EAs.

164 irst-pass extraction was two-thirds lower in AAs versus EAs in the overnight-fasted state.

165 strongly associated with acute rejection in AAs and graft loss in all patients.

166 he crude relative risk of acute rejection in AAs was reduced by 46% when including tacrolimus variabi

167 The present results in AAs indicate that genetic variants influencing opioid se

168 In contrast, insulin was similar in AAs and EAs after the 20-25 min intravenous insulin infu

169 Larger studies in AAs will be needed to fully elucidate the underlying det

170 s' association with blood pressure traits in AAs.

171 dds ratios to determine the risk of incident AA and vitiligo associated with AD diagnosed in or befor

172 ies were analyzed; 862,817 of these included AA.

173 ndings highlight the importance of including AA populations in genetics research on SUDs and the util

174 rs7428372) were replicated in an independent AA sample (Gelernter et al.).

175 l immunotherapy in patients with HDM-induced AA and AR, their effect on subsequent guideline updates

176 VPC31143-induced AA contraction was sensitive to pertussis toxin (PTX), t

177 life-course SES improvement had intermediate AA compared to extreme SES categories, suggesting revers

178 d neural efficiency, especially in HIV-LMX1A-AA carriers who might have greater dopaminergic reserve.

179 on in HIV participants, especially the LMX1A-AA carriers (LMX1A genotype by HIV status, cluster-corre

180 zzy logic screened 6 MOS sensors (LY2/G, LY2/AA, LY2/GH, LY2/gCT1, T30/1, and P30/1) to deconvolute t

181 tients with MDM2rs2279744 TT or MDM2rs937283 AA genotypes was significantly reduced compared with tha

182 mation is observed for homo-sequence 2-mers (AA.DD) where there are no competing folding equilibria.

183 Moreover, AA-induced PPARalpha up-regulation leads to repression o

184 In an independent set of opioid-naive AA children being treated for surgical pain, rs73568641-

185 curity system for a patient with PAR, and no AA was 159euro in 2013.

186 did not find differences between AA and non-AA mothers in the effect of maternal vitamin D supplemen

187 ], 17.6 ng/mL [8.3 ng/mL]) compared with non-AA women (n = 400; 27.1 ng/mL [9.7 ng/mL], P < .001).

188 t tacrolimus CV was higher in AAs versus non-AAs (39.9 +/- 19.8 % vs 34.8 +/- 15.8% P < 0.001).

189 otentially provides a mechanism to reject np AAs, some have pathological associations.

190 nt breast cancers developed in 103 (4.1%) of AA patients (mean follow-up interval of 6.8 years) and 1

191 ed and fifteen participants of EA and 366 of AA in the MGH CAMP study (Cardiology and Metabolic Patie

192 est genome-wide association meta-analysis of AA to date.

193 evidence that hydrogen(s) present at C10 of AA play a critical role in the catalysis of prostaglandi

194 There were 147 incident cases of AA and 98 incident cases of vitiligo over 2 years of fol

195 omen's Health Study, a prospective cohort of AA women enrolled in 1995 and followed biennially.

196 in costs with severity of PAR and control of AA.

197 This results in a cycle of AA-enrichment in pericentral hepatocytes, membrane relea

198 k in our understanding of the development of AA amyloidosis.

199 We investigated the effects of AA on colonoscopy complications, specifically bowel perf

200 ylcholine receptor-dependent exacerbation of AA and BPD in mice.

201 wed lower expression in the hair follicle of AA patients.

202 miRs contributing to increased incidence of AA and BPD in the progenies.

203 as a strategy to overcome these instances of AA therapy resistance.

204 genesis and emphasize the systemic nature of AA supporting the need for systemic therapeutic strategi

205 relationship between the estimated number of AA MMs and risk of GF was observed for HLA-DRB1 in decea

206 e an explanation for the lysosomal origin of AA amyloidosis.

207 termination of the KIE during oxygenation of AA and LA by mammalian enzymes including cyclooxygenase

208 The enzymes that catalyze the oxygenation of AA begin by abstracting hydrogen from one of three bis-a

209 n macrophages for COX and LOX oxygenation of AA is similar to KIEs determined in previous reports usi

210 increase in the PKIE for COX oxygenation of AA.

211 implicates microRNAs in the pathogenesis of AA.

212 derstanding of the unique pathophysiology of AA.

213 Recurrence of AA amyloidosis was diagnosed in 2 patients during the fi

214 pericentral hepatocytes, membrane release of AA, and generation of proinflammatory eicosanoids and ma

215 spholipase A2 (PLA2) promotes the release of AA, we investigated the role of PLA2 in local and system

216 ure to cigarette smoke increases the risk of AA and bronchopulmonary dysplasia (BPD) in children and

217 Use of AA did not significantly increase risk of perforation (o

218 Use of AA was associated with an increased risk of aspiration p

219 67 vitamin D-related genes in AA women only.AA women had lower 25(OH)D concentrations than did EA wo

220 OPLS-AA reveals moderate beta-structure propensity coupled wi

221 CHARMM36, CHARMM22*, CHARMM22/cmap, and OPLS-AA) and two water models (standard and modified TIP3P).

222 Fourth, two force fields, OPLS-AA and CHARMM22* have unique features setting them apart

223 s an intuitive interface for generating OPLS-AA/1.14*CM1A(-LBCC) force field parameters for organic l

224 al-life data on the progression of AR and/or AA in patients receiving AIT.

225 The selective detection of glucose or AA from their mixture is for the first time demonstrated

226 variable analysis showed patients with TT or AA genotypes had a significantly higher risk of SCCOP re

227 EA) and 2,030 African American participants (AA) free of diagnosed diabetes from the ARIC Study.

228 propriate ligand-mediated activation by PDGF-AA.

229 the presence of fibrotic growth factor, PDGF-AA, results in increased proliferation of PDGFRalpha+ ce

230 s in osteoclasts, with the promoters of PDGF-AA and BMP2 having Creb binding sites.

231 The expression of PDGF-AA and BMP2 was positively regulated by the p38 MAPK-Cre

232 , likely due to decreased expression of PDGF-AA and BMP2.

233 PDE levels of PDGF-AA, platelet glycoprotein VI, integrin-linked kinase-1,

234 In wild-type cells treated with PDGF-AA, c-Cbl becomes enriched in the cilium, and the recept

235 vered new PDGF:VEGFR2 interactions with PDGF-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:R2 KD

236 clinical trials in children with persistent AA receiving omalizumab therapy and observational studie

237 Increased plasma AA concentrations were observed mainly in subjects with

238 th obesity (NAFLD-Ob) display altered plasma AAs compared to controls (CTs); and b) if AA concentrati

239 ene (GC/DBP) rs4588 functional polymorphism (AA vs. CC: -16.7 nmol/L (95% CI: -26.2, -7.1); CA vs. CC

240 orbed Ru(NH3)6(3+) on aptamer and preventing AA from scavenging photogenerated holes to the photoacti

241 es of 20 patients with FMF and biopsy-proven AA amyloidosis that were transplanted between 1995 and 2

242 by Abeles, is now available in a quaternary AA context for the first time.

243 SAA is a protein precursor of reactive AA amyloidosis, the major complication of chronic inflam

244 l attenuated the production of 5-LOX-related AA derivatives.

245 significant variety of biologically relevant AA side chains are tolerated including those for alanine

246 a pair of frontal H-bonds with the relevant AA partner.

247 The GTF2I rs13227433 AA genotype, previously associated with lower social anx

248 ele of a myelin-specific gene (CNP rs2070106-AA) associated with catatonia in 2 independent schizophr

249 with higher methadone dose in the OD sample (AA and EA: n=1410, genetic score P=1.3 x 10(-3)).

250 lates of C. neoformans var. grubii (serotype AA) and of hybrids with C. neoformans var. neoformans (s

251 peripheral blood from 32 moderate-to-severe AA adults with 43 moderate-to-severe AD patients and 30

252 o less than 12 years with moderate-to-severe AA.

253 hannels could emerge primarily from a single AA substitution (asparagine-->threonine) via a single nu

254 whereas that of alternative acceptor sites (AA) is significantly increased post-fertilization when c

255 2000 to December 31, 2009 in adult solitary AA KTX recipients, with at least 5 years of follow-up.

256 In a population-based cohort study, AA for outpatient colonoscopy was associated with a sign

257 clear export signal (NES) at the N terminus (AAs 176-192) that contributes to CASZ1 nuclear-cytoplasm

258 e a critical region at the CASZ1 N terminus (AAs 23-40) that mediates the CASZ1b nuclear localization

259 We found that AA binds to and stabilizes the ligand-binding domain of

260 The study found that AA identity persisted as a significant risk factor for T

261 Our data revealed that AA significantly represses collagen expression and impro

262 The findings suggest that AA women with T2D are at increased risk of developing ER

263 This finding suggests that AA identity is associated with inherent susceptibility f

264 enal artery-ligated rat heart, suggests that AA-driven cardioprotection primarily arises from PPARalp

265 Results indicated that AAs relative to EAs obtained less sleep (341 vs. 381 min

266 The AA monomers were prepared via the highly reliable Michae

267 The AA-induced PPARalpha-bound TAK1 level thereby shows inve

268 Subjects with asthma and the AA/AG genotypes had a 5% decrease in FEV1 /FVC (P<.001).

269 of teeth to explore the color source at the AA level.

270 Analyses in the AA adolescent/young adult (offspring from COGA families)

271 and 87 447 participants were included in the AA and vitiligo analyses, respectively.

272 .5% clove and 12.5% green mate increased the AA and TPC, while FM with added sweet potato pulp had th

273 We therefore measured the AA profile of 44 subjects with NAFLD without diabetes an

274 say, site-specific miR-30b regulation of the AA risk genes IL2RA, STX17, and TNXB was validated.

275 IEs determined in previous reports using the AA isotopologue deuterated at carbon 13 (C13).

276 4, P adj = 0.007 for XPC), compared with the AA and GG genotypes, respectively.

277 including gametocytes, more often than their AA counterparts (OR 3.01 95% CI 1.38-6.57, P = 0.006).

278 Because these AAs are involved in glutathione synthesis, we hypothesiz

279 rase-binding motif (TBM) on TRF1 (13R/18G to AA) disrupts its interaction with TNKS1 concomitant recr

280 tion were less often parasitemic compared to AA adults (odds ratio [OR] 0.50 95% confidence interval

281 ar lean mass (LM; 3.0% and 2.1%) compared to AA genotype, with greater arm LM (0.8%) in T allele carr

282 rriers and leg LM (2.1%) for TT, compared to AA genotype.

283 ucose and insulin concentrations compared to AA/AG-carriers (p = 0.003 and p = 0.042).

284 -1) of oral methadone, an effect specific to AAs.

285 y in which preorganization of the ubiquitous AA-platform submotif precedes the formation of the docki

286 alpha-(1'-fluoro)-beta-(phenylsulfonyl)vinyl AA-esters undergo smooth sulfone-stannane interchange to

287 lpha-(1'-fluoro)-beta-(tributylstannyl)vinyl AA-esters.

288 lts showed that PGJ increased the viscosity, AA, and TPC, while GSF increased the ash and total fiber

289 Both carrying rs660895-G (AG vs AA: odds ratio [OR] = 0.81; GG vs AA: OR = 0.56; p-trend

290 5-G (AG vs AA: odds ratio [OR] = 0.81; GG vs AA: OR = 0.56; p-trend = 0.003) and ever smoking (OR = 0

291 with high dietary fat intake >/=37% (GG vs. AA/AG, OR 2.36 [1.02-5.49], p = 0.045).

292 ing plum quality and bioactive compounds was AA+RO.

293 To determine whether AA identity remains associated with TNBC for women with

294 being observed for those fruits coated with AA+RO.

295 we matched persons who had colonoscopy with AA (1:1) with those who did not.

296 , IFN-gamma producing cells were linked with AA duration.

297 IT with perennial allergens in patients with AA and AR, including use of different diagnosis and seve

298 We investigated the association of SES with AA in more than 5,000 individuals belonging to three ind

299 Costs of PAR with or without AA are poorly documented.

300 and earlier hypertension diagnoses in young AAs; this relationship appears to follow an additive mod