ライフサイエンスコーパス: AGA

1 AGA developed earlier and more frequently in arteries of

2 AGA displays variability in its time of onset, severity

3 AGA genome-wide association studies signals are enriched

4 AGA has a negative socioemotional effect on affected ind

5 AGA is an independent predictor of mortality from DM and

6 AGA is rarely used in E. coli, and arginine clusters at

7 AGA, defined as smooth muscle cells forming a neointima

8 AGAs had a negative impact on failure-free survival (FFS

9 AGAs were present in 34% of patients at diagnosis, inclu

10 gestational age of 33.3 +/- 1.8 wk and to 11 AGA infants (8 boys) with a mean (+/-SD) gestational age

11 ed labeling with carbodiimide-activated [14C]AGA to identify peptides 120-127, 234-237, 625-630, and

12 re validated by bisulfite pyrosequencing (30 AGA, 21 SGA) and also analyzed in cord blood.

13 ing of nuclear factors to these sites are 5'-AGA-3' (-282 to -280) in binding site I and 5'-ACAG-3' (

14 At either treatment age, AAV9/AGA administration led to (1) dose dependently increased

15 ely termed additional genetic abnormalities (AGAs).

16 is of early DR, showing that the accumulated AGA within the diabetic retina elicits the microglial ac

17 allosteric activation by N-acetylglutamate (AGA), a sensor of excess amino acids.

18 tion is a requirement for N-acetylglutamate (AGA), which induces an active enzyme conformation and do

19 MOP, mannopinic acid (MOA), agropinic acid (AGA), and the agrocinopines.

20 treatment with 18-alpha-glycyrrhetinic acid (AGA).

21 with 7-amino-1,3-naphthalenedisulfonic acid (AGA) yielded unique cross-ring cleavages similar to thos

22 developed to study microglial response after AGA treatment and the mechanistic basis behind this resp

23 that AGAA is the optimal primer whereas AG, AGA, and AGAACC were inefficient primers.

24 o delivered appropriate for gestational age (AGA) babies (controls, >10th to <90th percentile).

25 roups: FGR, appropriate-for-gestational age (AGA) with markers of placental dysfunction, healthy smal

26 e of appropriate weight for gestational age (AGA), FGR babies have smaller placentas with reduced act

27 those born appropriate for gestational age (AGA).

28 ng who were appropriate for gestational age (AGA).

29 nfants born appropriate for gestational age (AGA; n = 72) and SGA infants receiving BRF (n = 46) or F

30 SGA than in appropriate-for-gestational-age (AGA) infants born prematurely.

31 nfants born appropriate-for-gestational-age (AGA) or small-for-gestational-age (SGA) to identify new

32 At the same time, Amadori-glycated albumin (AGA)-like epitopes were featured in the regions of micro

33 ted by using the adaptive genetic algorithm (AGA) and subsequently synthesized by a hydride route wit

34 Androgenetic alopecia (AGA) has now become a common disorder, yet treatment opt

35 Androgenetic alopecia (AGA) is a common heritable and androgen-dependent hair l

36 Androgenetic alopecia (AGA) is a condition of scalp hair growth characterized b

37 Androgenetic alopecia (AGA) is associated with trichodynia, anxiety, low self-e

38 Early androgenetic alopecia (AGA) is patterned hair loss occurring before age 30 year

39 Androgenetic alopecia (AGA) is the most common type of hair loss, and there is

40 Presence of androgenetic alopecia (AGA) might be such a predictor.

41 DPCs) taken from male androgenetic alopecia (AGA) patients undergo premature senescence in vitro in a

42 Androgenetic alopecia (AGA), a hereditary disorder that involves the progressiv

43 Androgenetic alopecia (AGA), also known as common baldness, is characterized by

44 inasteride treatment of androgenic alopecia (AGA) is safe but do not assess quality of safety reporti

45 The Amplatzer (AGA Medical Corporation, Golden Valley, MN, USA) family

46 TCRs was the presence of CDR3 fitting to an AGA(G(n))GG-like amino acid motif.

47 rities, percentage African genetic ancestry (AGA) has been suggested as a risk factor associated with

48 selective MMP-12 inhibitors (CGA, CGA-1, and AGA) and the methodology to obtain MMP-12 selectivity fr

49 hree BamA L6 alterations, DeltaRGF, AAA, and AGA, produced a conditional lethal phenotype, concomitan

50 The rare codons AGG and AGA comprise 2% and 4%, respectively, of the arginine co

51 homogenous in terms of demographic data and AGA severity.

52 ests that the link between these factors and AGA is still unclear.

53 icant association between hormone levels and AGA or IR grade severity.

54 rential zinc status at birth between SGA and AGA infants born prematurely at similar stages of gestat

55 rs a high level of resistance to both HU and AGAs in a CpxR-dependent manner.

56 tress response can protect cells from HU and AGAs.

57 ession analysis of BAB and BAN and annotated AGA risk loci with differentially expressed genes.

58 rotective against aminoglycoside antibiotic (AGA)-induced hair cell death.

59 The aminoglycoside antibiotics (AGAs) are calcium-sensing receptor (CaR) agonists that a

60 Aminoglycoside antibiotics (AGAs) are nephrotoxic, with most of the damage confined

61 otics, including aminoglycoside antibiotics (AGAs), and toxic small molecules, such as hydroxyurea (H

62 Immunoglobulin (Ig)G-based antigliadin (AGA) tests generally were poor in both parameters wherea

63 e either small (SGA; n = 38) or appropriate (AGA; n = 65) for gestational age.

64 or and the dnaY gene which encodes tRNA(Arg)(AGA/AGG) Isolation of the recombinant GP alpha1 in a hig

65 tion and accelerated graft arteriosclerosis (AGA) in long-term cardiac allografts, hearts were transp

66 erity of accelerated graft arteriosclerosis (AGA) in transplanted organs, although the precise mechan

67 tion and accelerated graft arteriosclerosis (AGA), also known as cardiac allograft vasculopathy (CAV)

68 rts with accelerated graft arteriosclerosis (AGA).

69 iency of the enzyme aspartylglucosaminidase (AGA) which is involved in glycoprotein degradation.

70 loss of the enzyme aspartylglucosaminidase (AGA), resulting in AGA substrate accumulation.

71 Automated glycan assembly (AGA) aims at accelerating access to synthetic oligosacch

72 ere, we show that automated glycan assembly (AGA) enables access to a 100-mer polysaccharide via a 20

73 Automated Glycan Assembly (AGA) has facilitated the procurement of synthetic glycan

74 Automated glycan assembly (AGA) is significantly more challenging, as highly branch

75 Automated glycan assembly (AGA) streamlines the synthesis of complex oligosaccharid

76 he American Gastroenterological Association (AGA) Clinical Practice and Practice Economics Committee.

77 is American Gastroenterological Association (AGA) Clinical Practice Update (CPU) Expert Review is to

78 is American Gastroenterological Association (AGA) Institute Clinical Practice Update is to review the

79 is American Gastroenterological Association (AGA) Institute Clinical Practice Update is to review the

80 is American Gastroenterological Association (AGA) Institute Clinical Practice Update was to rapidly r

81 he American Gastroenterological Association (AGA) Institute on "Evaluation and Management of Occult a

82 he American Gastroenterological Association (AGA) Institute on "Use of Gastrointestinal Medications i

83 he American Gastroenterological Association (AGA) Institute Technology Assessment on "Image-Enhanced

84 he American Gastroenterological Association (AGA) membership.

85 he American Gastroenterological Association (AGA) on Anorectal Testing Techniques.

86 he American Gastroenterological Association (AGA) on constipation.

87 he American Gastroenterological Association (AGA) on Diagnosis and Treatment of Gastroparesis.

88 he American Gastroenterological Association (AGA) on Hemorrhoids.

89 he American Gastroenterological Association (AGA) on treatment of patients with dysphagia caused by b

90 he American Gastroenterological Association (AGA) standards for office-based gastrointestinal endosco

91 cognized by mtRF1a, the release mechanism at AGA and AGG codons remains a debated issue.

92 F1, mitoribosomes accumulate specifically at AGA and AGG codons.

93 neuronal elongation complexes are stalled at AGA codons due to deficiencies in a tRNA(Arg)UCU tRNA an

94 ection or accelerated graft atherosclerosis (AGA) in cardiac allograft recipients.

95 er, and its parameters were compared between AGA and IUGR, as well as between the severe and non-seve

96 olabile linker that allows for bidirectional AGA and ready introduction of various aglycons.

97 the C-terminal region is involved in binding AGA.

98 fat, and fat mass index than did those born AGA, with a dose-response effect across 2 subcategories

99 ose born SGA without catch-up and those born AGA.

100 This use of both AGA and AGG occurs rarely in other mammals, and this put

101 to the hCPS conformational change induced by AGA.

102 n from oligosaccharide fragments prepared by AGA and linear as well as branched beta-oligoglucans is

103 1-mer oligosaccharide fragments, prepared by AGA, yielded a multiple-branched 151-mer polymannoside.

104 The arginine codon AGA is a common codon in eukaryotic genes but is particu

105 The rare arginine codons AGA and AGG (AGR) present a case study in codon choice,

106 y high frequency of the rare arginine codons AGA and AGG when compared to genes of Escherichia coli o

107 y high frequency of the rare arginine codons AGA and AGG, as well as dual rare Arg codons at three po

108 ne, encoding the arginyl tRNA for the codons AGA and AGG.

109 The Amplatzer mVSD device (AGA Medical Corp.) offers excellent closure rates and lo

110 retinal microglial TNF-alpha release during AGA treatment.

111 Early AGA in men is frequently reported as the phenotypic equi

112 , and testosterone levels) of men with early AGA and to compare it with the PCOS profile; the seconda

113 Men with early AGA could be considered as male phenotypic equivalents o

114 ceipt among participants carrying the FCGR3B-AGA haplotype (comprising minor alleles of the 3 FCGR3B

115 The FCGR3B-AGA haplotype also influenced whether a combined Env-spe

116 assessing for eligibility in the finasteride-AGA pivotal trials.

117 US Food and Drug Administration approval for AGA.

118 AGA with finasteride, 1.25 mg/d or less, for AGA, only 31% met inclusion criteria for the pivotal tri

119 dependent and ranges from +1.05 kcal/mol for AGA/TTT to -1.05 kcal/mol for CGC/GTG.

120 unctional single-nucleotide polymorphism for AGA and eczema.

121 guanine bases in DNA (with a preference for AGA triplets), preventing its expression and replication

122 r which genes at these loci are relevant for AGA.

123 potentially being near the binding site for AGA.

124 Effective therapies for AGA include autologous transplantation of androgen-resis

125 Emerging therapies for AGA include hair follicle-activating peptides, mRNA-cont

126 linical data repository who were treated for AGA with finasteride, 1.25 mg/d or less, for AGA, only 3

127 99m)Tc-AGA-1 and (99m)Tc-AGA-2, derived from AGA.

128 is, we analyzed bald and non-bald scalp from AGA individuals for the presence of hair follicle stem a

129 were immunoglobulins, IgA/IgG anti-gliadin (AGA), and endomysial antibodies (EMA).

130 in CII, the immunodominant CII610-618 (GPAGT AGA R) within CB10 and the subdominant CII445-453 (GPAGP

131 small-for-gestational age (SGA), and healthy AGA (referent).

132 Compared to healthy AGA (N = 1,429), children with FGR (N = 250) were at hig

133 Any patient with a positive IgA AGA, EMA, or only IgG AGA in the presence of IgA deficie

134 nt with a positive IgA AGA, EMA, or only IgG AGA in the presence of IgA deficiency was offered a smal

135 In AGA NSCLC, tyrosine kinase inhibitors (TKIs) were associ

136 In AGA, it has been proposed that the inhibitory actions of

137 Recent advances in AGA technology pave the way for the production of novel

138 position; induction of a minigene ending in AGA stimulates bypassing at the latter but not the forme

139 tation that results in Thr122Lys exchange in AGA, and compared this mutant form to one carrying the w

140 Although iNOS is expressed in macrophages in AGA, its role in the pathogenesis of AGA is unknown.

141 aspartylglucosaminidase (AGA), resulting in AGA substrate accumulation.

142 sponse to AGAs and thus could play a role in AGA-induced nephrotoxicity.

143 lso identify a predicted promoter variant in AGA (the gene that encodes aspartylglucosaminidase) that

144 s support substantial ancestral variation in AGA.

145 ts with these compounds results in increased AGA activity and processing, implicating that these subs

146 and localized in lysosomes, but exhibits low AGA activity due to impaired processing of the precursor

147 ver, the efficacy of oral minoxidil for male AGA is yet to be evaluated in comparative therapeutic tr

148 Treatment with 2 microM AGA, an uncoupling agent, blocked the spread of Lucifer

149 rsus controls was 3.13 (P=0.03) and for mild AGA versus control patients was 1.61 (P=0.45).

150 ith moderate to severe AGA vs normal or mild AGA had a significantly higher risk of mortality from DM

151 acid change through a sequence modification (AGA) of the original tumor mutation (AGG) by codon degen

152 rg tRNA due to ribosome stalling at multiple AGA and AGG codons on the overexpressed int mRNA underli

153 or pharmacological chaperones for the mutant AGA.

154 We show that T122K mutated AGA is expressed in normal amounts and localized in lyso

155 ervention trials with agents that neutralize AGA effects may emerge as a new therapeutic approach to

156 A new AGA synthesizer enables rapid temperature adjustment fro

157 ic alterations (other AGA; n = 137), and non-AGA (n = 164).

158 ors (ICIs) conferred survival benefit in non-AGA patients (HR 0.45, 95% CI 0.25-0.84, P = 0.012).

159 VSDs) using the new Amplatzer mVSD occluder (AGA Medical Corp., Golden Valley, Minnesota).

160 g the new Amplatzer Membranous VSD Occluder (AGA Medical Corp., Golden Valley, Minnesota) in the U.S.

161 and Amplatzer PFO Occluder [disc occluder] [AGA Medical/St. Jude Medical, St. Paul, Minnesota]) eval

162 erspective describes the state-of-the art of AGA and aspects of the technology where additional impro

163 ion has been performed on the association of AGA with health-related quality of life (HRQOL).

164 To examine the possible cellular basis of AGA toxicity, acute and chronic responses to AGA treatme

165 not defined, it is known that the binding of AGA to CPS leads to a conformational change in which a p

166 ollicle may contribute to the development of AGA.

167 peated doses (every 48 h for eight doses) of AGA-1 at 0.3-10.0 mg/kg cleared hepatic GL-3, whereas hi

168 orting the role of these cells as drivers of AGA pathogenesis.

169 sustained, and dose-dependent elimination of AGA substrate in body fluids; (3) significantly rescued

170 Intravitreal injection of AGA per se in normal rats resulted in increases of Iba-1

171 To investigate mechanisms of AGA, we cultured DP cells (DPC) from balding and non-bal

172 on-fasting glucose, compared with mothers of AGA offspring.

173 for oxidative stress in the pathogenesis of AGA both in relation to cell senescence and migration bu

174 strate that MAC promotes the pathogenesis of AGA in long-term cardiac allografts.

175 ages in AGA, its role in the pathogenesis of AGA is unknown.

176 or cells plays a role in the pathogenesis of AGA.

177 Although the site of AGA interaction is not defined, it is known that the bin

178 scribed finasteride for routine treatment of AGA, most would have been excluded from the pivotal stud

179 ovel therapeutic strategies for treatment of AGA.

180 profile for finasteride in the treatment of AGA.

181 Codon usage in kamA includes the use of AGA for all 29 arginine residues.

182 Appropriate use of PPIs was based on AGA guidelines.

183 f biopsy-proven acute allograft rejection or AGA (assessed by coronary angiography).

184 sive method for detecting acute rejection or AGA after heart transplantation.

185 M199A) does not increase resistance to HU or AGAs.

186 other actionable genomic alterations (other AGA; n = 137), and non-AGA (n = 164).

187 opriate use and interpretation of percentage AGA in understanding health disparities has been complic

188 Correlation of percentage AGA with SSDH measures was described.

189 female [57.7%]), with a mean (SD) percentage AGA of 75.0% (14.0%).

190 been complicated by the fact that percentage AGA is correlated with genetic and nongenetic factors.

191 t-genetic codes of other invertebrate phyla, AGA and AGG specify arginine, and ATA specifies isoleuci

192 ould no longer base pair to form a predicted AGA triloop.

193 iral vector encoding human alpha-gal A (rAAV-AGA) was constructed and injected into the hepatic porta

194 , alpha-gal A activity in the livers of rAAV-AGA-injected Fabry mice was 20-35% of that of the normal

195 ns of liver toxicity occurred after the rAAV-AGA administration.

196 An essential requirement for tagging at rare AGA codons is a scarcity of the cognate tRNA; supplement

197 ng and reveals tagging caused by single rare AGA codons.

198 t Int protein expression depends on the rare AGA tRNA.

199 (sarcospan) to be the functionally relevant AGA genes at the 7p21.1 and 12p12.1 risk loci, respectiv

200 the presence of the pentasaccharide sequence AGA*IA (A(NAc,6S)-GlcUA-A(NS,3,6S)-I(2S)-A(NS,6S)).

201 6A37A38 in the anticodon loop, only tRNA(Ser)AGA, tRNA(Ser)CGA, tRNA(Ser)UGA, and selenocysteine tRNA

202 wo nucleus-encoded serine tRNAs, tRNA-serine(AGA) and tRNA-serine(GCT).

203 bulin (Ig)G titer, the odds ratio for severe AGA versus controls was 3.13 (P=0.03) and for mild AGA v

204 disease in patients with moderate or severe AGA, regardless of whether MetS is present.

205 Subjects with moderate to severe AGA vs normal or mild AGA had a significantly higher ris

206 ay for eight doses) of the highly sialylated AGA-1 glycoform; 4 d later, enzyme activity was retained

207 treated intravitreally with A717, a specific AGA-neutralizing antibody, or murine IgG.

208 (1) dose dependently increased and sustained AGA activity in body fluids and tissues; (2) rapid, sust

209 of either a putative (T)AGC hot spot or a (T)AGA non-hot spot motif.

210 more likely to undergo mutation than the (T)AGA non-hot spot motif.

211 cells which bear plasmids expressing the T4 AGA tRNA gene.

212 we report two (99m)Tc-radiotracers, (99m)Tc-AGA-1 and (99m)Tc-AGA-2, derived from AGA.

213 radiochemical stability compared to (99m)Tc-AGA-1.

214 (99m)Tc-AGA-2 displayed faster blood clearance in mice and bette

215 (99m)Tc-AGA-2 uptake detected by autoradiography was significant

216 Based on this, (99m)Tc-AGA-2 was chosen as the lead tracer and tested in murine

217 m)Tc-radiotracers, (99m)Tc-AGA-1 and (99m)Tc-AGA-2, derived from AGA.

218 ] wk), but remained shorter and lighter than AGA infants.

219 The AGA believes that patient safety is best protected if th

220 The AGA board requested that two members knowledgeable about

221 The AGA Institute Future Trends Committee (FTC) developed th

222 Clinical Practice Updates Committee and the AGA Governing Board to provide timely guidance on a topi

223 Clinical Practice Updates Committee and the AGA Governing Board to provide timely guidance on a topi

224 Clinical Practice Updates Committee and the AGA Governing Board to provide timely perspective on a t

225 and identified Cys-1327 and Cys-1337 as the AGA-responsive proximate cysteines.

226 fic peptide release activity of mtRF1 at the AGA and AGG codons.

227 R but not EDA2R as the candidate gene at the AGA risk locus on chromosome X.

228 ed by the Committee in March 1999 and by the AGA Governing Board in May 1999.

229 the Committee on March 20, 2001, and by the AGA Governing Board on April 18, 2001.

230 ice Committee on January 8, 2004, and by the AGA Governing Board on February 13, 2004.

231 by the committee on May 16, 1999, and by the AGA governing board on July 18, 1999.

232 nomics Committee on May 17, 1998, and by the AGA Governing Board on July 24, 1998.

233 Committee on September 13, 2001, and by the AGA Governing Board on May 18, 2001.

234 y the Committee on March 4, 2000, and by the AGA Governing Board on May 21, 2000.

235 omics Committee on March 4, 2000, and by the AGA Governing Board on May 21, 2000.

236 committee on September 25, 1999, and by the AGA Governing Board on November 25, 1999.

237 Committee on September 27, 1998, and by the AGA Governing Board on November 8, 1998.

238 actice Committee on May 16, 2004, and by the AGA Governing Board on September 23, 2004.

239 by the Committee on May 16, 2004, and by the AGA Governing Board on September 23, 2004.

240 mentary was commissioned and approved by the AGA Institute Clinical Practice Updates Committee and th

241 review was commissioned and approved by the AGA Institute Clinical Practice Updates Committee and th

242 review was commissioned and approved by the AGA Institute Clinical Practice Updates Committee and th

243 he Committee on February 22, 2006 and by the AGA Institute Governing Board on April 20, 2006.

244 s Committee on February 22, 2006, and by the AGA Institute Governing Board on April 20, 2006.

245 he Committee on January 19, 2006, and by the AGA Institute Governing Board on April 20, 2006.

246 he FTC on July 12, 2006, and accepted by the AGA Institute Governing Board on July 22, 2006.

247 omics Committee on June 20, 2006, and by the AGA Institute Governing Board on July 24, 2006.

248 mics Committee on March 12, 2007, and by the AGA Institute Governing Board on May 19, 2007.

249 the Committee on March 12, 2007, and by the AGA Institute Governing Board on May 19, 2007.

250 mics Committee on August 3, 2007, and by the AGA Institute Governing Board September 27, 2007.

251 Clinical Practice Update was produced by the AGA Institute.

252 proximal tubule and can be stimulated by the AGA neomycin.

253 ecommendations therein were prepared for the AGA Institute Clinical Practice and Economics Committee.

254 However, the AGA makes no recommendation in favor of, or against, the

255 LH/FSH ratio were was also increased in the AGA group.

256 significantly smaller in the SGA than in the AGA infants on an absolute basis (13.3 +/- 2.8 and 25.2

257 Moreover, the AGA non-hot spot motif mutates at as high a rate as the

258 The idea that portions of the AGA effector site might be derived from an ancestral glu

259 e SGA infants was 1.30 +/- 0.2 kg and of the AGA infants was 1.84 +/- 0.3 kg (P = 0.0001).

260 presents the official recommendations of the AGA Institute on "Endoscopic Therapy for Gastroesophagea

261 One or two nucleotide mutations of the AGA motif on the loop significantly reduced HEV replicat

262 e largely reversed by supplementation of the AGA tRNA in cells which bear plasmids expressing the T4

263 Based on the AGA clinical pathway, FIB-4 < 1.3 and LSM < 8 kilopascal

264 ave not been available, a situation that the AGA believes puts patients at risk.

265 Here it is reported that the AGA neomycin and gentamicin elicit acute, phosphatidylin

266 , MD, a medical writer under contract to the AGA Institute, and Michael Stolar, PhD, staff liaison to

267 n a topic of high clinical importance to the AGA membership, and underwent internal peer review by th

268 n a topic of high clinical importance to the AGA membership, and underwent internal peer review by th

269 n a topic of high clinical importance to the AGA membership.

270 ult outpatients with moderate-severe UC, the AGA suggests early use of advanced therapies and/or immu

271 generally lower accuracy associated with the AGA tests make them unsuitable for screening purposes.

272 ey to high yields and compatibility with the AGA workflow.

273 gnaling underlying the renal toxicity of the AGAs.

274 her, these observations demonstrate that the AGAs induce both acute and chronic cell fate changes in

275 Replacement of either all three AGA codons or the two closest to the 3' end of the gene

276 6 to 42% misincorporation of lysine at three AGA codons in a well-expressed protein.

277 al 6.6%, 119.1%) among SGA cases compared to AGA controls.

278 investigate whether CaR could contribute to AGA-induced nephrotoxicity, the acute responses to vario

279 AGA toxicity, acute and chronic responses to AGA treatment in OK cells and in CaR stably transfected

280 We administered an online survey to AGA members from 2004-2006.

281 lls express CaR-like proteins and respond to AGAs with intracellular Ca2+ mobilization and extracellu

282 -PLC-dependent ERK activation in response to AGAs and thus could play a role in AGA-induced nephrotox

283 ng, and depleting the available pool of tRNA(AGA) enhances tagging and reveals tagging caused by sing

284 rcity of the cognate tRNA; supplemental tRNA(AGA) suppresses tagging, and depleting the available poo

285 phrotoxicity, the acute responses to various AGAs in the proximal tubule-derived opossum kidney (OK)

286 LAT1, LAT2, SNAT5, glutamate: EAAT1) versus AGA [IBR 20th-80th].

287 e 10th percentile at birth, while 65.1% were AGA.

288 Coexpression of T122K with wildtype AGA results in processing of the precursor into subunits

289 d more than 380 genomic loci associated with AGA, including genes involved in androgen and WNT pathwa

290 ignificantly diminished in SGA compared with AGA infants (mean [95% CI of difference]: FVC: 127 versu

291 f metabolites with SGA and LGA compared with AGA risk, with false discovery rate (FDR) adjustment.

292 Compared with AGA-BRF infants, SGA-BRF infants had normal HMW adiponec

293 Compared with AGA-BRF infants, the catchup growth of SGA infants was c

294 Eligible men with AGA aged 18 to 55 years classified using the Norwood-Ham

295 m clinical trials of finasteride in men with AGA is very limited, is of poor quality, and seems to be

296 th the 32 controls, the 57 participants with AGA showed significantly increased mean (SD) levels of t

297 OL or psychiatric disorders in patients with AGA were included.

298 UA codon, but not in a control sequence with AGA at the test position; induction of a minigene ending

299 of 7 of 10 of the transplanted vessels with AGA that were examined.

300 postnatal age (mean [SD]: SGA 6.8 [2.4] wk, AGA 5.9 [2.3] wk), but remained shorter and lighter than