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 is an independent predictor of mortality from DM and

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

4 AGA, defined as smooth muscle cells forming a neointima

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

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

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

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

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

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

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

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

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

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

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

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

17 those born appropriate for gestational age (AGA).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 tress response can protect cells from HU and AGAs.

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

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

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

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

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

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

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

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

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

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

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

48 rts with accelerated graft arteriosclerosis (AGA).

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

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

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

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

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

54 he American Gastroenterological Association (AGA) membership.

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

56 he American Gastroenterological Association (AGA) on constipation.

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

58 he American Gastroenterological Association (AGA) on Hemorrhoids.

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

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

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

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

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

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

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

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

67 to the hCPS conformational change induced by AGA.

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

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

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

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

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

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

74 retinal microglial TNF-alpha release during AGA treatment.

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

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

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

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

79 US Food and Drug Administration approval for AGA.

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

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

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

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

84 potentially being near the binding site for AGA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 or pharmacological chaperones for the mutant AGA.

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

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

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

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

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

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

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

111 ollicle may contribute to the development of AGA.

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

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

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

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

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

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

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

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

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

121 profile for finasteride in the treatment of AGA.

122 ovel therapeutic strategies for treatment of AGA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 6A37A38 in the anticodon loop, only tRNA(Ser)AGA, tRNA(Ser)CGA, tRNA(Ser)UGA, and selenocysteine tRNA

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

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

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

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

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

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

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

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

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

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

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

149 The AGA board requested that two members knowledgeable about

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 gnaling underlying the renal toxicity of the AGAs.

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

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

190 6 to 42% misincorporation of lysine at three AGA codons in a well-expressed protein.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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