ライフサイエンスコーパス: ATA

1 ATA also did not affect Jak3, which is activated in thes

2 ATA also mimicked PRL activation of serine kinases ERK1

3 ATA occurred in 43% of patients after the Maze procedure

4 ATA occurred in 86 patients (43%) after the Maze procedu

5 ATA was low in nonballooned, atherosclerotic vessels (FP

6 ATA was measured through exposure of arterial segments e

7 y after surgery (n=12), or to control (air 1 ATA) (n=15).

8 e, we performed whole-exome sequencing in 19 ATAs that were paired with normal DNA samples and identi

9 the control group breathed 21% oxygen at 1.3 ATA; both treatment groups received 90-min air pressure

10 were randomized to pretreatment with HBO (3 ATA) immediately prior to (n=13), or posttreatment immed

11 let, d(A(3)TA(3)C(5)T(3)AT(3)C(5)T(3)GT(3)) (ATA) and d(AGTGAC(5)TCACTC(5)TCGCT) (GTG), and their con

12 res to hyperbaric oxygen rCBF decreased at 4 ATA, decreased for the initial 30 min at 5 ATA then grad

13 HBOT group received 80 bid, 7 days/week 1.5 ATA/90-min HBOTs and the sham-treated normobaric air gro

14 4 ATA, decreased for the initial 30 min at 5 ATA then gradually increased, and increased within 30 mi

15 ted with large increases in NO(x) at 5 and 6 ATA and always preceded EEG discharges as a sign of CNS

16 ased throughout 75 min of HBO2 at 4, 5 and 6 ATA.

17 BF) measurement were exposed to 100% O2 at 6 ATA (absolute pressure).

18 increased, and increased within 30 min at 6 ATA.

19 were treated with HBO2 at 3.5 atm absolute (ATA) for 60 min and exhibited an anti-allodynic effect,

20 er compressions at 2.0 atmospheres absolute (ATA) at 1 of 3 randomly preassigned oxygen fractions, re

21 n the HBO chamber at 3 atmospheres absolute (ATA) HBO for 1 h.

22 the FP-based assay: aurintricarboxylic acid (ATA) (IC50=1.4 muM), suramin sodium salt (IC50=3.6 muM),

23 the PMCA4 inhibitor aurintricarboxylic acid (ATA) inhibits and reverses cardiac hypertrophy induced b

24 AK)-STAT signaling [aurintricarboxylic acid (ATA), (E)-2-cyano-3-(3,4-dihydrophenyl)-N-(phenylmethyl)

25 can be activated by aurintricarboxylic acid (ATA), a negatively charged triphenylmethane derivative (

26 We show that aurintricarboxylic acid (ATA), a nonpeptide activator of cellular MEK/mitogen-act

27 o determine whether aurintricarboxylic acid (ATA), an endonuclease inhibitor known to inhibit apoptos

28 h can be blocked by aurintricarboxylic acid (ATA), an inhibitor of apoptosis; and (4) marginal releas

29 Aurintricarboxylic acid (ATA), an inhibitor of endonuclease activity and other pr

30 c YopH inhibitor is aurintricarboxylic acid (ATA), which exhibits a Ki value of 5 nm for YopH and dis

31 icular injection of aurintricarboxylic acid (ATA, 20 micrograms/5 microliters); (b) the inhibition of

32 signing artificial transcription activators (ATAs) that specifically control genes linked to human di

33 arterial wall-associated thrombin activity (ATA) after angioplasty.

34 Autonomous thyroid adenomas (ATAs) are a frequent cause of hyperthyroidism.

35 Utility of antithrombotic agents (ATAs) in these settings is restricted by inadequate phar

36 peculiarities of both beta-amidothioamides (ATAs) and 1,2-diaza-1,3-dienes (DDs).

37 ative transcriptional activator proteins, an ATA must minimally contain a DNA-binding domain (DBD) an

38 were more likely to have a genotype with an ATA haplotype than those whose arthritis remained restri

39 igh-level IL-10 secretion, while the ACC and ATA haplotypes produced intermediate and low levels of I

40 In contrast, the ACC and ATA haplotypes were more frequent in children with gingi

41 ate phyla, AGA and AGG specify arginine, and ATA specifies isoleucine.

42 an efficient method of prescreening GGAA and ATA microsatellite clones for Alu repeats with probes de

43 at the Janus kinase inhibitors, WHI-P154 and ATA, efficiently blocked STAT1 phosphorylation in a conc

44 nd old mice with an anti-myostatin antibody (ATA 842) for 4 wk increased muscle mass and muscle stren

45 pe transcription factor, Atypical Arbuscule (ATA), that acts as the central regulator of AM-related g

46 otent and selective YopH inhibitors, such as ATA, should be useful reagents to delineate YopH's cellu

47 ), 26 patients with aspirin-tolerant asthma (ATA) (11 steroid naive; mean age, 47 +/- 18 years; FEV(1

48 nd 14 patients with aspirin-tolerant asthma (ATA).

49 eroidal aromatase inhibitor (AI) atamestane (ATA) combined with toremifene (TOR; complete estrogen bl

50 onses in rats exposed at 4 to 6 atmospheres (ATA) of HBO2 and correlated them with brain interstitial

51 Thy-1 glycoprotein (anti-Thy-1 autoantibody [ATA]) is produced by B-1 cells that are positively selec

52 Increased anti-thymocyte/Thy-1 autoreactive (ATA) BCR cells in the B1 B cell subset by transgenic exp

53 In a Thy-1 null environment, BM ATA B cells progress to a normal follicular stage in spl

54 ant and poly(A)-rich microsatellite classes (ATA, AATA) are frequently associated with an evolutionar

55 hich a genomically encoded isoleucine codon (ATA) is converted to a methionine codon (ATI) in a regio

56 In contrast, ATA B-CLL did not develop from other B cell subsets, eve

57 Participants received daily ATA 500 mg with TOR 60 mg (ATA + TOR), or letrozole 2.5

58 Splenectomy did not eliminate ATA production and transfer of tolerant splenic B cells

59 This 15-bp core has the palindromic ends ATA and TAT, and it matches the consensus for LysR famil

60 Prescreening with primers designed for ATA microsatellite class resulted in the reduction of th

61 Furthermore, ATA 842 treatment also increased insulin-stimulated whol

62 Furthermore, ATA afforded significant neuronal protection and prevent

63 ed in a normal or non-NarI sequence (5'-GATG*ATA-3') and that the rate of incision for AAF-DNA adduct

64 d a triple nucleotide change, c.1470-1472TCC>ATA (p.Asp490Glu-Pro491Tyr), in one European kindred.

65 s in the translation initiation codon (ATG-->ATA) and in codon 31 (TCA-->TGA) of the beta(2)-microglo

66 An initiator methionine mutation (ATG-->ATA) in two late-onset patients was expressed at a signi

67 Two hits, ATA and NF023, obtained in both screens were confirmed i

68 ther B cell subsets, even when the identical ATA BCR was expressed on a Thy-1 low/null background.

69 proximately 90% of serum immunoglobulin M in ATA micro kappa mice.

70 mutation occurs with high frequency (27%) in ATAs.

71 e second most frequent genetic alteration in ATAs.

72 We further show that two of the inhibitors, ATA and PV6R, indeed inhibit the exonuclease activity of

73 The hazard ratios (LET/ATA + TOR) were 1.00 (95% CI, 0.92 to 1.08) for TTP, 0.9

74 n prolactin (PRL)-dependent Nb2 lymphocytes, ATA sustained cell growth in the absence of hormone and

75 ts received daily ATA 500 mg with TOR 60 mg (ATA + TOR), or letrozole 2.5 mg (LET).

76 Median TTF was similar at 9.24 months (ATA + TOR) versus 10.44 months (LET).

77 Nonetheless, ATA-positive selection was evident by self-antigen-depen

78 Administration of ATA by injection into the right cerebral ventricle 1 h b

79 The time course of ATA after angioplasty was assessed in 44 rabbits.

80 The average duration of ATA was 5.7+/-5.0 days.

81 ular context, we have examined the effect of ATA on T-cell signaling in human Jurkat cells transfecte

82 In this study, we examined the effects of ATA on expression of mRNAs encoding glutamate receptor s

83 responding control triplexes, the folding of ATA is accompanied by a lower counterion uptake and a si

84 define the incidence and natural history of ATA after the Maze procedure.

85 The lack of ATA, which represents the ortholog of Required For Arbus

86 n a separate set of experiments, 4 microg of ATA was administered intraventricularly 1 hour before is

87 Four micrograms of ATA was administered intraventricularly 1 hour before is

88 d-type plants revealed an additional role of ATA in restricting mycorrhizal colonization of the root

89 nit (GNAS) are found in approximately 70% of ATAs.

90 Delivery of ATAs using biomimetic synthetic carriers, host blood cel

91 ts hold promise for extending the utility of ATAs in the management of acute thrombotic disorders thr

92 DSs that have the potential to help optimize ATA pharmacokinetics, target drug delivery to sites of t

93 Results of studies with AT1A null mice or ATA X AT1B dual null mice and AT2-deleted animals indica

94 8.8% of patients without early postoperative ATA (P=0.8).

95 7.0% of patients who had early postoperative ATA and 8.8% of patients without early postoperative ATA

96 between the incidence of early postoperative ATA and the late recurrence of AF.

97 ined for all episodes of early postoperative ATA that occurred during the first 30 days after the pro

98 The peak incidence of early postoperative ATA was on postoperative day 8.

99 gen at 2.4 atmospheres of absolute pressure (ATA) and the control group breathed 21% oxygen at 1.3 AT

100 However, unlike PRL, ATA did not regulate Stat1 or Stat3.

101 OR occurred in 30% of patients receiving ATA + TOR and in 36% of patients receiving LET (P < .1).

102 ts (AEs) were similar for patients receiving ATA + TOR versus LET, and serious AEs were 10% v 11%, re

103 TTP for patients receiving ATA + TOR was identical to that for patients receiving L

104 evident by self-antigen-dependent high serum ATA production, comprising approximately 90% of serum im

105 resulting in the production of natural serum ATA, arises independently from the major pathway of BM B

106 rtificial DBDs to create potent and specific ATAs.

107 by transgenic expression yielded spontaneous ATA B-CLL/lymphoma incidence, enhanced by TCL1 transgene

108 intravenous infusion of r-hirudin suppressed ATA measured 24 hours after angioplasty in the focally a

109 the residue at C4 of the heterodiene system, ATAs can act as hetero-mononucleophiles or hetero-dinucl

110 chaeal consensus promoter sequence [TTTA(A/T)ATA] was found 32 nucleotides upstream from that transcr

111 However, atrial tachyarrhythmias (ATA) are a common early complication after the operation

112 nstrated persistent atrial tachyarrhythmias (ATAs).

113 affinity for ACRAMTU was observed in d(TATAT ATA)(2), followed by d(CGCGCGCG)(2) and d(GAG ATCTC)(2).

114 We demonstrate that ATA can effectively block the inhibitory activity of Yop

115 These findings suggest that ATA is neuroprotective in ischemia by blocking the trans

116 y than the GCC haplotype (P = 0.02), and the ATA/ATA genotype was associated with lower IL-10 product

117 s proposed to catalyze the first step in the ATA pathway, converting the substrates L-arginine and py

118 monstrate the functional significance of the ATA haplotype and reveal a significant association of ge

119 cant level in COS cells, suggesting that the ATA codon may be utilized to a clinically important exte

120 This ATA haplotype was associated with lower transcriptional

121 865 patients were randomly assigned (434 to ATA + TOR and 431 to LET) in 60 centers in the United St

122 e 5'-UTR of CRHR1, with or without an ATG-to-ATA mutation in the upstream ORF, and the main ORF of lu

123 The arginine transaminase (ATA) pathway represents one of the multiple pathways for

124 Here, using ATA micro kappa transgenic mice we show that cells with

125 To determine whether ATA can block the activity of YopH in a cellular context

126 hough the mechanism and specificity by which ATA activates Jak2, Stat5, and ERKs in Nb2 cells are sti

127 While ATA blocked DNA laddering resulting from either beta A4

128 IA compared with steroid-naive patients with ATA and healthy subjects (152.3 +/- 30.4 and 36.6 +/- 7.

129 and 8 patients with AIA and 8 patients with ATA received placebo.

130 Twelve patients with AIA and 6 patients with ATA were randomly assigned to receive 624 mg of aspirin,

131 Of the patients with ATA, 59% had atrial fibrillation (AF), 14% had atrial fl

132 ischemic controls in animals pretreated with ATA that was significantly less (p < 0.05) than the 48%

133 Pretreatment with ATA virtually eliminated TUNEL staining at 4 days.

134 tients demonstrated first-degree AVB without ATA, 32 of whom developed AVB from operative day 7 to 15