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1                                              ATA also did not affect Jak3, which is activated in thes
2                                              ATA also mimicked PRL activation of serine kinases ERK1
3                                              ATA diameters of TEVAR patients increased at a rate of 0
4                                              ATA influences may be an important new mechanism of coex
5                                              ATA length in both TEVAR and control patients increased
6                                              ATA occurred in 43% of patients after the Maze procedure
7                                              ATA occurred in 86 patients (43%) after the Maze procedu
8                                              ATA was low in nonballooned, atherosclerotic vessels (FP
9                                              ATA was measured through exposure of arterial segments e
10                                              ATAs were seen only in participants with greater than 70
11 ared to HC at baseline (NERD vs HC P = 0.04, ATA-CRSwNP vs HC P < 0.05).
12 y after surgery (n=12), or to control (air 1 ATA) (n=15).
13 ared to ATA-CRSwNP and HC (median NERD 9.1%, ATA-CRSwNP 2.1%, and HC 0.4%; P < 0.01).
14 r 1(AERD) (vs cluster 2(AERD)) and cluster 1(ATA) (vs cluster 2(ATA)) were older and had higher body
15 r combinations included U1RNP and ACA (13%), ATA and ACA (7%) and U1RNP and PmScl (5%).
16 % versus 20%; VTA >=200 bpm, 22% versus 14%; ATA, 25% versus 12%; appropriate therapy, 30% versus 20%
17 5 atmospheres absolute (ATA) at rate of 0.15 ATA/min with 100% oxygen for 90 minutes, applied immedia
18 e, we performed whole-exome sequencing in 19 ATAs that were paired with normal DNA samples and identi
19 er 2(AERD)) and cluster 1(ATA) (vs cluster 2(ATA)) were older and had higher body mass index, more se
20 iodine (RAI) therapy after the 2009 and 2015 ATA guidelines.
21  collected from patients with NERD (n = 26), ATA-CRSwNP (n = 17), and HC (n = 21) at baseline and aft
22 the control group breathed 21% oxygen at 1.3 ATA; both treatment groups received 90-min air pressure
23  were randomized to pretreatment with HBO (3 ATA) immediately prior to (n=13), or posttreatment immed
24 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
25 res to hyperbaric oxygen rCBF decreased at 4 ATA, decreased for the initial 30 min at 5 ATA then grad
26  HBOT group received 80 bid, 7 days/week 1.5 ATA/90-min HBOTs and the sham-treated normobaric air gro
27 4 ATA, decreased for the initial 30 min at 5 ATA then gradually increased, and increased within 30 mi
28 that produces T > C base substitutions in 5'-ATA-3' sequences.
29 ard ratio [HR] 1.71; VTA >=200 bpm, HR 1.58; ATA, HR 1.87; appropriate therapy, HR 1.62; inappropriat
30 ted with large increases in NO(x) at 5 and 6 ATA and always preceded EEG discharges as a sign of CNS
31 ased throughout 75 min of HBO2 at 4, 5 and 6 ATA.
32 BF) measurement were exposed to 100% O2 at 6 ATA (absolute pressure).
33  increased, and increased within 30 min at 6 ATA.
34 ed that certain trinucleotides, such as AAT, ATA, ATT, TAT, and TTA, are favored during protein misfo
35  were treated with HBO2 at 3.5 atm absolute (ATA) for 60 min and exhibited an anti-allodynic effect,
36 er compressions at 2.0 atmospheres absolute (ATA) at 1 of 3 randomly preassigned oxygen fractions, re
37 BO, pressurized to 2.5 atmospheres absolute (ATA) at rate of 0.15 ATA/min with 100% oxygen for 90 min
38 n the HBO chamber at 3 atmospheres absolute (ATA) HBO for 1 h.
39 the FP-based assay: aurintricarboxylic acid (ATA) (IC50=1.4 muM), suramin sodium salt (IC50=3.6 muM),
40 the PMCA4 inhibitor aurintricarboxylic acid (ATA) inhibits and reverses cardiac hypertrophy induced b
41 AK)-STAT signaling [aurintricarboxylic acid (ATA), (E)-2-cyano-3-(3,4-dihydrophenyl)-N-(phenylmethyl)
42 can be activated by aurintricarboxylic acid (ATA), a negatively charged triphenylmethane derivative (
43        We show that aurintricarboxylic acid (ATA), a nonpeptide activator of cellular MEK/mitogen-act
44 o determine whether aurintricarboxylic acid (ATA), an endonuclease inhibitor known to inhibit apoptos
45 h can be blocked by aurintricarboxylic acid (ATA), an inhibitor of apoptosis; and (4) marginal releas
46                     Aurintricarboxylic acid (ATA), an inhibitor of endonuclease activity and other pr
47 c YopH inhibitor is aurintricarboxylic acid (ATA), which exhibits a Ki value of 5 nm for YopH and dis
48 icular injection of aurintricarboxylic acid (ATA, 20 micrograms/5 microliters); (b) the inhibition of
49 signing artificial transcription activators (ATAs) that specifically control genes linked to human di
50  arterial wall-associated thrombin activity (ATA) after angioplasty.
51                 Autonomous thyroid adenomas (ATAs) are a frequent cause of hyperthyroidism.
52            Utility of antithrombotic agents (ATAs) in these settings is restricted by inadequate phar
53  peculiarities of both beta-amidothioamides (ATAs) and 1,2-diaza-1,3-dienes (DDs).
54 ative transcriptional activator proteins, an ATA must minimally contain a DNA-binding domain (DBD) an
55  were more likely to have a genotype with an ATA haplotype than those whose arthritis remained restri
56 igh-level IL-10 secretion, while the ACC and ATA haplotypes produced intermediate and low levels of I
57                     In contrast, the ACC and ATA haplotypes were more frequent in children with gingi
58 ate phyla, AGA and AGG specify arginine, and ATA specifies isoleucine.
59 an efficient method of prescreening GGAA and ATA microsatellite clones for Alu repeats with probes de
60 at the Janus kinase inhibitors, WHI-P154 and ATA, efficiently blocked STAT1 phosphorylation in a conc
61   Th e most common combination was U1RNP and ATA (35%).
62 nd old mice with an anti-myostatin antibody (ATA 842) for 4 wk increased muscle mass and muscle stren
63  strongly associated with antitopoisomerase (ATA) and anticentromere antibody-positive subsets of SSc
64 and lengths of the ascending thoracic aorta (ATA).
65 pe transcription factor, Atypical Arbuscule (ATA), that acts as the central regulator of AM-related g
66  and severity of arterial transit artifacts (ATAs) at ASL imaging.
67 otent and selective YopH inhibitors, such as ATA, should be useful reagents to delineate YopH's cellu
68 transporting ABCBs, which we now refer to as ATAs.
69 Over time, the American Thyroid Association (ATA) guidelines have increasingly promoted more limited
70 ed that such 'asymmetric tail associations' (ATAs) are common between ecological variables, and are i
71 ), 26 patients with aspirin-tolerant asthma (ATA) (11 steroid naive; mean age, 47 +/- 18 years; FEV(1
72 nd 63 patients with aspirin-tolerant asthma (ATA), both with 23 variables.
73 nd 14 patients with aspirin-tolerant asthma (ATA).
74 eroidal aromatase inhibitor (AI) atamestane (ATA) combined with toremifene (TOR; complete estrogen bl
75 onses in rats exposed at 4 to 6 atmospheres (ATA) of HBO2 and correlated them with brain interstitial
76 Thy-1 glycoprotein (anti-Thy-1 autoantibody [ATA]) is produced by B-1 cells that are positively selec
77 Increased anti-thymocyte/Thy-1 autoreactive (ATA) BCR cells in the B1 B cell subset by transgenic exp
78 lost CD1d in B1 B cells generating strong B1 ATA B cell leukemia/lymphoma.
79              In a Thy-1 null environment, BM ATA B cells progress to a normal follicular stage in spl
80 ant and poly(A)-rich microsatellite classes (ATA, AATA) are frequently associated with an evolutionar
81 ith papillary thyroid carcinomas up to 4 cm, ATA guideline changes corresponded with increased TL and
82 hich a genomically encoded isoleucine codon (ATA) is converted to a methionine codon (ATI) in a regio
83                                 In contrast, ATA B-CLL did not develop from other B cell subsets, eve
84                  Participants received daily ATA 500 mg with TOR 60 mg (ATA + TOR), or letrozole 2.5
85                Splenectomy did not eliminate ATA production and transfer of tolerant splenic B cells
86     This 15-bp core has the palindromic ends ATA and TAT, and it matches the consensus for LysR famil
87                      The sensory off-flavor "ATA" and a content of 0.5 ug/L 2-aminoacetophenone were
88       Prescreening with primers designed for ATA microsatellite class resulted in the reduction of th
89                                 Furthermore, ATA 842 treatment also increased insulin-stimulated whol
90                                 Furthermore, ATA afforded significant neuronal protection and prevent
91 ed in a normal or non-NarI sequence (5'-GATG*ATA-3') and that the rate of incision for AAF-DNA adduct
92                              Both rpoS ATG &gt; ATA and DeltarpoS strains exhibited stronger virulence-r
93                               The rpoS ATG &gt; ATA SNP was associated with enhanced EAEC-specific virul
94 polymorphism (SNP) in the start codon (ATG &gt; ATA) of rpoS, encoding the alternative sigma factor S.
95 d a triple nucleotide change, c.1470-1472TCC&gt;ATA (p.Asp490Glu-Pro491Tyr), in one European kindred.
96 s in the translation initiation codon (ATG--&gt;ATA) and in codon 31 (TCA-->TGA) of the beta(2)-microglo
97      An initiator methionine mutation (ATG--&gt;ATA) in two late-onset patients was expressed at a signi
98                                    Two hits, ATA and NF023, obtained in both screens were confirmed i
99  cofactor, resulting in cells with more holo ATA catalyst and higher catalytic activity.
100  antibodies (SSc-Abs): anti-topoisomerase I (ATA), anti-centromere (ACA), anti-RNA polymerase III (AR
101 ther B cell subsets, even when the identical ATA BCR was expressed on a Thy-1 low/null background.
102 proximately 90% of serum immunoglobulin M in ATA micro kappa mice.
103 D and HC (P < 0.01 and P = 0.01), but not in ATA-CRSwNP.
104 mutation occurs with high frequency (27%) in ATAs.
105 e second most frequent genetic alteration in ATAs.
106 12), or with autoantibody subtypes including ATA (P = 0.126, OR = 0.74, 95% CI = 0.51-1.08), ACA (P =
107  We further show that two of the inhibitors, ATA and PV6R, indeed inhibit the exonuclease activity of
108                       The hazard ratios (LET/ATA + TOR) were 1.00 (95% CI, 0.92 to 1.08) for TTP, 0.9
109 n prolactin (PRL)-dependent Nb2 lymphocytes, ATA sustained cell growth in the absence of hormone and
110 ts received daily ATA 500 mg with TOR 60 mg (ATA + TOR), or letrozole 2.5 mg (LET).
111       Median TTF was similar at 9.24 months (ATA + TOR) versus 10.44 months (LET).
112                                 Nonetheless, ATA-positive selection was evident by self-antigen-depen
113                            Administration of ATA by injection into the right cerebral ventricle 1 h b
114                           The time course of ATA after angioplasty was assessed in 44 rabbits.
115                      The average duration of ATA was 5.7+/-5.0 days.
116 ular context, we have examined the effect of ATA on T-cell signaling in human Jurkat cells transfecte
117    In this study, we examined the effects of ATA on expression of mRNAs encoding glutamate receptor s
118 responding control triplexes, the folding of ATA is accompanied by a lower counterion uptake and a si
119  define the incidence and natural history of ATA after the Maze procedure.
120                                  The lack of ATA, which represents the ortholog of Required For Arbus
121 n a separate set of experiments, 4 microg of ATA was administered intraventricularly 1 hour before is
122                           Four micrograms of ATA was administered intraventricularly 1 hour before is
123 d-type plants revealed an additional role of ATA in restricting mycorrhizal colonization of the root
124 nit (GNAS) are found in approximately 70% of ATAs.
125                                  Delivery of ATAs using biomimetic synthetic carriers, host blood cel
126 ing storage effects to show the influence of ATAs.
127 tus also was associated with the severity of ATAs (P = .002).ConclusionArterial transit artifacts wer
128 ts hold promise for extending the utility of ATAs in the management of acute thrombotic disorders thr
129 DSs that have the potential to help optimize ATA pharmacokinetics, target drug delivery to sites of t
130    Results of studies with AT1A null mice or ATA X AT1B dual null mice and AT2-deleted animals indica
131 8.8% of patients without early postoperative ATA (P=0.8).
132 7.0% of patients who had early postoperative ATA and 8.8% of patients without early postoperative ATA
133 between the incidence of early postoperative ATA and the late recurrence of AF.
134 ined for all episodes of early postoperative ATA that occurred during the first 30 days after the pro
135    The peak incidence of early postoperative ATA was on postoperative day 8.
136 gen at 2.4 atmospheres of absolute pressure (ATA) and the control group breathed 21% oxygen at 1.3 AT
137                         However, unlike PRL, ATA did not regulate Stat1 or Stat3.
138     OR occurred in 30% of patients receiving ATA + TOR and in 36% of patients receiving LET (P < .1).
139 ts (AEs) were similar for patients receiving ATA + TOR versus LET, and serious AEs were 10% v 11%, re
140                   TTP for patients receiving ATA + TOR was identical to that for patients receiving L
141 evident by self-antigen-dependent high serum ATA production, comprising approximately 90% of serum im
142 resulting in the production of natural serum ATA, arises independently from the major pathway of BM B
143 rtificial DBDs to create potent and specific ATAs.
144 by transgenic expression yielded spontaneous ATA B-CLL/lymphoma incidence, enhanced by TCL1 transgene
145 intravenous infusion of r-hirudin suppressed ATA measured 24 hours after angioplasty in the focally a
146 the residue at C4 of the heterodiene system, ATAs can act as hetero-mononucleophiles or hetero-dinucl
147 chaeal consensus promoter sequence [TTTA(A/T)ATA] was found 32 nucleotides upstream from that transcr
148 chyarrhythmia (VTA), atrial tachyarrhythmia (ATA), ICD therapies, VTA burden (using Andersen-Gill rec
149            However, atrial tachyarrhythmias (ATA) are a common early complication after the operation
150 nstrated persistent atrial tachyarrhythmias (ATAs).
151 affinity for ACRAMTU was observed in d(TATAT ATA)(2), followed by d(CGCGCGCG)(2) and d(GAG ATCTC)(2).
152                          We demonstrate that ATA can effectively block the inhibitory activity of Yop
153 irical example using diatoms illustrate that ATA influences can be comparable in magnitude to other m
154                  These findings suggest that ATA is neuroprotective in ischemia by blocking the trans
155  to other mechanisms of coexistence and that ATAs can make the difference between species coexistence
156 y than the GCC haplotype (P = 0.02), and the ATA/ATA genotype was associated with lower IL-10 product
157 s proposed to catalyze the first step in the ATA pathway, converting the substrates L-arginine and py
158 monstrate the functional significance of the ATA haplotype and reveal a significant association of ge
159 cant level in COS cells, suggesting that the ATA codon may be utilized to a clinically important exte
160 iation of the HLA-DPB1*13:01 allele with the ATA(+) subset of SSc in both AA and EA patients demonstr
161                                         This ATA haplotype was associated with lower transcriptional
162  865 patients were randomly assigned (434 to ATA + TOR and 431 to LET) in 60 centers in the United St
163 higher rates of overlap features compared to ATA patients.
164 ted sputum eosinophilic count as compared to ATA-CRSwNP and HC (median NERD 9.1%, ATA-CRSwNP 2.1%, an
165 e 5'-UTR of CRHR1, with or without an ATG-to-ATA mutation in the upstream ORF, and the main ORF of lu
166                   The arginine transaminase (ATA) pathway represents one of the multiple pathways for
167                                  Here, using ATA micro kappa transgenic mice we show that cells with
168 yclohexanone, E. coli cells expressing WT-Vf-ATA form either diastereomer of the amine product in >10
169 ts had a higher rate of first VTA, fast VTA, ATA, and appropriate and inappropriate ICD therapy (VTA
170  patients had a high risk and burden of VTA, ATA, and ICD therapies with a lower survival rate.
171 D, 59 asthmatics who tolerated aspirin well (ATA), and 51 healthy controls.
172                         To determine whether ATA can block the activity of YopH in a cellular context
173 hough the mechanism and specificity by which ATA activates Jak2, Stat5, and ERKs in Nb2 cells are sti
174                                        While ATA blocked DNA laddering resulting from either beta A4
175 cantly lower, in AERD clusters compared with ATA clusters.
176 IA compared with steroid-naive patients with ATA and healthy subjects (152.3 +/- 30.4 and 36.6 +/- 7.
177  and 8 patients with AIA and 8 patients with ATA received placebo.
178 Twelve patients with AIA and 6 patients with ATA were randomly assigned to receive 624 mg of aspirin,
179                         Of the patients with ATA, 59% had atrial fibrillation (AF), 14% had atrial fl
180 -ETE and leukotriene E(4) than patients with ATA.
181 ischemic controls in animals pretreated with ATA that was significantly less (p < 0.05) than the 48%
182                            Pretreatment with ATA virtually eliminated TUNEL staining at 4 days.
183                            Participants with ATAs (n = 16) were more likely to be symptomatic than we
184 tients demonstrated first-degree AVB without ATA, 32 of whom developed AVB from operative day 7 to 15
185 ly to be symptomatic than were those without ATAs (n = 28) (P = .004).

 
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