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1                                              DOA presents in the first decade of life and manifests a
2                                              DOA was found proportional to the phase shift between th
3 tectic solvents for 3-deoxyanthocyanidins (3-DOA) from sorghum bran was developed.
4                                       Four 3-DOA were identified in extracts using HPLC-QTOF-MS/MS, w
5 acts obtained using ChPA exhibited highest 3-DOA content and strongest in vitro antioxidant activitie
6  temperature: 90 degrees C, time: 67 min), 3-DOA yield was 0.86 +/- 0.01 apigeninidin mg/g.
7 disruption, leading to a higher release of 3-DOA.
8          We therefore screened a panel of 35 DOA patients for mutations in OPA1.
9 th losartan or 2',5'-dideoxyadenosine (2',5'-DOA, an adenylyl cyclase inhibitor) but not by PD123319
10 ich was abrogated by AG1478 but not by 2',5'-DOA.
11 ich was abrogated with co-treatment of 2',5'-DOA.
12 ylthioadenosine (MTA), 5'-deoxyadenosine (5'-DOA), and 6-amino-6-deoxyfutalosine.
13 orted missense variant iPSC line (c.1334G>A, DOA plus [DOA]+ iPSC) and CRISPR/Cas9 corrected controls
14    As a case study, the degree of agreement (DOA) statistics for potential evapotranspiration (PET) w
15                             OPA1+/-, DOA and DOA+ iPSC showed no differentiation deficit compared to
16 of the complex was observed for both HRD and DOA pathway substrates.
17                              Both malate and DOA did not alter the sensitivity of isoprene emission t
18 13% improvement in the direction of arrival (DOA) root mean square error (RMSE) and a 57.7% improveme
19 termine incident sound direction of arrival (DOA).
20        This study used direction-of-arrival (DOA) localization to track the position of goose-beaked
21 mutated in autosomal dominant optic atrophy (DOA) (Kjer type), an inherited neuropathy of the retinal
22 s with LHON, 19 with Dominant Optic Atrophy (DOA) and 22 healthy controls.
23                      Dominant optic atrophy (DOA) and axonal peripheral neuropathy (Charcot-Marie-Too
24 ients with autosomal dominant optic atrophy (DOA) harbor pathogenic OPA1 mutations and certain missen
25            Autosomal dominant optic atrophy (DOA) is a retinal neuronal degenerative disease characte
26                      Dominant optic atrophy (DOA) is the commonest form of inherited optic neuropathy
27            Autosomal dominant optic atrophy (DOA) is the most common form of hereditary optic neuropa
28            Autosomal dominant optic atrophy (DOA) is the most common inherited optic neuropathy, char
29 afferent function in dominant optic atrophy (DOA).
30 th isolated forms of Dominant Optic Atrophy (DOA).
31  transport, and isoprene emission rates, but DOA feeding did not affect any of these processes except
32 at ~98% of individuals express the canonical DOA*0101 allele, and the remaining individuals mostly ex
33                                  Clinically, DOA remains a fairly homogeneous entity despite the grow
34          Although the two genes encoding DO (DOA and DOB) are considered nonpolymorphic, there are ra
35 horylation site in vitro for both Drosophila DOA and tobacco PK12 LAMMER kinases.
36 and the remaining individuals mostly express DOA*0102, which we found was a gain-of-function allele.
37  no licensed disease-modifying therapies for DOA and the disease mechanisms driving RGC degeneration
38              This differs substantially from DOA, in which a more stable visual function is evident w
39  values for the SWME method also had greater DOA statistics than that for the OAME method over relati
40       The SWME method tended to have greater DOA statistics for PET than the OAME method with all ava
41                                 Although HLA-DOA had been shown previously to be regulated by CIITA,
42  PSMB9, HLA-DQB1, HLA-DQB2, HLA-DMA, and HLA-DOA), increased CD8 T-cell tumor infiltration (P=7.6x10(
43 pendent risk of a synonymous mutation at HLA-DOA, a non-classical HLA gene, on anti-citrullinated pro
44 ing function is selectively inhibited by HLA-DOA were 3-fold more numerous during rejection among rej
45 ction, likely because of a dysfunctional HLA-DOA gene product.
46 ated significant repression of the first HLA-DOA exon closest to rs9296068.
47 transgenic mice that expressed the human HLA-DOA and HLA-DOB genes under the control of a dendritic c
48 ss II transactivator (CIITA), identified HLA-DOA and HLA-DOB as being up-regulated by CIITA.
49  linkage disequilibrium (LD) patterns in HLA-DOA and HLA-DRB1, explaining the observed HLA-DOA varian
50 inor allele G of the SNP rs9296068, near HLA-DOA, as being significantly different (P = .018) between
51 OA and HLA-DRB1, explaining the observed HLA-DOA variant risk heterogeneity among ethnicities, which
52 titative trait loci (cis-eQTL) effect on HLA-DOA expression.
53                   HLA-DO, encoded by the HLA-DOA and HLA-DOB genes, has been shown to function as a m
54 egion to a 90-kb segment upstream of the HLA-DOA gene.
55 rected p=0.036), located in proximity to HLA-DOA.
56 hat natural variation occurring in the human DOA gene impacts DO function and can be linked to specif
57                                           In DOA retinal ganglion cells and the optic nerve degenerat
58 is the common outcome in chronic LHON and in DOA.
59 ickness was decreased in chronic LHON and in DOA.
60 se mechanisms that contribute to RGC loss in DOA, as well as potential therapeutic interventions.
61                          The gene mutated in DOA, Optic Atrophy Type 1 (OPA1), encodes a dynamin-rela
62 -specific, indicating that the penetrance in DOA is much lower than the 98% reported previously.
63       The present study demonstrates that in DOA, loss of macular RGCs is the earliest pathologic eve
64 eport here that the Drosophila family member DOA, human SK-G1, and the Saccharomyces cerevisiae KNS1,
65  line, in conjunction with the generation of DOA patient-derived iPSC carrying OPA1 variants, namely,
66 itochondrial dysfunction in a mouse model of DOA and documented the visual and neurologic progression
67 istent with it being an in vivo substrate of DOA kinase.
68                                     OPA1+/-, DOA and DOA+ iPSC showed no differentiation deficit comp
69 irtually indistinguishable from classic OPA1-DOA.
70 ic optimization (SOA), dynamic optimization (DOA), and direct approaches (DA).
71 e inhibitors malate and diethyl oxalacetate (DOA) in the strong isoprene emitter hybrid aspen (Populu
72 ense variant iPSC line (c.1334G>A, DOA plus [DOA]+ iPSC) and CRISPR/Cas9 corrected controls.
73 ontribute to optic nerve dysfunction in pure DOA.
74 ed with data from patients with OPA1-related DOA and further analyzed for age dependency dividing pat
75 notype as compared with classic OPA1-related DOA.
76 ge-matched patients affected by OPA1-related DOA.
77                    Single sensor phase shift DOA measurement presented a resolution better than 3 deg
78                            We show here that DOA is expressed as at least two different protein isofo
79 tified in any LHON patients, indicating that DOA and LHON are genetically distinct.
80          Although it was recently shown that DOA kinase is essential for normal sexual differentiatio
81 study, we show that natural variation in the DOA gene also impacts DO function.
82 leotide polymorphisms genetically linked the DOA*0102 common allele, a gain-of-function variant, with
83 e-chaotic coded metasurface ensures that the DOA estimation is sensitive to the polarization state of
84 gly suggesting that the mechanism underlying DOA is haploinsufficiency.
85 ploinsufficiency is the mechanism underlying DOA it is unlikely that this figure will be mutation-spe
86 nts, namely, the c.2708_2711delTTAG variant (DOA iPSC), and previously reported missense variant iPSC
87         OPA1 disease alleles associated with DOA display selective defects in several activities, inc
88 n 60% of genetically confirmed patients with DOA carry variants in the nuclear OPA1 gene, which encod
89 ectors were overall thinner in patients with DOA since early age compared to patients with WS, in whi
90 NFL and GC-IPL were smaller in patients with DOA than in healthy controls (P < 0.0001).
91 er plexiform layer (GC-IPL) of patients with DOA were evaluated by optical coherence tomography (OCT)
92                                Patients with DOA who belonged to families showing evidence of linkage
93 nce early age as compared with patients with DOA, who displayed a more stable visual function over th
94 e studied 39 patients from 28 pedigrees with DOA harboring heterozygous mutations in the OPA1 gene al
95 nteracts in the yeast two-hybrid system with DOA, the LAMMER protein kinase of Drosophila.