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1 ed with vitelliform macular degeneration, or Best disease.
2 pants: Forty-five individuals diagnosed with Best disease.
3  mutation spectrum of BEST1 in patients with Best disease.
4 gs, mfERG amplitudes, prevalence estimate of Best disease.
5  is proposed as a new large animal model for Best disease.
6 pensity for the macula to develop lesions in Best disease.
7 altered electrooculogram of individuals with Best disease.
8 ed in the dominantly inherited eye disorder, Best disease.
9  the potential of gene augmentation to treat Best disease, a dominant macular dystrophy caused by ove
10                                              Best disease, an autosomal dominant inherited macular de
11  approach for some individuals with dominant Best disease and that non-responders are candidates for
12 ubjects, 39 unrelated probands with familial Best disease, and 57 unrelated probands with the ophthal
13 tive eye diseases such as Stargardt disease, Best disease, and age-related macular degeneration.
14                               The lesions in Best disease are primarily restricted to the macula, a s
15 atients with the ophthalmoscopic features of Best disease are probably affected with some other macul
16 described previously in Danish patients with Best disease are reviewed.
17      Patients with the clinical diagnosis of Best disease are significantly more likely to have a mut
18 al appearance typical of and consistent with Best disease at various stages, except that the presenta
19                                              Best disease (BD) is an inherited degenerative disease o
20 the 57 probands with a clinical diagnosis of Best disease but no family history revealed 16 with muta
21 robands with the ophthalmoscopic findings of Best disease but no family history were screened for seq
22 nopathy as well as in two models of dominant Best disease caused by different mutations in regions en
23 monotherapy or in combination to achieve the best disease control and minimize overall toxicity.
24 two other alleles previously associated with Best disease, cotransfection with wild-type bestrophin-1
25  is common in the fundus of individuals with Best disease, diagnosis is based on a reduced ratio of t
26                                An eye from a Best disease donor with a T6R mutation was found to have
27                   It not only results in the best disease-free term survival rates, but also provides
28              Fifteen of the 20 patients with Best disease had more than 1 visit, and the imaging stud
29                     A prevalence estimate of Best disease in Denmark based on the number of diagnosed
30                             A third dominant Best disease iPSC-RPE model did not respond to gene augm
31         We then subjected all three dominant Best disease iPSC-RPE models to gene editing, which prod
32                                              Best disease is a macular dystrophy caused by mutations
33                     On clinical examination, Best disease is characterized by an elevated lesion bene
34         Our frequency estimate confirms that Best disease is one of the most common causes of early m
35           Vitelliform macular dystrophy (VMD/Best disease; MIM*153700) is an early-onset autosomal do
36             Of the 39 probands with familial Best disease, mutations were detected in all 39 (33 by S
37 -causing mutations were found in one or more Best disease or AMD patients.
38                                              Best disease, or vitelliform macular degeneration, is an
39                      Unaffected (n = 11) and Best disease patients (n = 7) were imaged at approximate
40              Physical activity is one of the best disease prevention strategies, and it is influenced
41 hic atrophy (GA), Stargardt disease (STGD1), Best disease, pseudoxanthoma elasticum (PXE), central ar
42 ose proximity to multiple seed nodes are the best disease-related candidate genes.
43 he best consistency between datasets and the best disease relevance.
44 s after the start of light adaptation, while Best disease subjects exhibited a significant increase i
45 jects, and the lack of a light peak phase in Best disease subjects is associated with an increase in
46  dark and light adaptation in unaffected and Best disease subjects, and to compare these changes to t
47 uded angle-closure glaucoma (four patients), Best disease (three patients), and central serous chorio
48 logy of two donors with clinically diagnosed Best disease were also examined.
49 ular manifestation of BEST1 mutation causing Best disease were ascertained retrospectively from the c
50 MD may actually have a late-onset variant of Best disease, whereas at the same time, a considerable f
51 tely sequenced in six probands with familial Best disease who showed no SSCP shift.