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1                                              Vogt et al. demonstrate that, in mice, maternal high-fat
2                                              Vogt-Koyanagi-Harada (VKH) disease affects primarily per
3 etinochoroidal atrophy may be acquired after Vogt-Koyanagi-Harada disease.
4 l atrophy that developed several years after Vogt-Koyanagi-Harada disease.
5  has been demonstrated in conditions such as Vogt-Koyanagi-Harada and Alezzandrini syndromes, the ocu
6 panic subjects are predominantly affected by Vogt-Koyanagi-Harada disease.
7                         Among uveitis cases, Vogt-Koyanagi-Harada syndrome (VKH) (odds ratio [OR] = 1
8 worse for uveitis related to Behcet disease, Vogt-Koyanagi-Harada disease, or sympathetic ophthalmia,
9 ced expression in bacteria grown in Dulbecco-Vogt modified Eagle's medium compared to bacteria grown
10       Indocyanine green angiography excluded Vogt-Koyanagi-Harada syndrome.
11     To identify new genetic risk factors for Vogt-Koyanagi-Harada (VKH) syndrome, we conducted a geno
12        Past medical history was relevant for Vogt-Koyanagi-Harada disease since the age of 19 and pos
13 ific syndromes, the incidence was greater in Vogt-Koyanagi-Harada syndrome (aHR, 3.37; 95% CI, 1.52 t
14                    In this issue of the JCI, Vogt et al. show that the B7 family-related protein V-se
15 ow recognised as separate: B. lantschouensis Vogt n. stat. and B. minshanensis Bischoff n. stat..
16 rative retinopathy is an uncommon feature of Vogt Koyanagi Harada (VKH) disease which might indicate
17 o observe the morphology of the palisades of Vogt (POV) with satisfactory resolutions.
18 ncontact method for imaging the palisades of Vogt by correlating OCT and confocal microscopy images.
19                       Pigmented palisades of Vogt revealed large superficial squamous cells and small
20 g of the limbus revealed normal palisades of Vogt structure and epithelial transition in the healthy
21 cessfully identified the limbal palisades of Vogt that constitute the corneal epithelial stem cell ni
22 he distinctive structure of the palisades of Vogt was found only in 2 of 6 harvested sites.
23                                 Palisades of Vogt were absent in all (100.0%) patients, and the corne
24 the thinnest stroma without any palisades of Vogt-like niche structure.
25 s reside, such as rete pegs and palisades of Vogt.
26 ation and anatomy of the limbal palisades of Vogt.
27  found to be involved in the pathogenesis of Vogt-Koyanagi-Harada (VKH) disease.
28 ort the proposed immunologic pathogenesis of Vogt-Koyanagi-Harada disease are discussed.
29 he aspect of Bowman's layer, the presence of Vogt's striae, and stromal opacities.
30                               Two reports of Vogt-Koyanagi-Harada syndrome in 4-year-old children are
31 including: Susac syndrome, Cogan syndrome or Vogt-Koyanagi-Harada disease; demyelinating conditions s
32 CGA) findings in patients with long-standing Vogt-Koyanagi-Harada (VKH) disease and their correlation
33 d long-term outcomes of uveitis secondary to Vogt-Koyanagi-Harada (VKH) disease in children.
34 ff exudative retinal detachment secondary to Vogt-Koyanagi-Harada syndrome, which was unresponsive to
35 ms (SNP) of IL-1 and IL-1R family genes with Vogt-Koyanagi-Harada (VKH) and Behcet's disease (BD) in
36  virus DNA in the vitreous of a patient with Vogt-Koyanagi-Harada syndrome is reviewed.
37 ce and features of glaucoma in patients with Vogt-Koyanagi-Harada (VKH) syndrome compared with nongla