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1 sty (1255 eyes [94.4%] for Fuchs endothelial corneal dystrophy).
2 represented (68.5%) among those with lattice corneal dystrophy.
3 n the development of this autosomal dominant corneal dystrophy.
4 n the development of this autosomal dominant corneal dystrophy.
5 first time the molecular basis of Meesmann's corneal dystrophy.
6 ge, four-generation family with Thiel-Behnke corneal dystrophy.
7 minant forms, Reis-Bucklers and Thiel-Behnke corneal dystrophy.
8 nd ulcer compared with those with hereditary corneal dystrophy.
9 ystrophy and some cases of Fuchs endothelial corneal dystrophy.
10 al anterior corneal involvement suspected of corneal dystrophy.
11 c improvement or regression of GCD2/Avellino corneal dystrophy.
12 keratectomy (PTK) in a patient with macular corneal dystrophy.
13 RNA in the treatment of an autosomal genetic corneal dystrophy.
14 e agent for TGFBIp-associated amyloidosis in corneal dystrophy.
15 factor beta-induced protein (TGFBIp)-linked corneal dystrophy.
16 eliminating endothelial rejection in macular corneal dystrophy.
17 patients undergoing DSAEK surgery for Fuchs corneal dystrophy.
18 delineate the pathogenic mechanisms of human corneal dystrophy.
19 s undergoing eye care for reasons other than corneal dystrophy.
20 olutionized our fundamental understanding of corneal dystrophies.
21 present a current review of the genetics of corneal dystrophies.
22 are responsible for four autosomal dominant corneal dystrophies.
23 ad a profound effect on our understanding of corneal dystrophies.
24 eration of the stromal matrix in the macular corneal dystrophies.
25 that they be categorized as CHST6-associated corneal dystrophies.
26 development of gene silencing therapies for corneal dystrophies.
27 IRIS Registry and primarily associated with corneal dystrophies.
28 rocessing that results in amyloidogenesis in corneal dystrophies.
29 FBI) gene cause clinically distinct types of corneal dystrophies.
30 tations give rise to phenotypically distinct corneal dystrophies.
31 may be indicated for patients with advanced corneal dystrophies.
32 strophy 1 (CHED1) and posterior polymorphous corneal dystrophy 1 (PPCD1) are autosomal-dominant corne
34 gies for primary DMEK were Fuchs endothelial corneal dystrophy (32.5%), pseudophakic bullous keratopa
37 vious transplant (39%), or Fuchs endothelial corneal dystrophy (9%) in 20 eyes (19 patients) with a G
38 ears, undergoing DSAEK for Fuchs endothelial corneal dystrophy (94% of eyes) or pseudophakic or aphak
42 stologically evident exacerbation of macular corneal dystrophy after PTK and emphasizes the relevance
43 of mutations, such as those that cause some corneal dystrophies and Alexander disease, than previous
44 It works well in the treatment of anterior corneal dystrophies and degenerations, but we are learni
45 type-phenotype correlations in TGFBI-related corneal dystrophies and highlight the importance of stru
46 Patients with decreased vision due to Fuchs corneal dystrophy and cataract can present with a number
47 n the corneal epithelium of mice resulted in corneal dystrophy and clouding that was apparent in newb
48 have extended the pedigree of Franceschetti corneal dystrophy and elaborated its natural history on
49 It also suggests a novel genetic locus for corneal dystrophy and enamel hypomineralization without
51 he psychological well-being of patients with corneal dystrophy and suggest that integrating mental he
52 microphthalmia-anophthalmia-coloboma (MAC), corneal dystrophies, and Axenfeld-Rieger syndrome (ARS).
59 symptoms of different epithelial and stromal corneal dystrophies are not specific; therefore, it is v
62 t at understanding the molecular genetics of corneal dystrophies as genetics is increasingly importan
63 , especially for eyes with Fuchs endothelial corneal dystrophy as the indication for primary DMEK wit
65 rovide a test-bed for therapies not only for corneal dystrophies but also for other keratinopathies c
66 genetic interaction between genes that cause corneal dystrophies can modulate the expressivity of the
67 chyonychia congenita and Messmann epithelial corneal dystrophy-causing missense mutations have been d
69 l dystrophy (CHED) is a heritable, bilateral corneal dystrophy characterized by corneal opacification
70 ystrophy (CFD) is a rare, autosomal dominant corneal dystrophy characterized by numerous small white
75 loss is due to the cataract versus the Fuchs corneal dystrophy (FCD) before determining the best surg
83 nse to oxidative stress in Fuchs endothelial corneal dystrophy (FECD) and normal corneal endothelial
84 compared susceptibility of Fuchs endothelial corneal dystrophy (FECD) and normal corneal endothelial
85 e development of advanced Fuchs' endothelial corneal dystrophy (FECD) and on central corneal thicknes
86 membrane (DM) in advanced Fuchs endothelial corneal dystrophy (FECD) and to image such changes by sl
87 e pathogenic mechanisms of Fuchs endothelial corneal dystrophy (FECD) could contribute to developing
103 overall cohort, 29.8% of Fuchs' endothelial corneal dystrophy (FECD) subgroup, and 27.4% of the bull
104 ients with comorbid KC and Fuchs endothelial corneal dystrophy (FECD) underwent uncomplicated Desceme
105 agy in the pathogenesis of Fuchs endothelial corneal dystrophy (FECD) using two alpha2 collagen VIII
106 consecutive patients with Fuchs endothelial corneal dystrophy (FECD) who underwent DMEK or triple-DM
110 elial dysfunction, include Fuchs endothelial corneal dystrophy (FECD), posterior polymorphous corneal
111 d the genetic aetiology of Fuchs endothelial corneal dystrophy (FECD), the most prevalent corneal dis
112 gene leads to early-onset Fuchs' endothelial corneal dystrophy (FECD), which progressively impairs vi
121 underwent DMEK mainly for Fuchs endothelial corneal dystrophy (FECD; 85.3%) or bullous keratopathy (
122 to 8 years after DMEK for Fuchs endothelial corneal dystrophy (FECD; n = 314), bullous keratopathy (
123 K for various indications (Fuchs endothelial corneal dystrophy [FECD]: n = 111; bullous keratopathy [
125 eceived two or more diagnoses of any type of corneal dystrophy, for an overall corneal dystrophy prev
126 24H and R555W, both associated with granular corneal dystrophy (GCD) characterized by the early-onset
128 tpatients clinically diagnosed with granular corneal dystrophy (GCD) prior to phototherapeutic kerate
129 ML) techniques for the diagnosis of granular corneal dystrophy (GCD), a rare inherited condition char
134 nsforming growth factor, beta-induced linked corneal dystrophies have recently been correlated to the
136 elopments in the surgical treatment of Fuchs corneal dystrophy have greatly enhanced our ability to r
137 in (TGFBIp) are linked to the development of corneal dystrophies in which abnormal protein deposition
139 The clinical finding of the granular-lattice corneal dystrophy in which deposits are located in the B
141 sification of Corneal Dystrophies classifies corneal dystrophies into four classes: epithelial and su
142 ation, refractive surgery, corneal edema, or corneal dystrophy, IOP and CCT readings were available f
146 g loss, whereas the ocular features comprise corneal dystrophy, lenticonus, dot-and-fleck retinopathy
148 atellite markers closely linked to the known corneal dystrophy loci, we excluded linkage between the
150 emonstrated blue deposits typical of macular corneal dystrophy, mainly in the stroma but also in the
152 uman corneas and corneas affected by macular corneal dystrophies (MCD) types I and II were examined b
153 tron x-ray diffraction patterns from macular corneal dystrophy (MCD) corneas contain an unusual refle
160 tive of a severe form of Meesmann Epithelial Corneal Dystrophy (MECD), when complexed with silicon-st
161 indications for DMEK were Fuchs endothelial corneal dystrophy (n = 28) and bullous keratopathy (n =
162 genetic sites are discovered for the various corneal dystrophies, new information will arise, allowin
164 we have identified another locus (CDB2) for corneal dystrophy of the anterior basement membrane/Bowm
165 ecurrent corneal erosions was diagnosed with corneal dystrophy of the Bowman layer after a clinical e
167 This study presents data on the impact of corneal dystrophies on quality of life compared to a hea
168 001 to 2009 were searched for a recording of corneal dystrophy on a claim submitted by an ophthalmolo
169 ectious keratitis, non-infectious keratitis, corneal dystrophy or degeneration, and corneal neoplasm.
171 promoter region cause posterior polymorphous corneal dystrophy (PPCD) 1 by inducing an ectopic expres
172 eal dystrophy (FECD), posterior polymorphous corneal dystrophy (PPCD) and congenital hereditary endot
173 tage of patients with posterior polymorphous corneal dystrophy (PPCD) confirms this previously report
175 oinsufficiency causes posterior polymorphous corneal dystrophy (PPCD), in a cohort of late-onset FCD
176 n humans is linked to posterior polymorphous corneal dystrophy (PPCD), in which an epithelial transit
179 ny type of corneal dystrophy, for an overall corneal dystrophy prevalence rate of 897 per million (10
180 e, within and between the different types of corneal dystrophies, raise questions that warrant furthe
181 Compared to the control group, patients with corneal dystrophies reported a significantly worse overa
182 lusion, our novel mouse model of TGFBI-R124C corneal dystrophy reproduces features of the human disea
183 ulation, these data provide an indication of corneal dystrophy's prevalence within insured subjects a
190 ant UBIAD1 variants associated with Schnyder corneal dystrophy (SCD), a human disorder characterized
191 s, a history of herpetic keratitis, Avellino corneal dystrophy, significant cataract, and uncontrolle
193 IGH3 (TGFbeta1) gene responsible for several corneal dystrophies, there has been an explosion of new
196 R124C mutation in TGFBI that causes lattice corneal dystrophy type1 (LCD1) and generated novel trans
197 omechanical properties of eyes with granular corneal dystrophy undergoing PTK, in an effort to preven
203 st of the reported dystrophies, and granular corneal dystrophy was the least common, being reported i
206 dysfunction resulting from Fuchs endothelial corneal dystrophy were enrolled in 6 corneal centers in
209 lopment of alternative, novel treatments for corneal dystrophies, which may substantially improve the
211 D1) are responsible for Schnyder crystalline corneal dystrophy, which is a genetic disease that cause
212 main is linked to the development of lattice corneal dystrophy with amyloid deposits in the superfici
213 tion of the quality of life in patients with corneal dystrophy with visual acuity, higher order aberr
214 ng keratoplasty for the treatment of macular corneal dystrophy without endothelial involvement were i
216 participants with EHR data, 2,393 (0.6%) had corneal dystrophy without prior surgery; they were predo