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1 sty (1255 eyes [94.4%] for Fuchs endothelial corneal dystrophy).
2 first time the molecular basis of Meesmann's corneal dystrophy.
3 ge, four-generation family with Thiel-Behnke corneal dystrophy.
4 minant forms, Reis-Bucklers and Thiel-Behnke corneal dystrophy.
5 eliminating endothelial rejection in macular corneal dystrophy.
6 patients undergoing DSAEK surgery for Fuchs corneal dystrophy.
7 s undergoing eye care for reasons other than corneal dystrophy.
8 represented (68.5%) among those with lattice corneal dystrophy.
9 n the development of this autosomal dominant corneal dystrophy.
10 n the development of this autosomal dominant corneal dystrophy.
11 are responsible for four autosomal dominant corneal dystrophies.
12 ad a profound effect on our understanding of corneal dystrophies.
13 eration of the stromal matrix in the macular corneal dystrophies.
14 tations give rise to phenotypically distinct corneal dystrophies.
15 olutionized our fundamental understanding of corneal dystrophies.
16 present a current review of the genetics of corneal dystrophies.
17 strophy 1 (CHED1) and posterior polymorphous corneal dystrophy 1 (PPCD1) are autosomal-dominant corne
22 of mutations, such as those that cause some corneal dystrophies and Alexander disease, than previous
23 It works well in the treatment of anterior corneal dystrophies and degenerations, but we are learni
24 Patients with decreased vision due to Fuchs corneal dystrophy and cataract can present with a number
25 n the corneal epithelium of mice resulted in corneal dystrophy and clouding that was apparent in newb
26 have extended the pedigree of Franceschetti corneal dystrophy and elaborated its natural history on
31 t at understanding the molecular genetics of corneal dystrophies as genetics is increasingly importan
32 rovide a test-bed for therapies not only for corneal dystrophies but also for other keratinopathies c
33 genetic interaction between genes that cause corneal dystrophies can modulate the expressivity of the
34 chyonychia congenita and Messmann epithelial corneal dystrophy-causing missense mutations have been d
36 l dystrophy (CHED) is a heritable, bilateral corneal dystrophy characterized by corneal opacification
37 ystrophy (CFD) is a rare, autosomal dominant corneal dystrophy characterized by numerous small white
40 loss is due to the cataract versus the Fuchs corneal dystrophy (FCD) before determining the best surg
48 nse to oxidative stress in Fuchs endothelial corneal dystrophy (FECD) and normal corneal endothelial
49 compared susceptibility of Fuchs endothelial corneal dystrophy (FECD) and normal corneal endothelial
50 e development of advanced Fuchs' endothelial corneal dystrophy (FECD) and on central corneal thicknes
59 agy in the pathogenesis of Fuchs endothelial corneal dystrophy (FECD) using two alpha2 collagen VIII
60 elial dysfunction, include Fuchs endothelial corneal dystrophy (FECD), posterior polymorphous corneal
61 d the genetic aetiology of Fuchs endothelial corneal dystrophy (FECD), the most prevalent corneal dis
65 to 8 years after DMEK for Fuchs endothelial corneal dystrophy (FECD; n = 314), bullous keratopathy (
66 eceived two or more diagnoses of any type of corneal dystrophy, for an overall corneal dystrophy prev
68 tpatients clinically diagnosed with granular corneal dystrophy (GCD) prior to phototherapeutic kerate
69 nsforming growth factor, beta-induced linked corneal dystrophies have recently been correlated to the
71 elopments in the surgical treatment of Fuchs corneal dystrophy have greatly enhanced our ability to r
72 in (TGFBIp) are linked to the development of corneal dystrophies in which abnormal protein deposition
74 The clinical finding of the granular-lattice corneal dystrophy in which deposits are located in the B
75 ation, refractive surgery, corneal edema, or corneal dystrophy, IOP and CCT readings were available f
78 atellite markers closely linked to the known corneal dystrophy loci, we excluded linkage between the
79 uman corneas and corneas affected by macular corneal dystrophies (MCD) types I and II were examined b
80 tron x-ray diffraction patterns from macular corneal dystrophy (MCD) corneas contain an unusual refle
86 indications for DMEK were Fuchs endothelial corneal dystrophy (n = 28) and bullous keratopathy (n =
87 genetic sites are discovered for the various corneal dystrophies, new information will arise, allowin
89 we have identified another locus (CDB2) for corneal dystrophy of the anterior basement membrane/Bowm
90 ecurrent corneal erosions was diagnosed with corneal dystrophy of the Bowman layer after a clinical e
92 001 to 2009 were searched for a recording of corneal dystrophy on a claim submitted by an ophthalmolo
93 eal dystrophy (FECD), posterior polymorphous corneal dystrophy (PPCD) and congenital hereditary endot
94 tage of patients with posterior polymorphous corneal dystrophy (PPCD) confirms this previously report
96 oinsufficiency causes posterior polymorphous corneal dystrophy (PPCD), in a cohort of late-onset FCD
97 n humans is linked to posterior polymorphous corneal dystrophy (PPCD), in which an epithelial transit
99 ny type of corneal dystrophy, for an overall corneal dystrophy prevalence rate of 897 per million (10
100 e, within and between the different types of corneal dystrophies, raise questions that warrant furthe
101 ulation, these data provide an indication of corneal dystrophy's prevalence within insured subjects a
106 ant UBIAD1 variants associated with Schnyder corneal dystrophy (SCD), a human disorder characterized
107 s, a history of herpetic keratitis, Avellino corneal dystrophy, significant cataract, and uncontrolle
109 IGH3 (TGFbeta1) gene responsible for several corneal dystrophies, there has been an explosion of new
111 omechanical properties of eyes with granular corneal dystrophy undergoing PTK, in an effort to preven
113 st of the reported dystrophies, and granular corneal dystrophy was the least common, being reported i
118 D1) are responsible for Schnyder crystalline corneal dystrophy, which is a genetic disease that cause
119 main is linked to the development of lattice corneal dystrophy with amyloid deposits in the superfici
120 ng keratoplasty for the treatment of macular corneal dystrophy without endothelial involvement were i
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