Publications by authors named "M Wolter-Roessler"

Background: A prospective study was carried out to evaluate postoperative visual acuity and patients satisfaction after implantation of a multifocal add-on IOL.

Patients And Methods: In 50 eyes of 25 patients operated by two surgeons "group A (MK) = 15 patients; group B (MWR) = 10 patients" with age-related cataract after "normal" cataract surgery, sulcus-fixated multifocal add-on IOLs (MS 714 PB Diff., Dr.

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Background: We report the results of the secondary implantation of retroiridally fixated irisclaw-lenses (Artisan(R)) to correct aphakia.

Patients And Methods: This retrospective study included all eyes that had undergone outpatient implantation of an Artisan IOL by the senior author (MK) between July 2004 and January 2008. We analysed 48 eyes of 46 patients (27 female, 19 male) aged 17 to 87 years.

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Background: To report the clinical, histopathological and immunohistochemical findings of two novel mutations within the TGFBI gene.

Methods: The genotype of 41 affected members of 16 families and nine sporadic cases was investigated by direct sequencing of the TGFBI gene. Clinical, histological and immunohistochemical characteristics of corneal opacification were reported and compared with the coding region changes in the TGFBI gene.

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Purpose: Different missense mutations in the TGFBI gene cause granular (Groenouw CDGG1, Avellino CDA, Reis-Bücklers CDB1) and lattice (Type I; Biber-Haab-Dimmer; CDL1) corneal dystrophies and, in some reports, corneal dystrophy Thiel-Behnke (CDB2). We report on the mutation spectrum and the genotype-phenotype correlations on the basis of clinical and histopathological examinations of 13 German families with TGFBI-linked corneal dystrophies.

Methods: In 31 patients with different corneal dystrophies, DNA was extracted from leukocytes of the peripheral blood and mutation analysis was performed by direct sequencing of the TGFBI gene.

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Background: Mutations of the BIGH3 gene were delineated as the underlying gene defect for corneal dystrophy Lattice Type I (CDL1) and corneal dystrophy Avellino type (CDA) in families with different regional provenance. Missense mutations in exon 4 with single base pair substitution which result in amino acid alterations Arg124Cys (CDL1) and ARG124His are described as hot spots. We report on histopathological and molecular genetic investigations in 2 German families and a single patient with CDL1 and CDA.

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