13 research outputs found

    Recidive d'une dystrophie de Groenouw de type I apres photokeratectomie therapeutique. Etude en biologie moleculaire du role de l'epithelium corneen. [Early recurrence of Groenouw type I corneal dystrophy after phototherapeutic keratectomy. Molecular biology study suggests epithelial genesis]

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    PURPOSE: Granular corneal dystrophy Groenouw type 1 (GGI) is a rare autosomal dominant disease caused by allelic mutations of the BIGH3 gene. The specific phenotype is characterized by granular opacities (white, sharply demarcated spots resembling bread crumbs) in corneal stroma, which cause recurrent corneal erosions and blurred vision. Phototherapeutic keratectomy (PTK) is an effective procedure that improves visual acuity, but recurrences are unavoidable. Though GGI deposits are well described, their origin is not completely known. The production of mutated keratoepithelin protein (a product of the BIGH3 gene) is the first step necessary for deposits to appear. Molecular biology experiments were conducted to determine the role of corneal cell types in the genesis of early recurrent deposits of post-PTK GGI. METHODS: Tissue specimens from a patient undergoing penetrating keratoplasty for recurrence of GGI (12 months after PTK) and five normal corneas were examined by hybridization in situ and immunohistology to study the expression of BIGH3 and location of keratoepithelin. RESULTS: Only one healthy cornea expressed BIGH3 mainly in the epithelium and less in keratinocytes and endothelial cells. In the GGI corneas, BIGH3 was highly expressed in the modified, hyperplastic epithelium. The keratoepithelin was accumulated under the epithelium where deposits were formed. CONCLUSION: This observation confirms that corneal epithelium is the main producer of mutated keratoepithelin on the cellular scale and thus constitutes the principal source of dystrophic deposit formation during recurrence

    Recidive d'une dystrophie de Groenouw de type I apres photokeratectomie therapeutique. Etude en biologie moleculaire du role de l'epithelium corneen. [Early recurrence of Groenouw type I corneal dystrophy after phototherapeutic keratectomy. Molecular biology study suggests epithelial genesis]

    No full text
    PURPOSE: Granular corneal dystrophy Groenouw type 1 (GGI) is a rare autosomal dominant disease caused by allelic mutations of the BIGH3 gene. The specific phenotype is characterized by granular opacities (white, sharply demarcated spots resembling bread crumbs) in corneal stroma, which cause recurrent corneal erosions and blurred vision. Phototherapeutic keratectomy (PTK) is an effective procedure that improves visual acuity, but recurrences are unavoidable. Though GGI deposits are well described, their origin is not completely known. The production of mutated keratoepithelin protein (a product of the BIGH3 gene) is the first step necessary for deposits to appear. Molecular biology experiments were conducted to determine the role of corneal cell types in the genesis of early recurrent deposits of post-PTK GGI. METHODS: Tissue specimens from a patient undergoing penetrating keratoplasty for recurrence of GGI (12 months after PTK) and five normal corneas were examined by hybridization in situ and immunohistology to study the expression of BIGH3 and location of keratoepithelin. RESULTS: Only one healthy cornea expressed BIGH3 mainly in the epithelium and less in keratinocytes and endothelial cells. In the GGI corneas, BIGH3 was highly expressed in the modified, hyperplastic epithelium. The keratoepithelin was accumulated under the epithelium where deposits were formed. CONCLUSION: This observation confirms that corneal epithelium is the main producer of mutated keratoepithelin on the cellular scale and thus constitutes the principal source of dystrophic deposit formation during recurrence

    Wrist Injuries in Tennis Players: A Narrative Review

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    The wrist/hand complex forms the crucial final link in the kinetic chain between the body and the racquet and therefore has a number of important roles in the production of all tennis strokes. However, the internal and external loads that are created at the wrist during these strokes have the potential to contribute to pain and injury. Therefore, the purposes of this narrative review are to (1) determine the extent of the problem of wrist pain/injury in tennis players, (2) identify bony and soft tissue structures of the wrist that are susceptible to damage as a result of tennis play and (3) explore factors that may influence the development of wrist pain/injury in tennis players. The epidemiological data revealed two important points. First, some evidence suggests wrist pain/injury accounts for a higher percentage of total injuries in more recent studies (2014–2015) than in early studies (1986–1995). Second, the relative frequency of wrist pain/injury compared with other well-recognized problem areas for tennis players such as the shoulder complex, elbow and lumbar spine is noticeably higher in more recent studies (2014–2015) than in early studies (1986–1995), particularly among females. Collectively, this would seem to indicate that the problem of wrist pain/injury has increased in the modern game. In fact, some wrist injuries appear to be related to the use of certain forehand grip types and the predominant use of the two-handed backhand. While the loads experienced at the wrist during tennis stroke production seem to be below threshold levels for a single event, the cumulative effects of these loads through repetition would appear to be an important consideration, especially when inadequate time is allowed to complete normal processes of repair and adaptation. This is supported by the evidence that most wrist injuries in tennis are associated with overuse and a chronic time course. The complex interaction between load, repetition, and training practices in tennis, particularly among young developing players who choose a path of early specialization, needs to be further explored
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