A Pathological Study on Rabbit Corneas after Laser In Situ Keratomileusis

A Pathological Study on Rabbit Corneas after Laser In Situ Keratomileusis

ABSTRACTS Abstracts of Published Articles in Nippon Ganka Gakkai Zasshi (Journal of the Japanese Ophthalmological Society) Clinical and Genetic Feat...

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ABSTRACTS

Abstracts of Published Articles in Nippon Ganka Gakkai Zasshi (Journal of the Japanese Ophthalmological Society)

Clinical and Genetic Features of Choroideremia Background: Choroideremia is an X-linked hereditary eye disease that causes progressive degeneration of the choroid and retina and frequently leads to legal blindness in later life. Recent molecular genetic studies have revealed mutations involving the Rab escort protein (REP-1) gene localized at Xq 21. Clinical Features: The clinical picture and rate of progression may vary among affected individuals in different families and within the same family. Usually, hemizygous males develop night blindness in their teenage years, followed by progressive peripheral visual field constriction and visual disability in late age. Heterozygous female carriers are mostly asymptomatic, but their fundi show characteristic pigment changes in the midperiphery closely resembling the fine mottling observed in the initial stage of the disease in males. Molecular Genetics: Assessment of the REP-1 gene in European and Japanese choroideremia patients has revealed a wide variety of mutations, including gross deletions and point mutations such as nonsense, frameshift, and splice-site mutations. All these mutations are thought to fail in intact REP-1 protein synthesis. Conclusions: The recent molecular studies may open a new chapter in the research on choroideremia as well as diagnosis and genetic counseling. (J Jpn Ophthalmol Soc 103:773–781, 1999) Norio Ohba* and Yasushi Isashiki† *Department of Ophthalmology, Kagoshima University Faculty of Medicine †Center for Chronic Viral Diseases, Kagoshima University Faculty of Medicine PII S0021-5155(00)00153-2

A Pathological Study on Rabbit Corneas after Laser In Situ Keratomileusis Purpose: To investigate pathological changes in rabbit corneas after laser in situ keratomileusis (LASIK). Jpn J Ophthalmol 44, 317–324 (2000) © 2000 Japanese Ophthalmological Society Published by Elsevier Science Inc.

Materials and Methods: We performed LASIK on rabbit corneas to theoretically correct 10.0 diopters of myopia. The corneas were studied pathologically at day 0, and 3 days, 1 week, 3 weeks, 4 months, and 9 months after LASIK. Results: At 3 days after LASIK, keratocytes in the ablated area changed morphologically into fibroblastic cells. And the structure of collagen fibers in the stroma was broken. These changes had disappeared almost entirely at 4 months after LASIK. There were no proliferative changes in the stroma of the ablated cornea 9 months after LASIK. No significant changes were observed in the endothelium. Conclusions: The damage to rabbit corneas induced by LASIK was mild to moderate under the present experimental conditions. (J Jpn Ophthalmol Soc 103: 782–789, 1999) Yuji Hosoda and Kiyoo Nakayasu Department of Ophthalmology, Juntendo University School of Medicine PII S0021-5155(00)00154-4

Genome Analysis of Adenovirus Type 7 and Adenovirus Type 11 Purpose: To study the epidemiology of adenovirus type 7 (Ad 7) conjunctivitis and adenovirus type 11 (Ad 11) conjunctivitis by determining genome types and subgenomic types. Materials and Methods: For Ad 7 I used twelve strains from patients with acute viral conjunctivitis and one strain from a patient with pneumonia. For Ad 11 I used seventeen strains from patients with cystitis. For Ad 7 genome typing, I used eleven DNA restriction endonucleases (REs) recognizing 6- or 7-base pair sequences and for Ad 11 genome typing, I used seven. For Ad 7 and for Ad 11 subgenome typing, I used Taq 1 and Hinf I which recognize 4- or 5-base pair sequences. Results: The thirteen Ad 7 strains all belonged to the same genome type and subgenome type. Ad 11 strains showed six genome types. Ad 11 p was the

0021-5155/00/$–see front matter