[Blockage of axoplasmic transport at the optic nerve head of normal albino rabbits (author's transl)].
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Biomedical subjects
Publications and source records attributed to E Chihara.
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Three patients with herpes zoster ophthalmicus were treated with an oral administration of colchicine and corticosteroid, while another seven were given systemic corticosteroid, vitamins, and sedatives. Colchicine inhibited the formation of new skin lesions but did not suppress the already grown vesicles. The effect of colchicine was attributed to a blockage of intra-axonal dissemination by neurotrophic virus.
3 early Mooren's ulcers were successfully treated by only one-time conjunctival excision adjacent to the ulcer, while in 2 other chronic vascularized Mooren's ulcers, repeated conjunctival excision was required for a final remission. The clinical outcome of these 5 eyes was better than that of 7 other eyes treated by conjunctival flap procedure, lamellar keratoplasty, topical eye drops or systemic medications. Four fragments of excised conjunctival tissue were examined histopathologically; the substantia propria was found to be infiltrated with plasma cells.
Distribution of nonaxoplasmically transported material along the optic pathway of the rabbit was studied after blockage of the axonal flow by vinblastine, and a clear pattern of distribution of the axoplasmic transport was deduced by subtraction from the pattern seen in nontreated animals. Vascular participation in the nonaxoplasmic transport was certified by autoradiographic studies. The theoretical pattern of distribution of axoplasmic transport in the optic system under ideal conditions was calculated from an idealized model system. From the comparison of theoretical and experimental patterns, partial obstruction of the axonal flow likely occurs at the optic foramen and chiasma.
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PURPOSE: To describe a new mutation of the trabecular meshwork-inducible glucocorticoid response protein (TIGR) gene in a Japanese patient with familial primary open angle glaucoma (POAG). METHODS: Standard ocular examinations were performed on the 44-year-old patient, his sister, and mother. DNA sequencing was used to identify the mutation. We also developed a DNA diagnostic method for detecting this missense mutation by polymerase chain reaction-induced mutation restriction analysis (PCR-IMRA). RESULTS: The patient, father, and sister had been diagnosed as having POAG. The patient and his sister had a Thr448Pro mutation (C-->A transition at the nucleotide number 1419) in exon 3. This mutation has not been reported before. CONCLUSIONS: Gene analysis is promising for an early diagnosis among the family members of familial POAG patients and will contribute to early therapy before an occurrence of irreversible visual impairment.
The retinas of 3 patients with typical retinitis pigmentosa (RP) were evaluated by optical coherence tomography (OCT), fluorescein angiography (FA), and fundus photography (FP). OCT showed that retinal thickness was decreased in the areas of the retina affected by RP, and nearly normal in the unaffected macular area. Reflectivity was partially decreased in the affected retinal areas and pigment masses were hyper-reflective. Reflectivity of the macular area was nearly normal except in the fovea, where it was decreased because of edema. Cystic spaces of the fovea were evident in Patient 1.