Biomedical subjects

S Okisaka

Publications and source records attributed to S Okisaka.

At least 19 recordsLinked to original sources

PubMed2001

[A case of fundus albipunctatus with a retinol dehydrogenase 5 gene mutation in a child].

BACKGROUND: We examined a family with fundus albipunctatus in which mutation of the retinol dehydrogenase 5(RDH 5) gene was suspected to be the cause of this disease. CASE: An 8-year-old girl had diffuse multiple white dots in her fundus except for the macula. She had good central vision. The amplitude of her electroretinogram wave was low, but it recovered after three hours of dark adaptation. Dark adaptometry showed an elevated threshold for rod adaptation. No visual field loss was observed. A homozygous missense mutation was found in exon 5 of the RDH 5 gene that substituted histidine for arginine at codon 280(Arg 280 His). Her mother had a normal fundus but was heterozygous for the same mutation. CONCLUSION: A missense mutation of RDH 5(Arg 280 His) was found in a Japanese family with fundus albipunctatus.

Alcohol Oxidoreductases↗

PubMed2000

The Contribution of Inflammatory Cell Infiltration to Conjunctival Inclusion Cyst Formation.

Purpose: The incidence of inclusion cysts was examined histopathologically in conjunctival disorders where inflammatory cell infiltration was seen in the subepithelial connective tissue.Method: The incidence of inclusion cysts was examined histopathologically in pterygium, vernal conjunctivitis, pyogenic granuloma and pingueculitis. The specimens of pinguecula were used as control.Results: Inclusion cysts were recognized in 5/(55) cases of pterygium, 2/(12) cases of vernal conjunctivitis, 1/(4) cases of pyogenic granuloma, and 1/(2) cases of pingueculitis. On the other hand no inclusion cyst was recognized in 20 cases of pinguecula in which no inflammatory cell infiltration was seen.Conclusions: Inflammatory cell infiltration may contribute to the formation of conjunctival inclusion cysts in pterygium, pingueculitis, vernal conjunctivitis and pyogenic granuloma.

Journal Article↗

PubMed2000

Purification and characterization of bovine cone arrestin (cArr).

To elucidate the quenching mechanism of phototransduction in vertebrate cone photoreceptors, a cDNA clone encoding cone specific arrestin (cArr) was isolated from a bovine retinal cDNA library using a human cArr cDNA probe. Affinity-purified anti-peptide antibody specific to cArr was prepared. Immunohistochemical staining displayed specific labeling of cArr in cone photoreceptors and immunoblotting identified a 46 kDa protein band. We purified cArr from bovine retinas by sequential column chromatography using DEAE-cellulose, gel filtration and mono Q columns. Binding studies revealed no binding of cArr to rhodopsin regardless of whether it was bleached and/or phosphorylated. cArr also failed to bind to heparin-Sepharose under conditions which rod arrestin (rArr) bound to the column. The present data suggest that cArr may play a role in the quenching of phototransduction in cone photoreceptors and that its activity therein is different to that of rArr.

Amino Acid Sequence↗

PubMed2000

Kerato-epithelin mutation (R 555 Q) in a case of reis-Bucklers corneal dystrophy

Background: Mutations in the kerato-epithelin gene on chromosome 5 q 31 are known to cause four distinct autosomal dominant diseases of the human cornea: Reis-Bucklers, granular, lattice, and Avellino corneal dystrophy. Mutation of arginin to glutamine in codon 555 (R 555 Q) in kerato-epithelin was recently reported in four blood-related patients with Reis-Bucklers corneal dystrophy.Case: A 42-year-old female has had photophobia with decreasing vison since the age of 20 years. Her corrected visual acuity was 0.5 in both eyes. She showed subepithelial opacities in both corneas characteristic of Reis-Bucklers corneal dystrophy.Method: The DNA was extracted from leukocytes according to standard protocols. The keratoepithelin gene was examined for a mutation by the polymerase chain reaction and direct sequencing.Findings: We identified kerato-epithelin mutation R 555 Q. The patient's two children and 50 controls did not show missense mutation.Conclusion: Kerato-epithelin mutation R 555 Q was present in a Japanese patient with Reis-Bucklers corneal dystrophy.

Journal Article↗

PubMed2000

[The contribution of inflammatory cell infiltration to conjunctival inclusion cyst formation].

PURPOSE: The incidence of inclusion cysts was examined histopathologically in conjunctival disorders where inflammatory cell infiltration was seen in the subepithelial connective tissue. METHOD: The incidence of inclusion cysts was examined histopathologically in pterygium, vernal conjunctivitis, pyogenic granuloma and pingueculitis. The specimens of pinguecula were used as control. RESULTS: Inclusion cysts were recognized in 5/55 cases of pterygium, 2/12 cases of vernal conjunctivitis, 1/4 cases of pyogenic granuloma, and 1/2 cases of pingueculitis. On the other hand no inclusion cyst was recognized in 20 cases of pinguecula in which no inflammatory cell infiltration was seen. CONCLUSIONS: Inflammatory cell infiltration may contribute to the formation of conjunctival inclusion cysts in pterygium, pingueculitis, vernal conjunctivitis and pyogenic granuloma.

Aged↗

PubMed1999

Effects of fluorescent light on growth of bovine retinal pigment epithelial cells in vitro incubated with linoleic acid or linoleic acid hydroperoxide.

Light-induced peroxidation of polyunsaturated fatty acids (PUFA) may generate lipid hydroperoxides, which may have toxic effects on retinal pigment epithelial (RPE) cells in vitro. We investigated the effects of cool-white fluorescent light on the RPE cells incubated with linoleic acids (LA) or linoleic acid hydroperoxides (LHP) and the influence of antioxidative enzymes. We measured the bovine RPE cell number after exposure to fluorescent light (610 and 1,200 lux) in the presence of LA or LHP. Furthermore, the effects of superoxide dismutase (SOD) and catalase on LA- or LHP-treated RPE cells were also examined. Both LA and LHP treatment increased RPE cell number under weak illumination (610 lux), but dose-dependently decreased the number of cells exposed to strong illumination (1,200 lux). With exposure to strong illumination, LA caused a greater reduction in RPE cell number than LHP. Multiple linear regression analysis showed that the number of RPE cells was significantly decreased in a manner dependent on the interactions of the illuminance of light and the concentrations of LA or LHP. The antioxidative enzymes significantly ameliorated the damage to RPE cells from LA or LHP and exposure to light. Therefore, the exposure to fluorescent light augmented the cytotoxic effects of LA and LHP on RPE cells, and this effect is likely to be mediated by reactive oxygen species.

Animals↗

PubMed1999

The localization of glutathione peroxidase in the photoreceptor cells and the retinal pigment epithelial cells of Wistar and Royal College of Surgeons dystrophic rats.

INTRODUCTION: If degenerating photoreceptor outer segments not phagocytized by RPE cells in the retina of Royal College Surgeons (RCS) rats were to undergo peroxidation, the distribution of glutathione peroxidase (GSH-PO) in the mitochondria or cytoplasm of the retina might be altered. We evaluated the immunocytochemical localization of GSH-PO to identify subcellular organelles in sections of the retinas of RCS rats. METHODS: Immunoblot analysis confirmed the presence of GSH-PO molecules in the retinas of RCS and Wistar rats aged 3 weeks. Sections were reacted with the F(ab) fragment of anti-rat alphaGSH-PO and then examined by laser scanning microscopy (LSM) and transmission electron microscopy (TEM). RESULTS: The size of the GSH-PO molecule in the retina was about 21 KD in the mitochondria and 23 KD in the cytosol in both strains of rats. LSM revealed fluorescent granules in the photoreceptor inner segments of the Wistar rats, and immunohistochemical TEM revealed GSH-PO in the mitochondria of their photoreceptor inner segments and retinal pigment epithelial (RPE) cells. In the RCS rats, the degenerating photoreceptor outer segments were clearly seen to be positive for anti-GSH-PO by conventional light microscopy (CLM). However, the photoreceptor inner segments of the RCS rats were negative for staining with anti-GSH-PO by LSM, and no GSH-PO could be detected in the mitochondria of the photoreceptor inner segments or RPE cells by immuno-TEM. CONCLUSION: Degeneration of the photoreceptor outer segments induced mitochondrial damage in the photoreceptor inner segments, and as a result GSH-PO shifted from the photoreceptor inner segments to the degenerating outer segments.

Animals↗

PubMed1999

[Histopathological observations on bullous keratopathy after argon-laser iridotomy].

PURPOSE: To elucidate histopathological mechanism of bullous keratopathy after argon-laser iridotomy (ALI). CASE AND METHOD: The patient was a 60-year-old female who underwent penetrating keratoplasty because of bullous keratopathy after 2 years and 2 months of ALI. The corneal specimen was fixed with a mixture of 2.5% formalin and 1.0% glutaraldehyde, and examined under light and electron microscopes. FINDING AND CONCLUSION: Laser-damaged endothelium produced a large amount of basement membrane-like material beneath Descemet's membrane. At the next stage, the severely damaged endothelium lost its organellae and cell membranes, and fell off. The surrounding healthy endothelium migrated into the damaged area and produced a small amount of material like basement membrane which covered Descemet's membrane. After that, stromal swelling, decrease of keratocytes, breaking and disappearance of Bowman's membrane, epithelial edema, connective tissue accumulation beneath basal cells, and epithelial detachment occurred in the laser-damaged area.

Corneal Diseases↗

PubMed1999

[Kerato-epithelin mutation (R 555 Q) in a case of Reis-Bücklers corneal dystrophy].

BACKGROUND: Mutations in the kerato-epithelin gene on chromosome 5 q 31 are known to cause four distinct autosomal dominant diseases of the human cornea: Reis-Bücklers, granular, lattice, and Avellino corneal dystrophy. Mutation of arginin to glutamine in codon 555 (R 555 Q) in kerato-epithelin was recently reported in four blood-related patients with Reis-Bücklers corneal dystrophy. CASE: A 42 year-old female has had photophobia with decreasing vision since the age of 20 years. Her corrected visual acuity was 0.5 in both eyes. She showed subepithelial opacities in both corneas characteristic of Reis-Bücklers corneal dystrophy. METHOD: The DNA was extracted from leukocytes according to standard protocols. The keratoepithelin gene was examined for a mutation by the polymerase chain reaction (PCR) and direct sequencing. FINDINGS: We identified kerato-epithelin mutation R 555 Q. The patient's two children and 50 controls did not show missense mutation. CONCLUSION: Kerato-epithelin mutation R 555 Q was present in a Japanese patient with Reis-Bücklers corneal dystrophy.

Adult↗

PubMed1998

Visual function in retinitis pigmentosa related to a codon 15 rhodopsin gene mutation.

To determine the phenotype of a Japanese family in which retinitis pigmentosa cosegregates with a rhodopsin gene mutation, i.e. an asparagine-to-serine change at codon 15 (Asn-15-Ser), 5 affected and 5 unaffected members of one pedigree underwent several ophthalmic examinations as well as Ganzfeld electroretinography (ERG) and multifocal ERG. Genomic DNA samples were analyzed by PCR amplification, sequencing and restriction enzyme digestion. A codon 15 rhodopsin gene mutation (Asn-15-Ser) was found in all affected members. The region of pigmentary degeneration was localized in the lower hemiretina, and visual field defects corresponded to the retinal pigmentary changes. Scotopic ERG amplitudes, rather than photopic ERG amplitudes, were reduced. Multifocal ERG revealed a low magnitude of response density, even for the upper hemiretina, which showed no bony corpuscle pigmentation. Visual function in sectorial retinitis pigmentosa associated with rhodopsin gene codon 15 mutation is on the basis of the rod-cone dystrophy, regardless of differences in phenotypic expression.

Adult↗

PubMed1998

Progression of visual field loss in patients with retinitis pigmentosa of sporadic and autosomal recessive types.

PURPOSE: We examined the natural course of patients with retinitis pigmentosa of the eight sporadic and five autosomal recessive forms over 5 years. METHODS: We measured the areas of the visual fields by Goldmann perimetry using a digitizer and a computer software. RESULTS: The visual field of V-4 isopters in 4 sporadic cases was approximately 200 cm2 during 30 years after the initial examination, but decreased down to 40 cm2 in the next 10 years. The visual field was reduced to half the normal field in 3 autosomal recessive cases early below the age of 25 years. In 4 sporadic and 2 autosomal recessive cases, the inferior temporal visual field was the widest at the onset of the disease, but exhibited the most severe loss. The superior nasal area was the narrowest initially, and showed the mildest progression. CONCLUSIONS: The visual field in retinitis pigmentosa is constricted age-dependently with severe loss of the inferior temporal visual area and mild damage to the superior nasal area.

Adolescent↗

PubMed1998

Pattern electroretinogram elicited by a dartboard pattern.

The receptive field size of retinal ganglion cells is closely related to their eccentricity from the fovea. To elicit larger pattern-reversal electroretinograms (P-ERGs), it may be useful to stimulate the retina with patterns having elements that parallel this change in receptive field size. We describe a dartboard pattern consisting of reversal elements that enlarge gradually from the central to the peripheral stimulus field. The utility of the dartboard pattern for eliciting P-ERG was investigated by comparing it with the conventional uniform checkerboard pattern, but with the other stimulus parameters remaining unchanged (96% contrast, 35.9 cd/m2 mean luminance, 3.3 rev/s temporal frequency, 15 degrees circular field). The dartboard pattern produced a significantly larger P50 amplitude than did the checkerboard pattern, while no difference in peak latency was found when 54 min of arc was used as a standard check size for the checkerboard pattern. The dartboard pattern for eliciting P-ERG should prove clinically useful.

Adult↗

PubMed1998

Automatic static threshold perimetry is useful for estimating the effects of laser photocoagulation on diabetic maculopathy.

Focal photocoagulation was performed on 18 eyes in 18 diabetes patients; a visual acuity test, fluorescein angiography and automated static threshold perimetry by Octopus automated static perimetry (program 31) were conducted before and 1, 3 and 6 months after krypton laser photocoagulation. Central field sensitivity and total loss were measured by automated static threshold perimetry. Group A (13 eyes) had a total loss of less than 150 dB. In these subjects, mild fluorescein leakage was detected within the area of the vascular arcade. In group B (5 eyes) with a total loss of greater than 150 dB, diffuse fluorescein leakage was also detected outside the vascular arcade. The central field sensitivity was reduced in 2 eyes of group B. The total loss worsened in 8 eyes of group A (61.5%) and 5 eyes of group B (100%). Inspection of photographs gave the impression that the degree of fluorescein leakage and the area of the avascular zone on fluorescein angiography accorded with total loss, thus suggesting that total loss reflects visual functions better than visual acuity or central field sensitivity. Therefore, automated static threshold perimetry appears to be a useful method for estimating visual functions after photocoagulation in diabetic maculopathy patients.

Adult↗

PubMed1998

Visual function and gene analysis in a family with Oguchi's disease.

A family with 1 case of retinitis pigmentosa (III-1) and 2 cases of Oguchi's disease (III-2, 3) was examined in terms of electrophysiology as well as molecular biology. The proband (III-3), a 42-year-old female, and 2 older brothers (III-1, 2, aged 52 and 45 years) and 2 unaffected members in the same family participated in this study. Corrected visual acuities of the individuals with Oguchi's disease (III-2, 3) were 1.2. On funduscopy, blood vessels stood out in relief against a metallic-appearing background and a Mizuo-Nakamura phenomenon was evident. Full-field electroretinograms (ERGs) recorded from the proband were indicative of rod dystrophy, but results of other electrophysiological examinations (multifocal ERG, pattern ERG and visual-evoked cortical potential recordings) were within normal limits. Patient III-1 had corrected visual acuities of RE 20 cm/m.m. and LE 30 cm/n.d., severe chorioretinal atrophy in both fundi, and full-field ERG revealed rod-cone dystrophy. Mutation of the arrestin gene (1147de1A) was detected in all 3 patients. Visual function in each patient coincides with that of retinitis pigmentosa or Oguchi's disease, respectively.

Adult↗

PubMed1998

[Effect of ultraviolet-filtering contact lens on rabbit eyes after exposure to ultraviolet light].

We evaluated the protective effect of a newly designed soft contact lens (SCL) on rabbit eyes. This SCL absorbs the ultraviolet B light of wavelengths between 280 nm and 320 nm. Three weeks after resecting the nictitating membrane, the rabbit corneas were covered either by the new SCL or a conventional SCL. The eyes were exposed to ultraviolet light from two 15 W lamps placed 20 cm anteriorly for 3 hours. Another three hours after the exposure, the cornea was examined first with a slitlamp biomicroscope after staining with fluorescein and then by histopathological means after enucleation. Six eyes wearing the new SCL showed moderate superficial punctate keratopathy. Six eyes wearing conventional SCL showed severe superficial keratopathy or corneal erosion. These findings were in good agreement with the histopathological findings. The new ultraviolet-filtering SCL was thus effective in protecting the rabbit cornea under our experimental conditions.

Animals↗

PubMed1998

[Pterygium and mast cells--expression of basic fibroblast growth factor increase in mast cells of the pterygium].

We examined the expression of basic fibroblast growth factor (bFGF) protein immunohistochemically, and bFGF specific messenger RNA (bFGF-mRNA) by in situ hybridization in the excised tissue of 5 cases of pterygium and 4 cases of normal conjunctiva. Immunohistochemical staining for bFGF showed strong positive staining in metachromatic mast cells stained with toluidine blue in the pterygium and in normal conjunctival specimens. The mean metachromatic mast cell count in pterygium specimens was increased significantly when compared with normal conjunctiva. In mast cells, bFGF positive rate was 84% in pterygium specimens, and 69% in normal conjunctival specimens. In situ hybridization indicated that the bFGFmRNA is located in most mast cells in pterygium specimens, but in only a few mast cells in normal conjunctival specimens. These results suggest that increased bFGF protein produced and stored by mast cells in the pterygium may contribute to its progression.

Female↗

PubMed1998

[Detection of parafoveal scotoma by multifocal electroretinograms].

We investigated the relation between multifocal electroretinograms (M-ERGs) and artificial parafoveal scotoma. M-ERGs were recorded from normal subjects using a circular piece of black paper attached to a monitor. Lower response density around the 10 to 15 degree parafovea region was not observed up to 3 degree scotoma (visual angle), but was detected above 5 degree scotoma in field topography of M-ERGs. The shape of the scotoma in field topography was not circular but somewhat oval. The results from two cases of parafoveal retinal degeneration were in good accordance with this basic study in normal subjects. We proved that detection of parafoveal scotoma by M-ERG is limited in comparison with the results obtained by automated static perimetry.

Electroretinography↗

PubMed1998

[Neuronal cell death mechanism in glaucomatous optic neuropathy].

Apoptosis of retinal ganglion cells has been observed in experimental glaucomatous models and human glaucomatous eyes in recent pathological studies. It seems that retinal ganglion cells in glaucomatous optic neuropathy die by a process similar to programmed cell death. Deprivation of neurotrophic factors, ischemia, chronic elevation of glutamate, and disorganized NO metabolism are suspected to be factors affecting neuronal loss in glaucoma, and most of these factors are known to activate the mechanism of cellular suicidal death. One of the common switches for the death mechanism seems to be in the mitochondria and to be controlled by Bcl-2 family proteins. A major goal of neuronal cell death research in glaucomatous neuropathy is to identify its molecular components and mechanisms of regulation. This information will lead to therapeutic agents that can modulate the cell death process in the treatment of glaucomatous neuropathy.

Animals↗