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M Uyama

Publications and source records attributed to M Uyama.

At least 73 records · Page 4Linked to original sources

[Indocyanine green infrared fluorescence angiography and vascular cast--preparation in experimental choroidal circulatory disturbance].

We performed experiments in 20 monkey eyes in order to clarify basic problems about interpretation of indocyanine green fluorescence angiography (ICG angiography). We severed the temporal group of posterior ciliary arteries to produce choroidal circulatory disturbance. ICG angiography was performed immediately, and 2 days, 4 days, and 2 weeks later. Following each ICG angiography, the eye was studied by plastic vascular cast technique with scanning electron microscopy. Immediately after occlusion, ICG angiography showed filling defect in the temporal choroidal hemisphere during the early phase. In the later phase, this area was gradually filled by the dye from choroidal arteries in the nasal hemisphere and the anterior ciliary arteries. Vascular cast preparations showed filling defect in the temporal choroidal hemisphere, corresponding with the early ICG angiogaphic findings. Both filling delay in ICG angiography and filling defect in vascular casts improved daily after occlusion. Two weeks after occlusion, The area of choroidal infarct temporal to the macula turned into chorioretinal atrophy. This area showed hypofluorescence in the early-phase ICG angiography and filling defect of the choriocapillaris in plastic casts. The early-phase ICG angiographic findings thus corresponded well with observations of vascular casts. We conclude that ICG angiography correctly reflects the actual circulatory disturbances in the choroid.

Animals↗

[Indocyanine green angiography of choroidal neovascularization in age-related macular degeneration].

One hundred forty eyes with choroidal neovascularization (ChNV) in age-related macular degeneration were examined with fluorescein and indocyanine green (ICG) angiography. ChNVs covered with subretinal hemorrhage, and ChNVs with retinal pigment epithelial (RPE) detachment were demonstrated at a higher rate and more clearly with ICG angiography than with fluorescein angiography. On the other hand, ChNVs in serous retinal detachment, and in disciform lesions were demonstrated more clearly with fluorescein angiography than with ICG angiography. These results show that ICG angiography is valuable for delineating "occult ChNVs" with subretinal hemorrhage or RPE detachment in age-related macular degeneration.

Aged↗

FGF receptor 1 expression in experimental choroidal neovascularization.

Fibroblast growth factor (FGF) is an important factor in neovascularization. To clarify the role of FGF, we demonstrated the expression of FGF receptor 1 mRNA in experimentally induced choroidal neovascularization using in situ hybridization. Krypton laser photocoagulation was applied to the posterior retina of colored rats to induce choroidal neovascularization; the eyes were removed at various intervals after photocoagulation. Chorioretinal sections were made, and FGF receptor 1 cDNA fragments were used to make antisense and sense probes for in situ hybridization. In normal chorioretinal tissue, stain indicating FGF receptor 1 mRNA was observed in the ganglion cells and the inner nuclear layer. After photocoagulation, FGF receptor 1 mRNA appeared in the retinal pigment epithelial cells, in melanocytes of the choroid and in the choroidal blood vessel wall of the photocoagulation lesions. This suggests that FGF is involved in the process of neovascularization. Previous studies have reported that the capillary endothelial cells and retinal pigment epithelial cells produce basic FGF in vitro; FGF may affect the cells in an autocrine or paracrine manner.

Animals↗

Gene expressions of basic fibroblast growth factor and its receptor in healing of rat retina after laser photocoagulation.

Basic fibroblast growth factor (bFGF) stimulates the mitogenesis of various cells and plays a key role in wound repair. Using in situ hybridization, we studied mRNA expressions of bFGF and one of its receptors, FGF receptor 1 (FGFR1), during wound repair of the rat retina after laser photocoagulation. Gene expressions of bFGF and FGFR1 were detected in the ganglion cell and inner nuclear layers of the normal adult rat retina. On day 3 following laser photocoagulation, proliferating retinal pigment epithelial (RPE) cells of the lesion showed intense gene expressions of bFGF and FGFR1. Macrophage-like cells that migrated into the lesion also showed gene expression of bFGF. These gene expressions decreased over time. The finding of elevated gene expressions of bFGF and FGFR1 after laser photocoagulation suggests the bFGF may be a factor in retinal wound repair.

Animals↗

Immunohistochemical features of the human retina and retinoblastoma.

The immunohistochemical features of 24 retinoblastoma specimens from 22 patients, 15 with unilateral and 7 with bilateral disease, were examined by the labelled streptavidin biotin (LSAB) method and compared with those of specimens from the remaining morphologically normal retina. In the normal retina, S-100 protein, glial fibrillary acidic protein (GFAP) and vimentin were detected in astrocytes and/or Müller cells. Neurofilament protein was seen in axons of the ganglion cells, synaptophysin was present in both plexiform layers, bcl-2 oncoprotein was seen in ganglion cells and bipolar cells, and neuron-specific enolase (NSE) was detected in ganglion cells, bipolar cells and photoreceptor cells and in their cell processes. While retinoblastoma (Rb) protein expression was noted in ganglion cells, bipolar cells, and some photoreceptor cells, p53 protein was not expressed at all. In all retinoblastomas, strong NSE expression and weak bcl-2 expression was observed in almost all tumour cells and synaptophysin was localized in rosette-forming cells, while tumour cells were devoid of S-100, GFAP, vimentin and neurofilament protein. These findings support the view that retinoblastomas are composed of neuron-committed cells. In addition, no Rb protein expression was detected in retinoblastomas, whereas p53 expression was found in 18 cases (75%).

Child↗

Adrenergic receptor-mediated Cl- transport in rabbit corneal endothelial cells.

Adrenoceptor-mediated Cl- transport in cultured rabbit corneal endothelium was examined using a Cl(-)-sensitive fluorescent dye. The intracellular Cl- concentration ([Cl-]i) in the endothelial cells was estimated to be about 30 mM. Noradrenaline (0.001-0.1 mM) transiently decreased the [Cl-]i in a dose-dependent manner. Such a decrease in [Cl-]i was completely antagonized by pretreatment with the alpha-adrenoceptor antagonist phentolamine (0.1 mM). The selective alpha 2-adrenoceptor agonist UK 14304-18 (5-bromo-6-[(4H,5H-imidazol-2-yl)amino]quinoxaline, 0.1 mM) persistently decreased the [Cl-]i, but neither the alpha 1-adrenoceptor agonist phenylephrine (0.1 mM) nor the beta-adrenoceptor agonist isoproterenol (0.1 mM) had any effect. The alpha 2-adrenoceptor agonist/antagonist yohimbine (0.1 mM) persistently and more strongly decreased the [Cl-]i than UK 14304-18 did. The yohimbine-induced decrease in the [Cl-]i was not further altered by UK 14304-18 or phenylephrine, but partly reversed by noradrenaline, isoproterenol and an adenylate cyclase activator, forskolin (0.1 mM). The yohimbine-induced decrease in [Cl-]i was inhibited by the carbonic anhydrase inhibitor acetazolamide (1 mM), and Cl-/HCO3- exchange inhibitors, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, but not by the H(+)-ATPase inhibitor N,N'-dicylohexylcarbodiimide. The forskolin-induced recovery in [Cl-]i was inhibited by the Na+/K+/Cl- cotransport inhibitor bumetanide (0.1 mM), but not by the Cl- channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Atrial natriuretic peptide stimulates Cl- transport in retinal pigment epithelial cells.

To study the regulatory role of atrial natriuretic peptide (ANP) on the Cl- transport activity of retinal pigment epithelial (RPE) cells, RPE cells from rabbits were cultured and exposed to ANP and other reagents under perfusion. The changes in intracellular Cl- concentration ([Cl-]i) were continuously recorded using a Cl(-)-sensitive fluorescent dye. The cGMP content was estimated by radioimmunoassay. ANP increased the cGMP content and the [Cl-]i in RPE cells. A guanylate cyclase activator, nitric oxide, and a cell permeable cGMP precursor, 8-Br-cGMP, also increased the level of cGMP and the [Cl-]i. A guanylate cyclase inhibitor, LY83583, an inhibitor of cGMP-dependent protein kinase, KT5823, and an inhibitor of Na+/K+/2Cl- cotransporter, bumetanide, diminished or abolished the ANP-induced increase in [Cl-]i. ANP facilitates Cl- accumulation in RPE cells, which is mediated by guanylate cyclase, cGMP-dependent protein kinase, and the Na+/K+/2Cl- cotransporter.

Aminoquinolines↗

[Choroidal neovascularization with indocyanine green infrared fluorescence angiography and vascular cast preparation].

Indocyanine green infrared fluorescence angiography (ICG angiography) was compared with the fluorescein angiography (FAG) to evaluate its benefit. Experimentally induced choroidal neovascularization (ChNV), by laser photocoagulation of monkey eyes was studied by means of cast preparation correlating with findings of ICG angiography. FAG could detect ChNV more clearly than ICG angiography. However, some (2/35 sites) ChNVs with subretinal hemorrhage could be detected only with ICG angiography. In the early phase, the densely distributed part or thick vessels of ChNV could be detected with ICG angiography. On the other hand, the loose part could not be detected. Cast preparation did not show morphologic difference between leaky and non-leaky lesions with ICG angiography. These results showed that ICG angiography could not produce clearer results than FAG. However, ChNVs covered with subretinal hemorrhage could be detected only with ICG angiography. ICG angiography has complementary value in conjunction with FAG in order to detect ChNVs.

Animals↗

[Protective effect of alpha-tocopherol in retinal light damage of pigmented rabbits--evaluation by nitro blue tetrazolium staining].

Free radicals are thought to be one of the causes of retinal light damage. Experiments were performed to identify the production of free radicals in light exposed retinas of rabbits using nitro blue tetrazolium (NBT) staining. In addition, a free radical scavenger, alpha-tocopherol, was administered systemically before light exposure to evaluate the protective effect against the retinal light damage. Pigmented rabbits were exposed to xenon light without long waves for 60 minutes. The eyes were enucleated immediately after light exposure, and incubated in the equilibrated media at 37 degrees C with 0.1 mM NBT solution for 60 minutes. After incubation, the eyes were embedded in paraffin, sectioned, and mounted without further staining. The same procedure was done to the tocopherol treated retinas. In the light exposed eyes, the NBT staining was markedly observed at the inner retina, and the staining was more remarkable than that of the non-exposed eyes. The tocopherol treated eyes showed weaker NBT staining in the inner retina than the non-treated eyes. The results suggest that free radicals are increased in the inner retina by light exposure and alpha-tocopherol suppresses production of free radicals.

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[Occurrence of choroidal neovascularization following photocoagulation treatment for central serous retinopathy].

Occurrence of choroidal neovascularization following laser photocoagulation treatment for central serous retinopathy (CSR) has been reported. We reviewed all the cases of photocoagulation treatment for CSR in our clinic during the past 25 years (1968-1993). Among 1,824 CSR-affected eyes which were treated, choroidal neovascularization occurred in 19 at the site of photocoagulation. In a careful reevaluation of pretreatment fluorescein angiograms, small choroidal neovascularizations were detected in 5 eyes, in which cases the diagnosis of CSR was incorrect. In 3 eyes, choroidal neovascularization was suspected and might have been masked. In the remaining 11 eyes, choroidal neovascularization was not seen. Our survey indicates that, in central serous retinopathy, when the age of the patient is over 50 years, and leakage is weak and parafoveal, choroidal neovascularization may be masked. Laser photocoagulation for these eyes should be conservative with careful, long-term observation.

Adult↗

[Effect of human interferon-beta on reconstruction of the choriocapillaris in monkeys following laser photocoagulation].

We studied the effect of human interferon-beta on reconstruction of the choriocapillaris following laser photocoagulation in monkey eyes. Moderate dye laser photocoagulation caused the occlusion of the choriocapillaris by the intraluminal thrombus in the photocoagulated lesions on the retina. After 3 days, immature endothelial cells began to migrate towards the center from the edge of the lesions. After 7 days capillaries were newly formed, and after 14 days the choriocapillaris in the lesions was almost reconstructed. Systemic administration of interferon-beta after photocoagulation suppressed the reconstruction of the choriocapillaris remarkably. These results suggest that interferon-beta inhibits proliferation and migration of the capillary endothelium on the retina. Interferon-beta may be effective as medication for the treatment of age-related macular degeneration.

Animals↗

[The effect of interferon-beta on experimental choroidal neovascularization].

We studied histologically the effect of systemic administration of human interferon-beta (IFN-beta) on experimental choroidal neovascularization which was caused by intensive laser photocoagulation at the posterior pole of monkey eyes. The regression of choroidal neovascularization was observed in IFN-treated monkeys. Histologically, retinal pigment epithelium (RPE) was remarkably abundant around choroidal neovascularization in the subretinal space, and the activity of neovascularization was weaker in IFN-treated monkeys than in untreated monkeys. These results indicate that IFN-beta promotes the proliferation of RPE and suppresses the activity of endothelial cells of neovascularization to cause regression of choroidal neovascularization. The results suggest that IFN-beta is clinically useful to treat the choroidal neovascularization of age-related macular degeneration.

Animals↗

[Expression of fibroblast growth factor receptor 1 in experimental choroidal neovascularization with in situ hybridization].

Fibroblast growth factor (FGF) is an important factor for neovascularization in vivo. In order to clarify the role of FGF in experimentally produced choroidal neovascularization, we demonstrated mRNA for FGF receptor 1 in situ hybridization. Krypton laser photocoagulation was applied to the posterior retina of colored rats to produce choroidal neovascularization experimentally. These eyes were removed at several different intervals after photocoagulation. Chorioretinal section were used for in situ hybridization. FGF receptor 1 cDNA fragment was used to make antisense and sense probes for in situ hybridization. In normal chorioretinal tissue, staining indicating the existence of FGF receptor 1 mRNA was seen in the ganglion cell layer and inner nuclear layer. After the photocoagulation, the staining was seen in the retinal pigment epithelial cells, melanocytes in the choroid, and choroidal blood vessel wall in the photocoagulated lesions. FGF receptor 1 mRNA was expressed through the development of choroidal neovascularization, and it appears that FGF is necessary for development of choroidal neovascularization. Previous workers showed that the capillary endothelial cells and retinal pigment epithelial cells produce basic FGF in vitro. It seems that FGF effects those cells in an autocrine or paracrine manner in vivo.

Animals↗

[A long-term course of experimentally produced choroidal neovascularization in the rat].

We studied morphologically a long-term course of experimental choroidal neovascularization (ChNV) induced by krypton laser photocoagulation in the rat retina. Fifty-two weeks after photocoagulation, ChNV was enveloped completely by the retinal pigment epithelium. Vascular endothelial cells of ChNV were thin, with many fenestrations and wide lumen. The ChNV maintained the morphological characteristics of mature leaky capillaries similar to choriocapillaris. The lumen of the neovascularizations tended to be compressed by massive collagen fibers produced by the retinal pigmented epithelium. We found that experimental ChNV in the rat retina retains the characteristics of leaky capillaries for a long time unlike that in the monkey ChNV.

Animals↗

[Dye leakage from choroidal neovascularization with indocyanine green angiography].

The ultrastructure of experimentally induced choroidal neovascularization was studied in correlation with dye leakage in indocyanine green (ICG) infrared fluorescence angiography. Newly formed vessels which demonstrated leakage of ICG extended into the subretinal space without enclosure of retinal pigment epithelium (RPE), and the endothelial cells were immature. Choroidal neovascularization which did not demonstrate leakage of ICG was enclosed by RPE without retinal detachment, and the endothelial cells were mature. The newly formed vessels with immature endothelium in the subretinal space that were covered with multiple layers of RPE demonstrated no leakage. These results show that ICG leaks form choroidal neovascularization which has immature vessels that are not enclosed by RPE and that extend into the subretinal space.

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[Effects of interferon-beta on repair of the retinal pigment epithelium after laser photocoagulation].

We studied the morphological effects of human interferon-beta on repair of the retinal pigment epithelium (RPE) after moderate dye laser photocoagulation in monkey eyes. In the control eyes, RPE cells were proliferating towards the center from the margin of the laser burn 3 days after photocoagulation. At day 14 after photocoagulation, a newly formed monolayer of RPE cells covered Burch's membrane to repair the lesion. In the eyes treated with interferon-beta by systemic administration, RPE cells had proliferated remarkably 3 days after photocoagulation. The RPE cells proliferated to form multiple layers on Burch's membrane even at day 14 after photocoagulation. These results suggest that interferon-beta promotes the proliferation to repair damaged RPE.

Animals↗

[Dark rim around choroidal neovascularization in indocyanine green angiography].

Experimentally produced choroidal neovascularization (ChNV) surrounded by a dark rim in indocyanine green (ICG) angiography was studied histopathologically. Dark rims were seen in 28% of ChNVs which were detected with ICG angiography 2 weeks after photocoagulation. During the developing stage of ChNV, the dark rim around it was seen in the early phase of ICG angiography, but in the late phase, the dark rim became unclear because of extravascular dye leakage. During the regressive stage, the dark rim was seen in all phases of angiography. It was especially clear in the late phase. Histopathologically, at the site of the dark rim the retinal pigment epithelial cells proliferated to surround the ChNV in the subretinal space during both stages. These results show that proliferated retinal pigment epithelium surrounding ChNV blocks the fluorescence of the choroid, and causes the dark rim. The dark rim is helpful for diagnosis of ChNV.

Animals↗

Immunohistochemical proof of intraneural localization of herpes simplex virus in experimental retinitis.

A unilateral intravitreal inoculation of herpes simplex virus type 1 (HSV-1) induced bilateral retinitis and encephalitis in the rat. Immunohistochemistry was employed to clarify the pathway of transmission of HSV-1 from the inoculated eye to the contralateral eye, and to identify localization of the viral antigen in the retina, optic nerve and brain. At an early stage of the post-inoculation period, HSV-1 immunoreactivity was first seen in the cytoplasm of Müller cells and then in various cells of the inner nuclear layer in the inoculated eye. At a later stage, HSV-1 immunoreactivity was seen in some retinal ganglion cells and optic nerve fibers in the inoculated eye. In the brain, HSV-1 was found in the optic chiasm, bilateral primary visual centers (bilateral suprachiasmatic nuclei, bilateral lateral geniculate nuclei, bilateral superior colliculus and bilateral pretectum) and bilateral visual cortex. HSV-1 was also demonstrated in the retinal ganglion cells, neural cells in the inner nuclear layer, and Müller cells in the contralateral eye. We found that HSV-1 antigen in the retina of the contralateral eye was transmitted through the optic nerve, visual pathway and nuclei, but not through the blood stream.

Animals↗