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Biomedical subjects

M Uyama

Publications and source records attributed to M Uyama.

At least 19 recordsLinked to original sources

Ciliochoroidal Detachment Following Scleral Buckling Surgery for Rhegmatogenous Retinal Detachment.

Purpose and Methods: We observed the peripheral choroid, ciliary body, and depth of the anterior chamber by ultrasound biomicroscopy (UBM) in 31 eyes with rhegmatogenous retinal detachment before and after scleral buckling surgery. Scleral encircling was performed in 11 eyes and segmental scleral buckling in 20 eyes.Results: With UBM, ciliochoroidal detachment was detected in all eyes (100%) following scleral encircling and in 8 eyes (40.0%) following segmental scleral buckling. After scleral encircling procedure, the eyes with preoperatively bullous and wide retinal detachment showed a severe ciliochoroidal detachment and edema of the ciliary body. Shallowing of the anterior camber occurred in all 11 eyes (100%) after scleral encircling and in 12 of 20 eyes (60.0%) after segmental scleral buckling. Marked shallowing with closure of the angle and elevated intraocular pressure occurred in 2 eyes.Conclusion: The results showed that careful postoperative examinations for the anterior segments, chamber angle, and intraocular pressure are necessary with slit-lamp examination and applanation tonometry after scleral buckling surgery.

Journal Article↗

Heterogeneity in ornithine cytotoxicity of bovine retinal pigment epithelial cells in primary culture.

Gyrate atrophy of the choroid and retina is a chorioretinal degeneration caused by hyperornithinemia and a deficiency of ornithine-delta-aminotransferase (OAT). We recently showed that ornithine exhibits cytotoxicity to human retinal pigment epithelial (RPE) cell lines treated with the OAT inhibitor, 5-fluoromethylornithine (5-FMOrn), and suggested that this system may be an in vitro model of gyrate atrophy. In the present study, in order to apply this system to primary cultured RPE cells, we freshly prepared RPE cells from bovine eyes and studied the effect of ornithine on cell damage. Two phenotypes, epithelioid and fusiform, which coexisted in the primary culture and epithelioid phenotype cells, but not fusiform ones, were severely damaged and partially detached from the substrate by 10 m m ornithine and 0.5 m m 5-FMOrn. Neither ornithine nor 5-FMOrn alone exhibited such cytotoxicity to both phenotypes of RPE cells. Proline significantly prevented the ornithine-induced cytotoxicity. Epithelioid and fusiform phenotypes isolated from the primary culture showed different distribution of actin filaments. A combination of ornithine and 5-FMOrn time-dependently inhibited [(3)H]thymidine incorporation in the epithelioid, but not fusiform, cells. Proline prevented the inhibition of [(3)H]thymidine incorporation by ornithine in 5-FMOrn-treated epithelioid cells. Furthermore, l -azetidine-2-carboxylic acid, a collagen synthesis inhibitor, reduced [(3)H]thymidine incorporation in epithelioid, but not fusiform, cells, which was reversed by proline. These results demonstrate that the epithelioid phenotype of bovine RPE cells becomes susceptible to ornithine following inactivation of OAT. The phenotypic cells and its prevention by proline may provide insight into biochemical triggers that induce gyrate atrophy.

Animals↗

Histopathological findings of X-linked retinoschisis with neovascular glaucoma.

BACKGROUND: X-linked retinoschisis (XLRS) is rarely complicated by neovascular glaucoma. Only a few reports of XLRS histopathological findings with neovascular glaucoma have been published. METHODS: A 41-year-old man with XLRS complicated by neovascular glaucoma in his left eye was examined with electroretinography, B-scan, ultrasound biomicroscopy and computed tomography. He was examined by ophthalmoscopy and fluorescein angiography in the other eye. An enucleation was performed in his left eye due to uncontrollable high intraocular pressure and persistent ocular pain. We examined the enucleated eye histopathologically. RESULTS: Examination of the enucleated eye showed nuclear sclerosis of the lens, pigmented retrolental membrane and retinoschisis which separated the inner layer of the retina and made a large space in the vitreous cavity without any apparent detachment of the outer layers of the retina. Sclerotic vessels were present histopathologically in both the inner and outer layers of the retina. There was a peripheral anterior synechia, ectropion uveae and a fibrovascular membrane, which contained many lumina of neovascularization, indicating marked rubeosis iridis. Small cystic spaces were observed in both the schitic retina in the peripheral region and the foveal schisis at the outer layer of the retina. The photoreceptor cells had become markedly atrophied and multiple regions of calcification were observed. The optic nerve showed severe atrophy with gliosis, but the central retinal artery and vein were still open within the nerve. CONCLUSIONS: These histopathological findings suggest that rubeosis iridis may have developed secondarily to retinal ischemia due to occlusion of the retinal blood vessels.

Adult↗

In vivo gene transfer into choroidal neovascularization by the HVJ liposome method.

PURPOSE: To evaluate the efficacy of the HVJ liposome method for gene transfer in rats with experimentally induced choroidal neovascularization. METHODS: Plasmid DNA containing the LacZ reporter gene, or fluorescein isothiocyanate (FITC)-labeled double-stranded phosphorothioate oligodeoxynucleotides (S-ODNs), was encapsulated in liposomes. The liposomes were coated with the envelope of inactivated hemagglutinating virus of Japan (HVJ). Intense laser burns were applied to the posterior pole of the retina of pigmented rats to induce choroidal neovascularization. Following photocoagulation, HVJ liposome suspension was injected into the vitreous. On days 3, 7, 14, and 28 after injection, the eyes were removed and fixed. The eyes injected with LacZ gene were reacted with X-gal, frozen, and cut into thin sections. The sections were examined for the expression of the LacZ gene by light microscopy. The enucleated eyes injected with double-stranded S-ODNs were frozen, cut into thin sections, and examined a confocal scanning laser microscope for FITC labeling. Eyes without injection of HVJ liposomes served as controls. RESULTS: Expression of LacZ genes (beta-galactosidase activity), or localization of FITC labeling, was observed mainly in the laser-induced choroidal neovascular tissue from 3 to 28 days after the intravitreal injection of HVJ liposome. CONCLUSIONS: We conclude that the HVJ liposome method achieved effective gene transfer into choroidal neovascular tissue. Thus, this method can be used as a nonviral gene therapy system for the treatment of choroidal neovascularization in vivo.

Animals↗

Uveal effusion syndrome: clinical features, surgical treatment, histologic examination of the sclera, and pathophysiology.

PURPOSE: To clarify clinical features and pathophysiology and to evaluate surgical outcome of subscleral sclerectomy for primary uveal effusion syndrome. DESIGN: Prospective, consecutive noncomparative case series. PARTICIPANTS: Nineteen eyes of 16 patients diagnosed with uveal effusion syndrome treated in our clinic between 1989 and 1998. METHODS: Patients were examined by routine ophthalmologic examinations, fluorescein and indocyanine green angiography; measurement of the axial length of the eyeball; magnetic resonance imaging; and echography. Subscleral sclerectomy (sclerectomy under the scleral flap) was performed at the equator on all patients. Histologic examination of excised sclera was carried out on all samples. Patients were followed for outcome over time. MAIN OUTCOME MEASURES: Reattachment of the choroid and retina with resolution of the serous fluid. RESULTS: Three subgroups were identified: In type 1, nanophthalmic eye; the eyeball is small (average axial length 16 mm) and high hypermetropic (average +16 diopters); in type 2, the eyeball size is normal (average axial length 21 mm) with small refractive error; and in type 3, the eyeball size is normal. Histologically, types 1 and 2 demonstrated abnormal sclera with disorganization of collagen fiber bundles and deposits of proteoglycans in the matrix, whereas type 3 showed normal sclera. Subscleral sclerectomy was effective for types 1 and 2, inducing postoperative resolution of the subretinal fluid. However, type 3 eyes were not helped by this technique. CONCLUSIONS: Primary uveal effusion syndrome is caused by abnormalities of the sclera and increased resistance to transscleral fluid outflow as subscleral sclerectomy is an effective treatment in types 1 and 2 only, correct preoperative classification is essential for early surgical management.

Adult↗

Enhancement of dedifferentiation and myoid differentiation of retinal pigment epithelial cells by platelet derived growth factor.

AIMS: To clarify factor(s) involved in morphological dedifferentiation of retinal pigment epithelial (RPE) cells in vitro from mitotically quiescent hexagonal cells to flattened cells that lack epithelial characteristics and concurrent myoid differentiation. METHODS: RPE cells which retained their differentiated hexagonal morphology were isolated from bovine eyes by mechanical pipetting. Dedifferentiation and myoid differentiation of RPE cells were examined by microscopic observation and immunohistochemical analysis using antibodies against cytokeratin, an epithelial marker, and alpha smooth muscle actin, a marker of myoid differentiation. The contractile ability of RPE cells was evaluated by collagen gel contraction assay. RESULTS: Platelet derived growth factor (PDGF) enhanced morphological changes in the RPE from hexagonal-shaped cells to flattened cells. Coincident with this morphological alteration, the expression of cytokeratin in RPE cells decreased and expression of alpha smooth muscle actin began and was increased in a time dependent manner. These alterations were completely blocked by collagen synthesis inhibitors. Interleukin 1beta, transforming growth factor beta1, insulin-like growth factor I, and basic fibroblast growth factor had little or no effect on the dedifferentiation. PDGF also potentiated the RPE induced collagen gel contraction. CONCLUSIONS: These results demonstrate that PDGF enhanced the dedifferentiation of RPE cells, the initial step of proliferative vitreoretinopathy (PVR), as well as myoid differentiation and collagen gel contraction. PDGF may have a versatile role in the pathogenesis of PVR involving collagen synthesis.

Actins↗

The second eye of Japanese patients with unilateral exudative age related macular degeneration.

AIM: To clarify the incidence of choroidal neovascularisation (CNV) and predisposing findings for development of CNV in the second eye of Japanese patients with unilateral exudative age related macular degeneration (AMD). METHODS: The second eyes of unilaterally affected patients with exudative (neovascular) AMD treated in our clinic during the past 10 years (1988-97) were carefully followed up for more than a year. Evidence of CNV was confirmed by fluorescein and indocyanine green angiography. Macular lesions in patients, in whom CNV developed in the second eye, were retrospectively evaluated from patient records. RESULTS: 170 patients met the criteria. The average follow up period was 47 months (range 12-108 months). All patients were Japanese. CNV developed in the second eye in 12 (7%) of 170 patients, 30.3 months on average after the first examination. Cumulative incidence of developing CNV in the second eye using Kaplan-Meier life table analysis was: 0.6% by 1 year, 5.6% by 3 years, and 12.3% by 5 years, and was relatively low compared with that in white patients. CNV developed most frequently from serous pigment epithelial detachment (PED) in the macula (58%). Soft drusen were not prevalent and risk of developing CNV was not very high (18%). CONCLUSION: It was confirmed that there were some differences in the incidence and predisposing findings for CNV developing in AMD among Japanese and other Asian patients compared with those in white people. It is important to recognise these differences between the two populations to understand the pathogenesis and epidemiology of AMD.

Adult↗

[Effects of corticosteroid on porcine retinal pigment epithelial cells in culture--2. Effects on phagocytosis and lysosomal activity].

PURPOSE: The effects of a corticosteoid on the phagocytosis and lysosomal activity of cultured porcine retinal pigment epithelium (RPE) cells were investigated. METHODS: After exposing cultured RPE cells to various concentrations (10, 50, 100, 500, 1,000 nM) of betamethasone sodium phosphate (betamethasone), the cells were incubated with latex microspheres for 6 hours. RESULTS: The number of latex microspheres phagocytized by the cultured RPE cells was inhibited by 50 nM betamethasone within 24 hours. Ten-nM betamethasone did not inhibit the proliferation of cultured RPE cells, but ingestion of latex microspheres by the cells was inhibited after 3 days. Lysosomal activity (acid phosphatase, beta-glucuronidase) of RPE cells was inhibited by a high concentration (500 nM) of betametasone. CONCLUSION: These results suggest that corticosteroid inhibits the phagocytosis and lysosomal activity of cultured RPE cells.

Acid Phosphatase↗

[Ciliochoroidal detachment following scleral buckling surgery for rhegmatogenous retinal detachment].

PURPOSE AND METHODS: We observed the peripheral choroid; ciliary body, and depth of the anterior chamber by ultrasound biomicroscopy (UBM) in 31 eyes with rhegmatogenous retinal detachment before and after scleral buckling surgery. Scleral encircling was performed in 11 eyes and segmental scleral buckling in 20 eyes. RESULTS: With UBM, ciliochoroidal detachment was detected in all eyes (100%) following scleral encircling and in 8 eyes (40.0%) following segmental scleral buckling. After scleral encircling procedure, the eyes with preoperatively bullous and wide retinal detachment showed a severe ciliochoroidal detachment and edema of the ciliary body. Shallowing of the anterior camber occurred in all 11 eyes (100%) after scleral encircling and in 12 of 20 eyes (60.0%) after segmental scleral buckling. Marked shallowing with closure of the angle and elevated intraocular pressure occurred in 2 eyes. CONCLUSION: The results showed that careful postoperative examinations for the anterior segments, chamber angle, and intraocular pressure are necessary with slit-lamp examination and applanation tonometry after scleral buckling surgery.

Adult↗

Changes in choriocapillaris and retinal pigment epithelium in age-related macular degeneration.

Retinal pigment epithelial cells (RPE) and the choriocapillaris are on opposite sides of Bruch's membrane and control transport in and out of the retina. In age-related macular degeneration (AMD), they may also be responsible for deposition of material in and on Bruch's membrane and the formation or regression of choroidal neovascularization (CNV). Indocyanine green (ICG) angiography can be used to visualize the choroidal vasculature and CNV. Filling of the choriocapillaris with ICG was delayed in subjects older than 50 years of age, and areas of hypofluorescence were observed in maculas of AMD subjects, often associated with CNV. Laser Doppler flowmetry of the choriocapillaris in the macula demonstrated that choroidal blood flow and volume are reduced in subjects older than 46 years of age and further decreased in subjects with AMD. The human choriocapillaris can be histologically studied in two dimensions by incubating the tissue for alkaline phosphatase activity, flat-embedding it in transparent polymer and sectioning it. Using this technique, choriocapillaris dropout was found to be associated with deposition of material in Bruch's membrane in diabetic subjects. When RPE are removed from Bruch's membrane, the choriocapillaris degenerates; the regeneration of choriocapillaris can be blocked by Genistein, a tyrosine kinase inhibitor. Finally, RPE cells may produce substances that both stimulate the formation and regression of CNV in animal models. These studies suggest that there may be a reduction in choriocapillaris flow in AMD, and this loss of choriocapillaris can be associated with the Bruch's membrane deposits that are hallmarks of AMD. Furthermore, RPE may stimulate the formation and regression of CNV and RPE loss can result in loss of choriocapillaris.

Adult↗

Idiopathic polypoidal choroidal vasculopathy in Japanese patients.

OBJECTIVE: To describe the vascular nature and clinical features of idiopathic polypoidal choroidal vasculopathy in Japanese patients. METHODS: Patients thought to have idiopathic polypoidal choroidal vasculopathy were examined with binocular ophthalmoscopy, slitlamp biomicroscopy with a contact lens, fluorescein angiography, and indocyanine green angiography. RESULTS: From January 1993 to December 1997, 35 eyes in 32 patients were diagnosed as having idiopathic polypoidal choroidal vasculopathy. Men were predominantly affected (22 patients [69%]). Most patients were unilaterally involved (29 patients [91%]) and elderly, with a mean age of 65.7 years (range, 44-82 years). Ocular manifestations were relatively mild, with serous or hemorrhagic detachments of the retinal pigment epithelium and neurosensory retina in the posterior pole. Most patients had a favorable course, although some experienced recurrence, and a few eyes developed disciform scarring. In all patients, indocyanine green angiograms demonstrated branching vascular networks with polypoidal dilations at terminals of the network beneath the retinal pigment epithelium. These lesions were mostly in the macula (33 eyes [94%]), with a few in the peripapillary area. CONCLUSIONS: Idiopathic polypoidal choroidal vasculopathy in Japanese patients differs from that in American patients. It seems that this disorder occurs in elderly Japanese patients and should be treated as a distinct clinical entity. It is probably a peculiar form of choroidal neovascularization beneath the retinal pigment epithelium. We propose the term "polypoidal choroidal neovascularization" for this disorder.

Adult↗

Transfection of basic fibroblast growth factor (bFGF) gene or bFGF antisense fene into human retinal pigment epithelial cells.

BACKGROUND: Transplantation of RPE cells offers a potential of restoring retinal pigment epithelium (RPE) function and has been shown to be effective in the dystrophic RCS rat model. Recently, RPE transplantation was attempted in patients with age-related macular degeneration. Basic fibroblast growth factor (bFGF) plays important roles in maintaining normal retinal function. The purpose of this study was to introduce bFGF sense or antisense cDNA into human RPE cells to alter the expression of bFGF. METHODS: Human bFGF sense cDNA or antisense cDNA was inserted into the pBK-CMV vector. For stable gene expression, we introduced the plasmids into RPE cells using the electroporation method. Following electroporation, transfected RPE cells were cultured and resistant cells were selected in the presence of antibiotic G418. We analyzed the expression of the transfected genes in the cloned RPE cells by polymerase chain reaction (PCR) and by reverse transcription (RT)-PCR. RESULTS: Cloned RPE cells in which the bFGF sense or antisense cDNA had been efficiently transfected were established. PCR and RT-PCR analysis demonstrated not only the presence but also the expression of bFGF sense or antisense cDNA in the transfected RPE cells. CONCLUSIONS: Human bFGF sense cDNA or antisense cDNA can be efficiently introduced into cultured RPE cells by the electroporation method. The successful expression of the genes into RPE cells demonstrated that this technique can be used to regulate bFGF expression and thus increase the scope of RPE transplantation for the treatment of retinal diseases.

Cells, Cultured↗

Expression of vascular endothelial growth factor and its receptor (KDR/flk-1) mRNA in experimental choroidal neovascularization.

PURPOSE: Vascular endothelial growth factor (VEGF) is an angiogenic peptide that has been suggested to be important in the pathogenesis of choroidal neovascularization. We investigated the transcription of VEGF and its receptor KDR/flk-1 genes during the development of experimentally induced choroidal neovascularization. METHODS: Rat VEGF or KDR cDNA was inserted in PGEM or pBluescript to prepare antisense or sense riboprobes. Multiple krypton laser burns were applied to the posterior pole of pigmented rat eyes according to a previously described protocol which produces choroidal neovascularization. At intervals of up to 4 weeks after photocoagulation, the eyes were removed and cut into thin sections. The sections were subjected to in situ hybridization with digoxigenin (DIG)-labeled single-strand rat VEGF and KDR cDNA riboprobes. RESULTS: In normal adult rat retinas, VEGF and KDR mRNA expression was mainly observed in the ganglion cell and the inner nuclear layers. During the development of neovascularization, VEGF and KDR mRNAs were detected in retinal pigment epithelial-like cells, fibroblast-like cells and endothelial cells in neovascular lesions. The level of expression was strongest at 1 week after photocoagulation in lasered lesions, and decreased by 4 weeks after photocoagulation. CONCLUSIONS: Our findings demonstrate that expression of VEGF and its receptor KDR may play a role in the formation of experimentally induced choroidal neovascularization. In this study, VEGF and its receptor were co-localized, suggesting that an autocrine and/or paracrine mechanism may be operative.

Animals↗

Phosphorothioate oligonucleotides induction into experimental choroidal neovascularization by HVJ-liposome system.

PURPOSE: The purpose of this study was to determine whether the inactivated hemagglutinating virus of Japan (HVJ)-liposome method can induce phosphorothioate oligonucleotides effectively into an experimentally-induced choroidal neovascularization of rats. We also examined whether antisense phosphorothioate oligonucleotides against VEGF could be induced into choroidal neovascularization as a therapeutic agent by the HVJ-liposome method. METHODS: The experiments were conducted on a rat model of choroidal neovascularization. FITC-labeled phosphorothioate oligonucleotides were coencapsulated in liposomes. The liposomes were coated with the envelope of inactivated HVJ and injected into the vitreous cavity following photocoagulation of pigmented rat eyes. The eyes were removed following injection, fixed, frozen and cut into thin sections. Induction of oligonucleotides was observed under a laser confocal scanning microscope for fluorescence and the development of choroidal neovascularization was evaluated histopathologically. RESULTS: Phosphorothioate oligonucleotides were effectively induced into ganglion cells and into the cells of the choroidal neovascularization induced by laser photocoagulation. Highly effective induction of oligos was observed 3 to 14 days after intravitreal injection of HVJ-liposomes after which the level decreased. Antisense oligonucleotides against VEGF were induced specifically into cells in the choroidal neovascularization, however neovascularization was still observed. CONCLUSIONS: Phosphorothioate oligonucleotides can be effectively induced into ganglion cells, and specifically into cells in choroidal neovascularization. Although antisense oligonucleotides against VEGF failed to prevent choroidal neovascularization, the HVJ-liposome method provided a highly effective means of inducing antisense oligos for in vivo antisense therapy.

Animals↗

Indocyanine green angiography and pathophysiology of multifocal posterior pigment epitheliopathy.

PURPOSE: To clarify the pathophysiology of multifocal posterior pigment epitheliopathy (MPPE), or bullous retinal detachment (RD)-an unusual manifestation of central serous chorioretinopathy (CSC)-we evaluated indocyanine green (ICG) angiographic findings of patients with MPPE. METHODS: Indocyanine green angiography was performed on 45 eyes of 26 patients with MPPE in our clinic during a 4-year period and compared with clinical and fluorescein angiographic (FA) findings. RESULTS: Ophthalmoscopically, in the posterior pole there were multiple yellowish-white retinal exudations, associated with flat, serous RD and bullous RD in the lower periphery. Fluorescein angiography demonstrated multiple massive leakages from the choroid into the subretinal space. These leakage sites corresponded to the retinal exudations. Indocyanine green angiography showed hyperfluorescence in the posterior pole of the choroid. The hyperfluorescence was first seen in the middle phase and became prominent in the late phase. This finding seems to be due to extravasation from the choriocapillaris. After laser photocoagulation of the leakage sites seen on FA, the leakages stopped and the retinal exudations and RD were resolved. Indocyanine green angiography, however, revealed hyperfluorescence in the posterior pole that was seen in active stage. DISCUSSION AND CONCLUSION: These ICG angiographic findings for MPPE show that hyperpermeability of the choroidal vessels may be the primary causative lesion. This is followed by an intrastromal accumulation of the extravasated choroidal fluid, which may be subclinical. Involvement of the retinal pigment epithelium may be secondary, and then the disease becomes manifest with RD. In MPPE, a severe form of CSC, the retinal pigment epithelium is involved extensively and widely, and prognosis is unfavorable. We conclude that MPPE and CSC represent opposite ends of a common morbid spectrum.

Adult↗

Natriuretic peptide receptors, NPR-A and NPR-B, in cultured rabbit retinal pigment epithelium cells.

We tried to detect natriuretic peptide (NP) receptor (NPR-A and NPR-B) mRNAs in cultured rabbit retinal pigment epithelium (RPE) cells and examined the regulation of their expression in relation to subretinal fluid absorption or RPE cell proliferation. RPE cells from 2-4 passages were grown to confluence on microporous membranes and analyzed for levels of expression of receptor mRNAs by quantitative RT-PCR and Northern blotting. The expression of NPR-B mRNA was approximately tenfold higher than that of NPR-A mRNA. The expression of NPR-A mRNA was not affected by treatments that may change subretinal fluid transport, while that of NPR-B mRNA was inhibited by transmitters involved in light- and dark-adaptation such as dopamine and melatonin. Expression of NPR-B mRNA was also suppressed by platelet-derived growth factor and transforming growth factor-beta. Furthermore, atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP), ligands for NPR-A and B, respectively, inhibited the proliferation of RPE cells, as analyzed by incorporation of [3H]thymidine. These findings suggest that ANP may be involved in constitutive absorption of subretinal fluid and that NPs form an important regulatory system of proliferation in RPE cells.

Acetazolamide↗

[Effects of local administration of interferon-beta on proliferation of the retinal pigment epithelium].

PURPOSE: We demonstrated effects of local administration of human interferon (IFN)-beta on the repair process of the rabbit retinal pigment epithelium (RPE). MATERIAL AND METHODS: We used adult pigmented rabbits in this experiment. We measured IFN-beta levels in the ocular tissues after sub-Tenon administration of human IFN-beta by means of enzyme-linked immunosorbent assay (ELISA) methods. Laser photocoagulation in moderate intensity was applied after IFN administration. The repair process of the RPE in laser lesion sites was examined histopathologically. RESULTS: Locally administrated IFN spread by diffusion into the intraocular tissues. The highest IFN level was detected in the choroid. In eyes treated with IFN, RPE cells proliferated vigorously to the center of the photocoagulated lesions on early stages after laser photocoagulation. Proliferation of RPE cells after laser photocoagulation was remarkable in eyes treated with large amounts of IFN. CONCLUSION: It was demonstrated histopathologically that sub-Tenon administration of IFN-beta promoted proliferation of RPE cells during the repair process after laser photocoagulation.

Administration, Topical↗

[Vascular endothelial growth factor promotes experimental choroidal neovascularization in monkey eyes].

PURPOSE: To evaluate the effect of vascular endothelial growth factor (VEGF) on experimental choroidal neovascularization (CNV) in monkey eyes through clinical, morphometric, and histological observations. METHOD: CNV was induced in both eyes of 6 rhesus monkeys by intense photocoagulation by red krypton laser. Immediately after photocoagulation, 2.5 micrograms of exogenous human VEGF was injected into the vitreous of the left eye in each animal. The right eyes served as controls. The eyes were enucleated 3 days to 12 weeks after photocoagulation and were examined by light and electron microscopy. RESULTS: VEGF-treated eyes developed remarkable serous retinal detachment around the sites of photocoagulation with manifest CNV one week after photocoagulation. Although there was no difference in the incidence of CNV between the treated and control eyes, the treated eyes showed more intense leakage of fluorescein from the CNVs for up to 4 weeks after treatment. Morphometrically, the CNVs were significantly larger and continued to grow longer in the treated than in the control eyes after one week of photocoagulation. Histologically, newly formed vessels with a distinct lumen were present in the treated eyes after 3 days of photocoagulation. CONCLUSION: Intravitreal injection of human VEGF promotes experimental choroidal neovascularization in monkey eyes.

Animals↗