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PubMed1992

Tractional elevations of the retina in patients with diabetes.

Tractional retinoschisis and tractional retinal detachment are both complications of proliferative diabetic retinopathy. The two conditions are frequently confused because they are similar in diagnostic features. We determined the respective incidence of tractional retinoschisis and tractional retinal detachment in 200 eyes with tractional elevations of the retina in patients with diabetes. In 39 eyes, the diagnosis was unequivocally tractional retinoschisis because the retinal elevation maintained its concave contour despite the development of retinal holes. In 65 eyes, tractional retinal detachment was diagnosed with equal certainty, either because pigment lines were present or because the elevation, after a retinal hole developed, rapidly became convex and extended to the ora serrata. The remaining 96 eyes, in which retinal holes or pigment lines were absent, were classified by other features that had been tested for significance in the already diagnosed eyes. On that basis, the diagnosis was retinoschisis in 46 eyes and retinal detachment in 50 eyes.

Diabetes Mellitus, Type 1↗
PubMed2003

The urokinase/urokinase receptor system in retinal neovascularization: inhibition by A6 suggests a new therapeutic target.

PURPOSE: The objective of the study was to determine the role of urokinase (uPA) and the urokinase receptor (uPAR) in retinal angiogenesis, and whether loss of uPAR or the inhibition of uPA/uPAR interactions could suppress the extent of retinal neovascularization in an animal model of ischemic retinopathy. METHODS: Retinal neovascularization was induced by exposing newborn mice to 75% oxygen on postnatal day 7 for 5 days, followed by exposure to room air on days 12 to 17. The expression of uPAR in the retina was investigated by RT-PCR and immunohistochemistry. The role of uPAR in ischemic retinopathy was investigated by quantitating the extent of retinal neovascularization in the uPAR(-/-) mouse. The effects of inhibiting the uPA/uPAR interaction on the development of retinal neovascularization were studied in this animal model with a uPA-derived peptide, A6. Animals were treated with an intraperitoneal injection of A6 at a dose of 5, 10, or 100 mg/kg once a day on days 12 to 16. Control animals included oxygen-exposed mice treated with similar amounts of PBS only on days 12 to 16. The effect of A6 on the expression of uPAR in the retina was examined by real-time RT-PCR. RESULTS: The expression of uPAR mRNA was upregulated in experimental animals during the period of angiogenesis and was localized to endothelial cells in the superficial layers of the retina. The uPAR(-/-) mouse demonstrated normal retinal vascular development; however, the absence of functional uPAR resulted in a significant reduction in the extent of retinal neovascularization. Histologic analysis of mice treated with A6 peptide showed significant inhibition of retinal neovascularization, and the response was dose dependent. The RT-PCR analysis of the retinas of the A6-treated animals showed a greater than twofold decrease in uPAR expression. CONCLUSIONS: Expression of the urokinase receptor uPAR is essential to the development of retinal neovascularization. Inhibition of the activity of uPAR suppresses retinal neovascularization, possibly through a reduction in cell-associated proteolytic activity, cell signaling, or cell-matrix adhesion necessary for cell migration during angiogenesis. The uPA/uPAR interaction may be an important therapeutic target in the management of proliferative retinopathies.

Animals↗
PubMed2000

Effects of inhibition of glycation and oxidative stress on the development of cataract and retinal vessel abnormalities in diabetic rats.

PURPOSE: To study effects of inhibition of glycation, and oxidative stress on the development of cataract and retinal vessel abnormalities in diabetic rats. METHODS: Diabetes was induced in male Wistar rats with streptozocin (STZ; 60 mg/kg BW, i.p.). Diabetic as well as strain matched control rats were fed 1) a normal diet, 2) addition of aminoguanidine in the drinking water (0.5 g/l for diabetic rats and 1.0 g/l for control rats) or 3) probucol in the pellets (1% w/w). After 6 months, the number of acellular vessels, endothelial cells and pericytes were counted in trypsin digested retinal vessel preparations, and the total retinal tissue amount of glutathione (GSH) and cysteine was measured with HPLC. RESULTS: Cataract formation occurred after 13 weeks in diabetic animals compared with 17 weeks for those treated with aminoguanidine, and 16 weeks for those treated with probucol (p < 0.001 in both cases). Aminoguanidine inhibited the formation of acellular collapsed capillary strands, 9 (3-14) vs. 18 (12-262) (median, range) per quadrant in untreated diabetic rats (p = 0.004), while probucol did not have any effect. Neither aminoguanidine, nor probucol influenced the endothelial/pericyte ratio. Diabetes caused a reduction in the GSH/cysteine ratio (10.7 +/- 0.6 vs. 15.3 +/- 1. 5) (mean +/- SD; p < 0.001). Probucol partly restored this imbalance (p < 0.05) whereas aminoguanidine did not. CONCLUSIONS: The results indicate that cataract formation in diabetes involves both glycation and oxidative stress processes. The reduced formation of acellular collapsed capillary strands by aminoguanidine suggests a potential role for glycation in vascular damage. The positive effect of probucol on cysteine/GSH metabolism imbalance indicates that derangements of one of the retinal defense systems against oxidative stress can be normalized by antioxidants.

Animals↗
PubMedDate not supplied

Retinal detachment in myopic eyes after laser in situ keratomileusis.

PURPOSE: To report the characteristics and surgical outcomes of rhegmatogenous retinal detachments in myopic eyes after laser in situ keratomileusis (LASIK). METHODS: Clinical charts of patients that developed rhegmatogenous retinal detachment after LASIK were reviewed. Surgery to repair rhegmatogenous retinal detachment was performed in 31 eyes (mean follow-up of 14 months after vitreoretinal surgery). RESULTS: A total of 38,823 eyes underwent surgical correction of myopia from -0.75 to -29.00 D (mean -6.00 D). Thirty-three eyes (27 patients; frequency .08%) developed rhegmatogenous retinal detachment after LASIK; detachments occurred between 12 days and 60 months (mean 16.3 mo) after LASIK. Eyes that developed a rhegmatogenous retinal detachment had a mean -8.75 D before LASIK. Most rhegmatogenous retinal detachment and retinal breaks occurred in the temporal quadrants (71.1%). Final best spectacle-corrected visual acuity (BSCVA) of 20/40 or better was obtained in 38.7% of the 31 eyes (two patients refused surgery). Poor final visual acuity (20/200 or worse) occurred in 22.6% of eyes. Information regarding visual acuity after LASIK and before the development of rhegmatogenous retinal detachment was available in 24 eyes; 45.8% (11/24 eyes) lost two or more lines of visual acuity after vitreo-retinal surgery. Reasons for poor visual acuity included the development of proliferative vitreo-retinopathy (n=5), epiretinal membrane (n=1), chronicity of rhegmatogenous retinal detachment (n=1), new breaks (n=1), displaced corneal flap (n=1), and cataract. CONCLUSIONS: Rhegmatogenous retinal detachment after LASIK for myopia is a serious complication. Final visual acuity may be limited by myopic degeneration, amblyopia, or delayed surgical repair.

Adolescent↗
PubMed1999

Rhegmatogenous retinal detachment after treatment of retinoblastoma.

PURPOSE: To determine the rate of retinal detachment after treatment of retinoblastoma, to describe the clinical features and management, and to discuss possible pathogenic mechanisms. METHODS: We retrospectively analyzed the charts of 80 patients (83 eyes) with retinoblastoma treated conservatively between 1963 and 1994, looking specifically for cases that developed a retinal detachment after treatment. RESULTS: Five patients (5 eyes, stages IVa to Vb) developed a retinal detachment after treatment. Of these, four had undergone external radiotherapy and one had an episcleral cobalt plaque. Retinal detachment developed within three months after radiotherapy and relentlessly progressed in all four eyes over a period of five months to four years. In the eye that received the episcleral cobalt plaque, the detachment remained localized inferiorly. Even though no retinal break could be detected in four eyes, the clinical features were suggestive of a rhegmatogenous detachment: there was retinal thinning adjacent to the regressed tumors, and the evolution was much longer than that of an exudative retinal detachment. A scleral buckling procedure was performed in two eyes and the retina was successfully reattached. The retinal detachment was not operated on in the three other eyes: the hole was too posterior in one eye; retinal surgery was refused in the second eye; and the retinal detachment remained localized inferiorly in the third eye. CONCLUSION: A retinal detachment developed in 6% of eyes after conservative treatment of retinoblastoma. The possibility of a rhegmatogenous origin should be considered even if no retinal break is detected. In the absence of tumor activity, a scleral buckling repair could be carefully considered if the retinal detachment threatens the macula, and if its evolution is not indicative of an exudative detachment.

Child, Preschool↗
PubMedDate not supplied

Deficiency of neuropilin 2 suppresses VEGF-induced retinal neovascularization.

Vascular endothelial growth factor (VEGF) plays a central role in the development of ocular neovascularization (NV) and is an excellent target for therapeutic intervention. VEGF acts through several receptors, including VEGF receptor 1, VEGF receptor 2, neuropilin-1 (Npn1), and Npn2, but the exact role of these receptors in the development of retinal NV is unknown. In this study, we investigated the expression of npn2 mRNA during new blood vessel growth in the retina and used npn2 knockout mice to assess the impact of deficiency of Npn2 on retinal NV. The level of npn2 mRNA in the retina increased during retinal vascular development, after exposure to hyperoxia, and after the onset of retinal ischemia. Immunohistochemistry showed colocalization of Npn2 with a vascular marker in retinal NV. Compared with littermate controls, mice deficient in Npn2 had significantly less ischemia-induced retinal NV and very little subretinal NV due to expression of a Vegf transgene. These data suggest that Npn2 facilitates VEGF-induced retinal NV and may constitute a useful target for therapeutic intervention in ocular diseases complicated by NV.

Animals↗
PubMed1993

Function and spatial distribution in developing chick retina of the laminin receptor alpha 6 beta 1 and its isoforms.

We have recently shown that the laminin-binding integrin receptor, alpha 6 beta 1, is prominently expressed in the developing chick retina, and its expression and activity are regulated during development on both retinal ganglion cells and other neural retinal cells. In the present study, we show that antibodies specific for the extracellular portion of the chick alpha 6 subunit dramatically inhibit interactions in vitro between embryonic day 6 neural retinal cells and laminin, showing that alpha 6 beta 1 functions as an important laminin receptor on developing retinal neurons. In previous work, we showed that alpha 6 mRNA levels on retinal ganglion cells decrease dramatically after E6 during the period that RGC axons innervate the optic tectum. In the present study, we show decreases in alpha 6 mRNA are not prevented by ablation of the optic tectum, indicating that tectal contact is not the major cause of this decrease. Within the embryonic retina, the alpha 6 subunit is codistributed, in part, with laminin, suggesting that it functions as a laminin receptor during retina development in vivo. Furthermore, two isoforms of the alpha 6 protein with distinct cytoplasmic domains generated by differential splicing have quite different distribution patterns in the retina, suggesting that these two isoforms may have different functions during retinal development.

Amino Acid Sequence↗
PubMed1997

Sustained closure of surgically repaired macular holes after retinal detachment with submacular fluid.

PURPOSE: To examine the behavior of surgically repaired macular holes when subsequent retinal detachment with submacular fluid develops and to correlate these observations with current theories of macular hole formation and closure. METHODS: We reviewed the medical records of four patients who underwent successful surgical closure of macular holes and subsequently developed rhegmatogenous retinal detachment with macular involvement. RESULTS: No reopening of the original macular hole occurred in any of the four patients. No focal macular attachment was seen that would suggest firm adherence of the macular hole edges to the underlying retinal pigment epithelium. CONCLUSIONS: When retinal detachment with submacular fluid develops in patients with a successfully closed macular hole, sustained closure of the macular dehiscence is typically seen. These findings support reapproximation of the hole edges with an associated retinal wound healing response as the mechanism of hole closure.

Aged↗
PubMed2001

Long-term follow-up of unoperated macular holes.

OBJECTIVE: To investigate the anatomic and visual acuity outcomes among patients with unoperated macular holes and at least 5 years of follow-up. DESIGN: Retrospective, noncomparative case series from an institutional practice setting. PARTICIPANTS: All patients with unoperated full-thickness macular holes evaluated at Bascom Palmer Eye Institute between January 1, 1968 and December 31, 1993 and observed for at least 5 years. METHODS: Demographic and clinical data were abstracted from patients' medical records and ophthalmologic photography records. For patients with bilateral macular holes, only one eye was included. MAIN OUTCOME MEASURES: Visual acuity and clinical features on initial examination, at 5 years, and at final follow-up. RESULTS: The study included 65 eyes of 65 patients with a median age of 65 years (range, 52-85 years) and a median follow-up of 9.3 years (range, 5-29 years). On initial examination at Bascom Palmer Eye Institute, the macular hole was stage 2 in 15 eyes (24%), stage 3 in 23 eyes (37%), and stage 4 in 25 eyes (40%). At final follow-up, the macular hole was stage 3 in 10 eyes (16%) and stage 4 in 53 eyes (84%). Visual acuity was 20/200 or worse in 35 eyes (54%) on initial examination, in 43 eyes (74%) at 5 years, and in 53 eyes (82%) at final follow-up. Poorer visual acuity on initial examination was a significant predictor of poorer final vision (P < 0.01). Other accompanying clinical features such as the presence of operculum, posterior vitreous detachment, and epiretinal membrane were not significantly associated with final vision. Throughout follow-up, there was a redistribution and reduced number of yellow nodular opacities at the level of the retinal pigment epithelium at the base of the macular holes and the development of retinal pigment epithelial atrophy around the macular holes. CONCLUSIONS: Long-term follow-up of unoperated macular holes demonstrates progression in hole size and stage, vision loss which generally stabilizes at the 20/200 to 20/400 level, a redistribution and reduced number of yellow nodular opacities at the level of the retinal pigment epithelium, and the development of retinal pigment epithelial atrophy surrounding the macular hole, resulting in a "bull's-eye" macular appearance.

Aged↗
PubMed1994

The role of B lymphocytes in experimental herpes simplex viral retinitis.

The purpose of this study was to examine B cell participation in experimental herpes simplex virus (HSV) retinitis. Passive immunization with anti-herpes antibody protects BALB/c mice from herpes simplex retinitis (HSR). Using anti-Mu antibody treatment, we modified the B cell population of C.B-17 mice, normally resistant to HSR, in order to test the hypothesis that such treatment would render them susceptible to HSR by impairing their early antibody response to anterior chamber (AC) inoculation with HSV. We analysed the effect of anti-Mu treatment on their susceptibility to HSR and then employed Polymerase Chain Reaction (PCR) and ELISA techniques to study the patterns of immunoglobulin gene and protein expression, and the T-cell receptor alpha/beta (TCR alpha/beta) gene expression after AC inoculation of HSV. Immunohistopathologic analysis revealed that 100% of the B cell deficient mice (B-) developed contralateral retinitis following AC inoculation, confirming the hypothesis that anti-Mu antibody treatment would convert HSR-resistant mice into HSR-susceptible ones. Transfer of B cells from naive congenic donor mice resulted in 67% of recipient B- mice developing contralateral retinitis. Transfer of anti-HSV antibody conferred nearly complete protection, with only 11% of mice developing retinitis (P < 0.005). PCR and ELISA analysis showed that both untreated and B- C.B-17 mice showed similar dynamic patterns of mRNA IgG isotype expression and of anti-HSV IgG isotypic antibody response following AC inoculation. Thus, we were forced to reject the hypothesis that an impaired early antibody response is primarily responsible for the increased HSR susceptibility seen in B- mice. In contrast, PCR analysis of TCR alpha/beta mRNA expression revealed dramatic differences between susceptible and resistant mice, suggesting that TCR V beta selection and usage may be a critical factor influencing HSR-sensitivity in this murine model, and that B cells (and immunoglobulin isotype) may play a role in TCR V beta selection and usage after ocular encounter with HSV.

Animals↗
PubMed1985

The influence of retinal afferents upon the development of layers in the dorsal lateral geniculate nucleus of mustelids.

The extent to which the development of a normal laminated lateral geniculate nucleus depends upon retinal afferents has been studied in normal and albino ferrets and in mink. Removal of all retinal afferents before they invade the nucleus (28 days in utero) or before they establish distinct monocular terminal fields (newborn, approximately 41 days post-conception) produces a nucleus that is smaller than normal and poorly separated from the adjacent perigeniculate and medial interlaminar nuclei. However, the nucleus is wedge-shaped, resembling a normal adult nucleus, in which a broad medial binocular segment is distinguishable from a narrower lateral monocular segment. There is a normal mediolateral gradient of cell sizes and some signs of a laminar differentiation, cells next to the optic tract being morphologically distinguishable from cells near the optic radiation, but no cell-free interlaminar zones are formed. The development of a monocularly innervated nucleus depends on the size of the surviving retinal input. In normally pigmented ferrets or mink the crossed retinofugal component is larger than the uncrossed component. In the monocular animals one sees essentially a monocular set of geniculate layers on each side, with an appropriate asymmetry. Each nucleus can be regarded as representing the survival of those layers which would have been innervated by the good eye, together with some additional geniculate territory that appears to be added to the surviving layers as retinogeniculate axons occupy territory normally innervated by the other eye. The crossed component of an albino ferret is abnormally large and the monocularly innervated contralateral nucleus is almost like that of a normal albino. There is a full complement of geniculate layers and interlaminar zones, which appears to develop without any binocular interactions. The ipsilateral retinogeniculate component of albinos is extremely small. In the monocular albino animals it forms discontinuous terminal patches, leaving sectors of the poorly differentiated nucleus uninnervated. These results show that in geniculate development there is a limited interaction between the two sets of retinal afferents. Each set plays a well defined and distinctive role, and one can replace the other to a limited extent only.

Afferent Pathways↗
PubMed1997

Development of serotoninergic chick retinal neurons.

Numerous neurotransmitters have been studied in detail in the developing retina. Almost all known neurotransmitters and neuromodulators were demonstrated in vertebrate retinas using formaldehyde-induced fluorescence, uptake autoradiography or immunohistochemistry procedures. Serotoninergic (5HT) amacrine neurons were described in the inner nuclear layer (INL) of the retina with their dendrites spreading within the inner plexiform layer (IPL). The present work describes the morphological pattern of development of serotoninergic amacrine neurons with a stratified dendritic branching pattern in the chick retina from embryonic day 12 to postnatal day 7. Serotoninergic-bipolar neurons are also described. SHT-amacrine neurons have round or pear-shaped somata and primary dendritic trees oriented toward the IPL that runs through the INL, showing several varicosities. Secondary dendrites then go through the INL, without any collateral branch. At the outer and inner margin of the IPL the primary and secondary dendrites originate an outer and an inner serotoninergic network, respectively. When the primary dendritic tree reaches the IPL it deflects laterally in sublayer 1-the outer serotoninergic network. Tertiary branches then arise from the secondary dendrite and deflect in the innermost sublayer of the IPL-the inner serotoninergic network. The final pattern of branching of 5HT amacrine cells was present at embryonic day 14 and was completely developed at hatching. Serotoninergic (5HT) bipolar neurons were also present in the INL at hatching. They are weakly immunoreactive and are probably a subset of bipolar cells that accumulate serotonin from the intersynaptic cleft and are not "true" 5HT neurons.

Animals↗
PubMed1995

[Reflection measurement during retinal laser coagulation in patients. Development of an automatically controlled dosimeter].

PURPOSE: Retinal laser coagulation has limited reproducibility, because every laser exposition is unpredictably affected by pigmentation and media opacities. This can lead to complications. A feedback-controlled dosimeter would make retinal laser treatment a safer, more reproducible and faster procedure. METHOD: A reflectometer was developed that allows monitoring of the reflection of laser light during standard photocoagulation. Hundreds of coagulations in rabbit eyes and about 12,000 coagulations in patients undergoing routine laser treatment were recorded. RESULTS: The results of the first reflectance measurements in humans are presented along with extensive animal studies. A typical reflectance history was found for different lesion intensities. The degree of retinal whitening correlates with reflectance characteristics. These characteristics allow an early prediction of lesion intensity. Motion during laser exposure affects each coagulation in a fashion similar to spot size and exposure time. CONCLUSION: Reflectometry is the currently most effective means of monitoring lesion development. An automatic dosimeter for retinal photocoagulation seems feasible.

Animals↗
PubMed1975

Ultrastructure and clinicopathologic correlation of idiopathic preretinal macular fibrosis.

Detailed light and electron microscopic examination of early idiopathic preretinal fibrosis lesions showed that the fibrosis consisted of a layer of glial cells on the retinal surface. Two cases supported the clinical observation that a glinting retinal reflex preceded the development of retinal folds and traction lines. In both cases there was a break in the inner limiting lamina through which glial cells migrated and, presumably, proliferated on the retinal surface. There was no evidence for vitreoretinal adhesions. The ultrastructural similarity of the lesion to preretinal glial membranes seen in other disease entities suggested the possibility of a common biochemical stimulus for glial cell migration and proliferation on the retinal surface.

Aged↗
PubMed1979

Proliferative diabetic retinopathy in patients with defects of platelet function.

A 71-year-old woman had von Willebrand's disease, an inheritable abnormality of platelet activity, and developed diabetic retinal neovascularization. A 59-year-old man had a myeoloproliferative disorder with thrombocythemia but may have had retinal changes before the development of his platelet dysfunction. The occurrence of diabetic proliferative retinopathy in patients with reduced platelet activity suggests that platelet induced microcirculatory abnormalities may not be required for neovascularization.

Aged↗
PubMed1982

Acute retinal necrosis.

Acute retinal necrosis represents a distinct, recently recognized clinical syndrome. Four patients who presented with rapid visual loss associated with uveitis and coalescent areas of retinal necrosis, followed by development of retinal detachments were examined. This paper emphasizes the following: (1) unilateral involvement does occur, (2) the distribution of lesions can be peripheral or central, and (3) early lesions are not associated with retinal vascular abnormalities either clinically or angiographically. Signs and symptoms are suggestive of an infectious process, possibly viral.

Acute Disease↗
PubMed1994

Ectopic expression of gamma interferon in the eye protects transgenic mice from intraocular herpes simplex virus type 1 infections.

Transgenic (rho gamma) mice provide a model for studying the influence of gamma interferon (IFN-gamma) produced in the eye on ocular and cerebral viral infection. To establish this model, we injected BALB/c- and C57BL/6-derived transgenic and nontransgenic mice of different ages intravitreally with herpes simplex virus type 1 (HSV-1) strain F. Eye and brain tissues of these mice were assessed for pathological and immunocytochemical changes. HSV-1 infection induced severe retinitis of the injected eyes and infection of the brain in all mice. In transgenic mice inoculated with HSV-1, the left, nontreated eyes were protected from retinitis, whereas nontransgenic mice developed bilateral retinitis. Additional intravitreal injection of IFN-gamma with the virus protected the noninoculated eyes of nontransgenic mice. Three-week-old nontransgenic mice died from HSV-1 infection, whereas transgenic mice of the same age and nontransgenic mice intravitreally treated with IFN-gamma survived. Ocular IFN-gamma production increased the extent of inflammation in transgenic mice but did not have a significant influence on the growth of HSV-1 until day 3 after inoculation and did not influence the neuroinvasion of this virus. Thus, the effects of IFN-gamma were not caused by an early block of viral replication. Possible mechanisms of IFN-gamma action include activation of the immune response, alteration of the properties of the virus, and direct protection of neurons.

Animals↗
PubMed1983

Acute retinal necrosis.

We treated 2 patients with unilateral acute retinal necrosis in association with uveitis. The disorder began as anterior uveitis, secondary glaucoma, and retinal vasculitis, and then developed into retinal necrosis within a few months. The aetiology was obscure and the appropriate treatment debatable. We also review reports of patients showing the same clinical characteristics, termed Kirisawa-type uveitis and bilateral acute retinal necrosis, and believe the disorders to be identical.

Acute Disease↗