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At least 307 records · Page 17Linked to original sources
PubMed2000

Retinal degeneration 6 (rd6): a new mouse model for human retinitis punctata albescens.

PURPOSE: To characterize the genetics and phenotype of a new mouse mutant with retinal degeneration, rd6, that is associated with extensive, scattered, small white retinal dots seen ophthalmoscopically. METHODS: The phenotype was characterized using ophthalmoscopy, fundus photography, electroretinography, light microscopy, immunocytochemistry, and electron microscopy. Genetic characterization and linkage analysis studies were performed using standard methods. RESULTS: The inheritance pattern of rd6 is autosomal recessive. Linkage analysis mapped rd6 to mouse Chromosome 9 approximately 24 cM from the centromere, suggesting that the human homolog may be on chromosome 11q23. Ophthalmoscopic examination of mice homozygous for rd6 revealed discrete subretinal spots oriented in a regular pattern across the retina. The retinal spots appeared by 8 to 10 weeks of age and persisted through advanced stages of retinal degeneration. Histologic examination revealed large cells in the subretinal space, typically juxtaposed to the retinal pigment epithelium. The white dots seen on fundus examination corresponded both in distribution and size to these large cells. By 3 months of age, the cells were filled with membranous profiles, lipofuscin-like material, and pigment. These cells reacted strongly with an antibody directed against a mouse macrophage-associated antigen. Photoreceptor cells progressively degenerated with age, and an abnormal electroretinogram was initially detected between 1 and 2 months of age. CONCLUSIONS: The fundi of mice homozygous for rd6 exhibit phenotypic similarities to the human flecked retinal disorder retinitis punctata albescens. Thus, rd6/rd6 mice may be a model for understanding the etiology of this or similar disorders. The relationship between the aberrant subretinal cells and the concomitant photoreceptor degeneration remains to be established.

Animals↗
PubMed2006

Preserved vision despite distinct retinal edema in central retinal artery occlusion.

BACKGROUND: In subtotal central retinal artery occlusion (CRAO), distinct retinal edema with acute onset irreversible visual loss is common. - METHODS: Clinical observation, fluorescein angiogram. - PATIENT: A 69-year-old patient presented with acute visual loss of his right eye. Risk factors for CRAO were arterial hypertension and diabetes mellitus. A further factor was a 60% stenosis of the right and a 90% stenosis of the left internal carotid arteries. - RESULT: Visual acuity at initial examination was 20/32 despite pronounced central retinal edema with characteristic cherry red spot of the macula. Fluorescein angiography demonstrated early filling of retinal vessels, only perfusion of the inferior macular vessels was delayed. Two months later retinal edema resolved and central visual acuity was 20/25. - CONCLUSION: In this patient, retinal edema most likely resulted from a transient retinal ischemia. Spontaneous reperfusion occurred early enough to allow functional recovery in the ischemic retina.

Aged↗
PubMed1987

Presence of retinal autoantigen in normal mice: absence in strains with retinal degeneration.

We examined the eyes of four strains of mice to determine if some or all contained an antigen which might cross-react with an antigen of guinea pig retina. To do this, we prepared guinea-pig antibody to guinea-pig retinal extract by immunizing Hartley guinea pigs with guinea-pig retinal extract in two different adjuvants. The retinal tissue of Balb/c and C57B1/6J mice stained well when we used the guinea-pig antibody to guinea-pig retinal extract. In contrast, the eyes of a subline, i.e., C57B1/6J-rd with retinal degeneration, did not stain. Likewise, the eyes of C3H/HeJ and SJL mice with abnormal retinas did not stain. The latter two strains are known to have retinal degeneration. The control studies were negative. This study shows that normal murine eyes have at least one antigen which cross-reacts with a guinea-pig retinal antigen. It also shows abnormal mouse retinas lack this antigen.

Animals↗
PubMed1980

Breakdown of blood. Retinal barrier in RCS rats with inherited retinal degeneration.

A breakdown in the blood-retinal barrier to certain proteins is described in mutant RCS rats with inherited retinal degeneration. Intravenously injected microperoxidase and horseradish peroxidase are extravasated from the outer (but not inner) retinal capillaries of these rats, at approximately 11 weeks of age and older. The number of affected capillaries increases with the age of the animals and progression of the retinal dystrophy until virtually all capillaries in the outer retina become permeable to these tracers. In such capillaries, enzyme reaction product is demonstrable in a greater proportion of luminal vesicles and in the majority of abluminal vesicles. Reaction product is also localized in cytoplasmic vacuoles, the basal laminae of endothelial cells and pericytes, and the perivascular spaces. The increased permeability of outer retinal capillaries in RCS rats appears to be due to an increase in transendothelial vesicular transport of the probe molecules. There was no evidence that either tracer permeated the interendothelial junctions or entered the basal laminae by reflux from the perivascular spaces. It is suggested that factors originating from the degenerated photoreceptor cells may play a role in stimulating the vesicular transport observed in permeable capillaries. In contrast to these findings, the outer retinal capillaries of RCS rats were not permeable to hemoglobin, catalase, or ferritin, regardless of the age of the animal or the degree of retinal degeneration. Since the vesicles that form at the luminal front are covered by a diaphragm, it is possible that this structure prevents entry of these larger proteins into the endothelial vesicle, even in capillaries that are demonstrably permeable to the smaller tracers.

Animals↗
PubMed1996

Sub-retinal pigment epithelial deposits in a dominant late-onset retinal degeneration.

PURPOSE: To determine the pathogenesis of an autosomal dominant late-onset retinal degeneration by studies of the retinal histopathology, phenotype of family members, and candidate genes for the disease. METHODS: The retina from an 80-year-old patient donor was prepared for light and electron microscopy, including special stains and immunocytochemistry. Family members were examined clinically and with retinal function tests. Rhodopsin, peripherin/RDS, and TIMP3 genes were screened for mutations, and linkage analysis was performed with short tandem repeat polymorphisms flanking these genes. RESULTS: Affected family members had nyctalopia in the sixth decade of life and severe visual loss developed by the eighth decade. The donor retina showed marked loss of photoreceptors except in the inferior periphery. A thick layer of extracellular deposits was present between the RPE and Bruch's membrane in all retinal regions. A 70-year-old affected family member had a retinopathy resembling retinitis pigmentosa. Her 42-year-old daughter had a patch of punctate yellow-white lesions in one fundus and abnormal dark adaptation. The 50-year-old son of the donor had normal fundi but abnormal dark adaptation and electroretinography. No mutations were detected in the coding sequence of the rhodopsin, peripherin/RDS, and TIMP3 genes. Rhodopsin and TIMP3 were further excluded with linkage analysis. CONCLUSIONS: This novel retinal degeneration shares histopathologic and clinical features with both Sorsby fundus dystrophy and retinitis pigmentosa. The sub-RPE deposits may disrupt the exchange of nutrients and metabolites between the retina and the choriocapillaris, leading to photoreceptor dysfunction and degeneration.

Adult↗
PubMed2001

Echographic evaluation of a patient with diabetes and dense vitreous hemorrhage: an avulsed retinal vessel may mimic a tractional retinal detachment.

PURPOSE: To report that an avulsed retinal vessel may appear as a tractional retinal detachment on echographic evaluation. METHODS: Case report. RESULTS: A 57-year-old diabetic woman presented with a nonclearing vitreous hemorrhage of 2 months duration in the left eye. Echography was consistent with a localized tractional retinal detachment on longitudinal sections; transverse sections demonstrated a pinpoint opacity in the vitreous cavity. Intraoperatively, an avulsed retinal vessel was noted in the area of echographic abnormality. CONCLUSION: An avulsed retinal vessel may mimic tractional retinal detachment on echography. Although trained ophthalmic echographers routinely perform both longitudinal and transverse sections during an echographic evaluation, less skilled observers must be aware of the importance of performing both longitudinal and transverse sections for accurate echographic diagnosis.

Diabetes Mellitus, Type 1↗
PubMed1997

Expression of c-fos and c-jun mRNA following transient retinal ischemia: an approach using ligation of the retinal central artery in the rat.

The expression of the proto-oncogenes c-fos and c-jun was examined by in situ hybridization at various timepoints following transient retinal ischemia by means of ligation of the retinal central artery in the rat. Ischemia of 90-minute duration resulted in the degeneration of neurons in both the ganglion cell layer and the inner nuclear layer at 48 hours after reperfusion. The expression of c-fos and c-jun messenger RNA throughout the entire inner nuclear layer was transiently coinduced following 90-minute retinal ischemia with a peak at 1 hour after reperfusion. This expression was also found in the ganglion cell layer at 3 hours after reperfusion. Weak signals for c-fos and c-jun mRNA were observed at 24 hours after reperfusion and returned to near control levels by 48 hours. c-jun protein expression was detected in the ganglion cell layer, the middle of the inner nuclear layer, and optic nerve head at 3 hours, but not 1 hour, after lethal ischemia/reperfusion; however, c-fos protein expression was not detected after reperfusion. Whereas no neuronal degenerative changes were found at 7 days after 30-minute ischemic retina, c-fos and c-jun messenger RNA were also induced at 1 hour postreperfusion. To our knowledge, this study is the first report to show expression patterns of immediate-early genes after retinal ischemia/reperfusion. These results suggest that changes in expression of c-fos and c-jun after transient retinal ischemia are similar to those after transient brain ischemia, and the selective occlusion of the central retinal artery will provide a useful model for studying ischemic neuronal degeneration in vivo in the rat retina.

Animals↗
PubMed1998

Tractional retinal detachment after branch retinal vein occlusion. Influence of disc neovascularization on the outcome of vitreous surgery.

OBJECTIVE: This study aimed to investigate the influence of disc neovascularization on the outcome of vitreous surgery for tractional retinal detachment (TRD) after branch retinal vein occlusion (BRVO). DESIGN: The study design was a retrospective case series. PARTICIPANTS: Twenty-two eyes of 22 patients who had undergone vitrectomy for TRD after BRVO at the Osaka National Hospital (Osaka, Japan) or the Surugadai Hospital of Nihon University (Tokyo, Japan) between 1985 and 1995 participated. Seven (32%) of 22 eyes had a TRD secondary to neovascularization of the optic disc (NVD) and neovascularization elsewhere (NVE; group I), and 15 (68%) had a TRD with NVE without NVD (group II). MAIN OUTCOME MEASURES: Visual acuities and retinal reattachment rates were measured. RESULTS: Sixteen (73%) of the 22 study eyes showed severe vitreous hemorrhage before surgery, and 11 eyes (50%) had received laser photocoagulation treatment before surgery. Fourteen (64%) of the study eyes achieved total retinal reattachment after initial vitrectomy, and 19 eyes (86%) were reattached completely at final examination. Thirteen eyes (59%) achieved a visual acuity of better than 0.1. Group I patients had a significantly higher rate of recurrent combined traction rhegmatogenous retinal detachment (P = 0.01) and a significantly worse final visual outcome (P = 0.01). CONCLUSIONS: Better surgical results are expected in eyes without NVD than with NVD among patients who undergo vitrectomy for TRD after BRVO. Although the authors were unable to determine the reason for this difference in the current study, they speculate that the degree of retinal nonperfusion, diffusible angiogenic factors, and distance of the site of occlusion from the disc may each affect visual and anatomic outcomes in these eyes.

Aged↗
PubMed2001

Evaluation of RLBP1 in 50 autosomal recessive retinitis pigmentosa and 4 retinitis punctata albescens Spanish families.

Defects in retinal vitamin A metabolism or in genes expressed in the retinal pigment epithelium (RPE) are related to nonsyndromic retinitis pigmentosa (RP). The RLBP1 gene encodes the cellular retinaldehyde-binding protein which, in the RPE and Müller cells of the retina, is thought to play a role in retinoid metabolism and visual pigment regeneration. We describe a study of the involvement of the RLBP1 gene in 50 autosomal recessive retinitis pigmentosa (ARRP) and four retinitis punctata albescens Spanish families. Cosegregation and homozygosity studies using an intragenic polymorphism and three close markers (D15S116, D15S127, and D15S130) ruled out RLBP1 as the cause of ARRP in 26 pedigrees. In the remaining families, SSCP analysis of the coding region and sequencing of the abnormal migrating bands did not detect any disease-causing mutation. These results indicate that mutations in the RLBP1 gene are not responsible for the ARRP or retinitis punctata albescens in this set of Spanish families. We did, however, identify two frequent polymorphisms (3'UTR + 167 G > T, T: 0.23 and G: 0.77; IVS6 + 20 T > C, T: 0.36 and C: 0.64), a silent substitution (S218S), and a rare variant (5'UTR-101 G > A).

Carrier Proteins↗
PubMedDate not supplied

Acute retinal necrosis presenting as central retinal artery occlusion with cilioretinal sparing.

PURPOSE: To report a case of acute retinal necrosis presenting as central retinal artery occlusion with cilioretinal sparing. METHODS: Single interventional case report. The findings of the ophthalmic examination, MRI, blood parameters, biopsy results and clinical course are reported. RESULTS: A forty two year old gentleman reporting sudden loss of sight, ophthalmic examination revealing uveitis, central retinal artery occlusion with cilioretinal sparing and peripheral necrotizing retinitis. CONCLUSIONS: Central retinal artery occlusion can be an early feature of acute retinal necrosis (ARN).

Adult↗
PubMedDate not supplied

Effects of hypertension on the retinal vein width at the retinal arterio-venous crossings.

PURPOSE: The study was designed to quantify retinal vein width changes at the arterio-venous crossing and to evaluate the effects of hypertension on vein widths at "vein posterior to the artery" (VPA) and "vein anterior to the artery" (VAA) crossings. METHODS: The width of the retinal veins was measured at points before and after the arterio-venous crossings by a computerized image analysis system in ten normal subjects and 35 hypertensive patients. Retinal vein width changes at fixed intervals from the arterio-venous crossing points, both VAA and VPA, were measured as a function of the stage of the hypertensive retinopathy in the subjects. RESULTS: Mean retinal vein width showed significant (p < 0.05) narrowing at VPA crossings at stages 2, 3 and 4 of hypertensive retinopathy. For the VAA crossings, there was no significant decrease in the width of the vein at any stage. There was no significant narrowing of the vein at VPA crossings in normal subjects or in stage 0 and stage 1 hypertensive retinopathy patients. CONCLUSIONS: The decrease in the width of the retinal vein in stages 2, 3 and 4 hypertensive retinopathy patients at VPA crossings can cause turbulence in blood flow, leading to intimal damage and occlusion. The absence of narrowing may explain the low incidence of branch retinal vein occlusions at VAA crossings.

Adult↗
PubMed1991

[A case of central retinal vein occlusion accompanied by central retinal artery occlusion].

A 81-year-old woman developed central retinal vein occlusion (CRVO) in her left eye subsequent to central retinal artery occlusion (CRAO). She noticed sudden visual loss in the left eye. At initial examination, her left visual acuity was 0.03, and only a small visual field was preserved at temporal area. The left fundus showed findings of mild non-ischemic CRVO. In addition white clouded retina was recognized at the left posterior pole which indicated CRAO. FAG showed remarkably prolonged arterial circulation, but no retinal capillary obliteration. Then retinal hemorrhage increased rapidly and her left eye developed hemorrhagic retinopathy. Two weeks after initial examination, FAG showed extensive retinal capillary obliteration. In this case it was supposed that central retinal artery occlusion due to arteriosclerosis produced ischemic capillaropathy and venous thrombosis, after which restoration of arterial circulation caused hemorrhagic retinopathy.

Aged↗
PubMed1988

Effects of laser wavelengths on experimental retinal detachments and retinal vessels.

We studied the effects of the yellow (577 nm), orange (595 nm) and red (630 nm) dye lasers, the argon blue-green (488, 514.5 nm) and green (514.5 nm) lasers, and the krypton red (647 nm) laser on experimentally produced serous and hemorrhagic retinal detachments and on retinal vessels in rabbits. Retinal detachments were created by either injecting balanced saline solution or partially hemolyzed blood under the retina. All laser wavelengths except the argon blue-green bypassed the sensory retina and produced no damage on either the sensory retina or the underlying retinal pigment epithelium with serous retinal detachment. Each laser wavelength, however, produced a specific effect on the detached retina with hemorrhagic fluid. Blue-green, green, yellow and orange wavelengths damaged the sensory retina more severely than the red wavelengths. Laser coagulation of the retinal vessels with the blue-green, green and orange wavelengths produced vasospasms.

Animals↗
PubMed2005

Correlation of retinal sensitivity measured with fundus-related microperimetry to visual acuity and retinal thickness in eyes with diabetic macular edema.

AIM: To determine whether significant correlations exist between retinal sensitivity measured by fundus-related microperimetry and the visual acuity and the foveal thickness measured by optical coherence tomography (OCT) in eyes with diabetic macular edema (DME). METHODS: A retrospective chart review of 32 eyes with DME and 17 normal healthy eyes that had undergone fundus-related microperimetry and OCT. The macular sensitivity was measured using the recently introduced fundus-related microperimeter, Micro Perimeter 1. The mean retinal sensitivities within the central 2 degrees and 10 degrees were correlated with the best-corrected visual acuity and OCT-measured foveal retinal thickness. RESULTS: The mean sensitivities in the central 2 degrees and 10 degrees were significantly lower in patients with DME than in normal subjects (P<0.0001). The mean retinal sensitivities in the central 2 degrees and 10 degrees were inversely correlated with visual acuity (r(2)=0.623, P<0.0001; r(2)=0.581, P<0.0001) and foveal thickness (r(2)=0.581, P<0.0001; r(2)=0.551, P<0.0001). CONCLUSIONS: The mean retinal sensitivities measured with fundus-related microperimetry were significantly lower in eyes with DME than in normal eyes. Because a significant correlation of the microperimeter-determined retinal sensitivity to visual acuity and foveal thickness was observed, the retinal sensitivities obtained by fundus-related microperimetry may be another measure that can be used to assess the effects of DME.

Adult↗
PubMed1998

Early embryonic interaction of retinal pigment epithelium and mesenchymal tissue induces conversion of pigment epithelium to neural retinal fate in the silver mutation of the Japanese quail.

The neural retina and retinal pigment epithelium (RPE) diverge from the optic vesicle during early embryonic development. They originate from different portions of the optic vesicle, the more distal part developing as the neural retina and the proximal part as RPE. As the distal part appears to make contact with the epidermis and the proximal part faces mesenchymal tissues, these two portions would encounter different environmental signals. In the present study, an attempt has been made to investigate the significance of interactions between the RPE and mesenchymal tissues that derive from neural crest cells, using a unique quail mutant silver (B/B) as the experimental model. The silver mutation is considered to affect neural crest-derived tissues, including the epidermal melanocytes. The homozygotes of the silver mutation have abnormal eyes, with double neural retinal layers, as a result of aberrant differentiation of RPE to form a new neural retina. Retinal pigment epithelium was removed from early embryonic eyes (before the process began) and cultured to see whether it expressed any phenotype characteristic of neural retinal cells. When RPE of the B/B mutant was cultured with surrounding mesenchymal tissue, neural retinal cells were differentiated that expressed markers of amacrine, cone or rod cells. When isolated RPE of the B/B mutant was cultured alone, it acquired pigmentation and did not show any property characteristic of neural retinal cells. The RPE of wild type quail always differentiated to pigment epithelial cells. In the presence of either acidic fibroblast growth factor (aFGF) or basic FGF (bFGF), the RPE of the B/B mutant differentiated to neural retinal cells in the absence of mesenchymal tissue, but the RPE of wild type embryos only did so in the presence of 10-40 times as much aFGF or bFGF These observations indicate that genes responsible for the B/B mutation are expressed in the RPE as well as in those cells that have a role in the differentiation of neural crest cells. They further suggest that development of the neural retina and RPE is regulated by some soluble factor(s) that is derived from or localized in the surrounding embryonic mesenchyme and other ocular tissues, and that FGF may be among possible candidates.

Animals↗
PubMed1998

Quantitative analysis of foveal retinal thickness in diabetic retinopathy with the scanning retinal thickness analyzer.

PURPOSE: This study sought to measure foveal retinal thickness in patients with diabetic retinopathy and to investigate the relationship between foveal thickness and visual acuity, biomicroscopic findings, and angiographic features. METHODS: A commercial scanning retinal thickness analyzer was used to measure retinal thickness. A laser slit was projected onto the retina and scanned in 400 milliseconds across the central area of the fundus. The image where the laser slit intersects with the retina was digitally recorded and analyzed. Retinal thickness was measured in 35 patients (35 eyes; patient age, 57 +/- 13 years) with diabetic retinopathy. Patients also were examined by fluorescein angiography and slit-lamp biomicroscopy to detect foveal thickening. RESULTS: Linear regression analysis indicated a significant correlation between foveal thickness and visual acuity (adjusted R2 = 0.72, P < 0.001). Foveal thickness was abnormal in 6 (100%) of 6 eyes in which foveal thickening was detected with slit-lamp biomicroscopy. Foveal thickness also was abnormal in 9 (31%) of 29 eyes that appeared normal by biomicroscopic examination. Foveal thickness was 136 +/- 65 microns in 7 eyes without leakage, 175 +/- 35 microns in 13 eyes with questionable leakage, and 291 +/- 120 microns in 7 eyes with definite leakage (P = 0.0075). CONCLUSIONS: Retinal thickness analysis is shown to be more sensitive than slit-lamp biomicroscopy for detecting small changes in retinal thickness. Retinal thickness analysis may prove to be a useful, noninvasive modality for the development or regression of macular edema.

Adult↗
PubMed2006

Loss of retinal progenitor cells leads to an increase in the retinal stem cell population in vivo.

Retinal stem cells [with the potential to produce either neural retinal progenitors or retinal pigment epithelial (RPE) progenitors] exist in the mammalian eye throughout life, and indeed the greatest absolute increase in the stem population occurs postnatally. The stem cells proliferate embryonically and thus may help to build the retina initially, but in postnatal mammals they clearly do not proliferate to regenerate the retina in response to injury. Using Chx10(orJ/orJ) and Mitf(mi/mi) mice, with small eye phenotypes due to the reduction of the neural retinal progenitor population and the retinal pigmented epithelial progenitor population, respectively, we now report that the retinal stem cell population, when assayed from the ciliary margin, increases 3-8-fold in both mutants. These findings suggest that the mammalian retinal stem cell population may be capable of responding to genetically induced signals from the progenitor populations.

Animals↗
PubMed1991

2-amino-4-phosphonobutyric acid exerts a light-dependent effect on post-gabaculine levels of retinal gamma-aminobutyric acid (GABA): evidence that ON synaptic pathways regulate retinal GABAergic transmission.

The effects of light, 2-amino-4-phosphonobutyric acid (APB), and kainic acid on rat retinal gamma-aminobutyric acid (GABA)-ergic transmission were studied by measuring levels of retinal GABA following subcutaneous injection of gabaculine, an irreversible inhibitor of GABA-transaminase. Post-gabaculine levels of retinal GABA in light-exposed rats were significantly greater than those in rats held in darkness. The synaptic mechanism of this effect of light was examined by measuring post-gabaculine levels of retinal GABA in rats placed into either lighted or darkened conditions after receiving unilateral intravitreal injections of APB, a glutamate analogue that selectively decreases the activity of ON synaptic pathways in the retina. APB attenuated the post-gabaculine accumulation of GABA in rats held in the light, but not in those placed into darkness. Furthermore, the light-dependent increment in post-gabaculine accumulation of retinal GABA was entirely APB sensitive, and the effect of APB was entirely light dependent. In contrast to APB, kainic acid stimulated the post-gabaculine accumulation of retinal GABA in vivo. Our findings suggest that APB and kainic acid influence GABAergic transmission at different sites in the retina and that some retinal GABAergic neurons are either ON or ON-OFF amacrine cells.

Aminobutyrates↗