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Retinal projections and retinal ganglion cell distribution patterns in a sturgeon (Acipenser transmontanus), a non-teleost actinopterygian fish.

Retinal projections in a sturgeon were studied by injecting biocytin or HRP into the optic nerve. The target areas are the preoptic area, thalamus, area pretectalis, nucleus of posterior commissure, optic tectum, and nuclei of the accessory optic tract. Furthermore, a few labeled fibers and terminals were found in a ventrolateral area of the caudal telencephalon. All retinal projections are bilateral, although contralateral projections were more heavily labeled. Retrogradely labeled neurons were found in the ventral thalamus bilaterally. Retinal projections in sturgeons are similar to those of other non-teleost actinopterygians and chondrichthyans (sharks), in terms of the targets and extent of bilateral projections. Distribution patterns of ganglion cells in the retina were examined in Nissl-stained retinal whole mount preparations. The highest density areas were found in the temporal and nasal retinas, and a dense band of ganglion cells was observed along the horizontal axis between the nasal and temporal areas of highest density. The density of ganglion cells in the dorsal retina is the lowest. The total number of ganglion cells was estimated to be about 5 x 10(4) in a retina. The existence of a low density area in the dorsal retina suggests reduced visual acuity in the ventral visual field.

Animals↗

Shape, number and localization of retinal tears in myopic over 8D, aphakic and traumatic cases of retinal detachment. An experience report.

For this experience report we have selected out of a total of 950 eyes with retinal detachment, 373 eyes and have sorted them out into three study groups: myopia over 8 d (197 eyes including 14 bilateral detachments), surgical aphakia (102 eyes) and traumatic detachment (74 eyes). With the help of tables and figures we tried to point out the form, number and localization of retinal tears in the eyes with retinal detachment in the above-mentioned groups. For fundus examinations we used routinely the binocular indirect ophthalmoscope without and with scleral depressor and the Goldmann three-mirror contact glass, also without and with scleral depressor. The striking features of the main types of retinal breaks in the three groups are commented, statistically analysed and compared.

Aphakia, Postcataract↗

Tumor necrosis factor and nitric oxide production by resident retinal glial cells from rats presenting hereditary retinal degeneration.

The inherited retinal dystrophy observed in Royal College of Surgeons (RCS) rats is a widely used model for the study of the photoreceptor degeneration that occurs in retinitis pigmentosa and macular degeneration. The visual cell degeneration is accompanied by an abnormal accumulation of microglial cells in the retina of RCS rats presenting the dystrophy. In the present study, we show that combined stimulation of RCS dystrophic retinal Müller glial (RMG) cells with interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) induced the release in culture supernatants of significantly higher amounts of tumor necrosis factor (TNF) and nitric oxide (NO) compared to nondystrophic congenic controls. In contrast, the levels of TNF and NO found in the supernatants from microglial cells were not significantly different in both strains. Interestingly, as shown by thymidine incorporation, microglial cells from RCS dystrophic rats have a prominent capacity of proliferation in culture medium compared to microglia isolated from RCS non dystrophic controls. Incubation of RMG cells and microglia with the stereoselective inhibitor of NOS, NG-monomethyl-L-arginine (L-NMMA), inhibited nitrite release in LPS + IFN-gamma-stimulated RMG cells and microglia. The addition of TGF-beta with LPS + IFN-gamma clearly inhibited TNF release in supernatants from both dystrophic and control rat RMG cells and microglia. While TGF-beta significantly inhibited nitrite synthesis in RMG cells, the effect on nitrite synthesis by microglia was very low. The retinal dystrophy observed in RCS dystrophic rats could result from an abnormal reactivity of RMG and microglial cells to release TNF and NO in response to stimulants. The immunomodulatory cytokine TGF-beta and inhibitors of NOS could be negative regulators in the cytokine network and nitrite synthesis thus interfering with the development of photoreceptor cell death.

Animals↗

Carriers of X-linked retinitis pigmentosa. A fluorophotometric determination of the permeability of the blood-retinal barrier.

The blood-retinal barrier permeability to fluorescein was studied in a single family with X-linked retinitis pigmentosa by an elaborate vitreous fluorophotometric method. Affected males showed a ten times increase of permeability compared with normals. In a group of seven obligate carriers the mean permeability was significantly increased by 45% compared with the mean permeability in a group of normals. Five of the seven carriers had permeabilities higher than the normal mean permeability + 2 SD, while two carriers had a permeability within the normal mean +/- 2 SD. Thus, this study supported that carriers of X-linked retinitis pigmentosa show deterioration of the blood-retinal barrier. However, the phenomenon is not present in all carriers and the permeability cannot be used as a completely safe indicator of the carrier state.

Adolescent↗

Thicknesses of macular retinal layer and peripapillary retinal nerve fiber layer in patients with hyperopic anisometropic amblyopia.

This prospective study was performed to measure the macular and the peripapillary retinal nerve fiber layer (RNFL) thicknesses using optical coherence tomography (OCT) in patients with anisometropic amblyopia. Thirty-one patients with hyperopic anisometropic amblyopia were included. The macular retinal thickness and the peripapillary RNFL thickness were measured using OCT. The mean refractive error was +3.71 diopters (D) and +1.00 D, the mean macular retinal thickness was 252.5 microm and 249.7 microm, and the mean RNFL thickness was 115.2 microm and 109.6 microm, inthe amblyopic eye and the normal eye, respectively. OCT assessment of RNFL thickness revealed a significantly thicker RNFL in hyperopic anisometropic amblyopia (P=0.019), but no statistically significant difference was found in macular retinal thickness (P>0.05). In conclusion, the amblyopic process may involve the peripapillary RNFL, but not the macula. However, further evaluation is needed.

Amblyopia↗

A brief review of retinitis pigmentosa and the identified retinitis pigmentosa genes.

The family of inherited ocular diseases that is collectively known as retinitis pigmentosa is a major cause of progressive retinal disease worldwide. As such, this family of diseases has been the object of much scientific scrutiny, both clinical and basic. The recent application of molecular genetic analyses has heralded the rapid elucidation of the underlying gene defects in many cases. In this article, the fundamental clinical and electroretinographic characteristics of retinitis pigmentosa will be recalled. Additionally, the current understanding of the genetic causes of retinitis pigmentosa will be reviewed, and the identified causative genes will be classified into groups related by function.

Animals↗

[The condition of the retinal vessels and intraocular and retinal pressure in patients with incipient forms of cerebrovascular atherosclerosis].

The authors examined 350 patients with initial forms of cerebrovascular atherosclerosis. Among the studied group 98 had discirculatory disorders. All patients were studied for the eye ground, intraocular and retinal pressure. The following clinical symptoms characterized this group of patients: antigiospasms, organic changes in the arterial vessels of the retina, changes in the peripapillar zones, in a normal eye retraction, a drop in the diastolic retinal pressure. Glaucoma was depicted in 27%. In patients with a tendency to cerebral paroxysms and transient disorders of cerebral circulation there were more distinct and more frequent symptoms of angiospasms, as well as signs of organic changes in the retinal arteries. The authors mark an increase in the systolic and retinal pressure and an asymmetry of it. Glaucoma was depicted in 3% of the cases.

Adult↗

[Retinal detachment, caused by hyperaemia of the choroid? Remarks on the supposed relationship between retinal detachment and "indirect trauma" (author's transl)].

It was recently stressed by Scheerer that retinal detachment in a highly myopic eye may be caused by hyperaemia of the choroid, presumably occuring during heavy physical labour which is performed by a non-trained person. Clinical studies have shown, however, that choroidal detachment, resulting from either hemorrhagic, or serous accumulation of fluid during operative procedures or during postoperative periods, is not followed by retinal detachment. Also experimental occlusion of large choroidal vessels, associated with hyperaemia in the choroidal vasculature, does not lead to retinal changes inducing the separation of the neuroretina from the pigment epithelium layer. Thus, it is concluded that choroidal hyperaemia, possibly occuring during heavy physical labour, has no relationship to the development of a retinal detachment in a "disposed" eye.

Aged↗

[Central retinal artery occlusion or branch retinal artery occlusion in the young associated with high lipoprotein (a) levels].

INTRODUCTION: High plasma lipoprotein (a) concentration is an independent risk factor for atherosclerosis and thrombosis. PATIENTS: We present the cases of two young women, one with central retinal artery occlusion and the other with branch retinal artery occlusion. Case 1: A 32-year-old woman was seen in our clinic complaining of a sudden decrease in visual acuity to 1/50 with a central visual field defect in the right eye. The fundus examination revealed an occlusion of the central retinal artery, which was confirmed by fluorescein fundus angiography. Thorough systemic evaluation showed no signs of cardiovascular disease, no coagulation abnormalities, and no clinical or biological evidence of a systemic disorder. On the other hand, hypercholesterolemia and elevated levels of lipoprotein (a) were detected. Case 2: A 35-year-old woman consulted complaining of a visual field loss in the left eye without reduction of visual acuity. Fundus examination and angiography showed the occlusion of the temporal-superior branch artery. A detailed systemic work-up revealed a pseudo-bicuspid aortic valve and high lipoprotein (a) levels. CONCLUSION: These two cases emphasize the importance of a thorough systemic evaluation of young adults with a retinal artery occlusion. High plasma lipoprotein (a) concentration is a risk factor which should not be neglected.

Adult↗

[Retinal vein occlusion. I. Pathophysiology of thrombosis and etiopathogenesis of retinal vein occlusion].

The author submits contemporary views on thrombosis. In all intravascular thromboses three mechanisms participate in varying extents: humoral, i.e. haemocoagulation, fibrinolytic and thrombocyte disorders, disorders of the vascular wall and rheological and haemodynamic disorders resp. Mechanisms of thrombosis are interlinked, activation of one group as a rule does not lead to the development of a thrombus unless it is particularly intense. As a rule combination with another group of factors is necessary. In case of venous thrombosis a key role is played by a combination of stasis and activation of the blood clotting system. In the aetiopathogenesis of occlusion of the retinal vein the author considers impairment of the vascular wall the key factor which leads to changes of the rheological conditions which predispose to thrombosis. The author describes the so-called critical retardation of the blood flow in the retinal vein as the critical level of changed rheological condition humoral factors begin to play a clinical role when in thrombogenesis. On this predisposed background humoral factors act and the result is occlusion of the retinal vein. The author considers occlusion proper a process which develops for a long time and the occlusion of the retinal vein is the final link of a long and very complicated process which is multifactorial and very variable.

Humans↗

Correlation between polarimetric retinal nerve fiber layer thickness and retinal sensitivity determined with frequency-doubling technology.

BACKGROUND AND OBJECTIVE: Correlation between polarimetric retinal nerve fiber layer thickness measured with variable corneal compensation and retinal sensitivity measured with frequency-doubling technology (FDT) and standard automated perimetry (SAP) was investigated. PATIENTS AND METHODS: Twenty-four consecutive patients with chronic open-angle glaucoma and 17 healthy control subjects (1 randomly selected eye for each subject) were evaluated. RESULTS: For all subjects, quadrant scanning laser polarimetry parameters correlated positively with both FDT and SAP mean sensitivity of the opposite hemifield (P< .001). Global scanning laser polarimetry parameters correlated positively with FDT-mean sensitivity, SAP-mean sensitivity, and FDT-mean deviation, and negatively with SAP-mean deviation (in SAP, mean deviation is positive in case of sensitivity loss) (P < or = .02). The nerve fiber indicator also correlated with FDT-pattern standard deviation and SAP-corrected loss variance (P < or = .01). Using un-logged sensitivity values, no further correlations were found. CONCLUSION: Our results show that a similar structure-function relationship exists between polarimetric retinal nerve fiber layer thickness determined with variable corneal compensation and retinal sensitivity measured with SAP and FDT.

Adult↗

Sequence variations in the retinal fascin FSCN2 gene in a Spanish population with autosomal dominant retinitis pigmentosa or macular degeneration.

PURPOSE: Only one mutation in the retinal fascin gene (FSCN2) has so far been associated with autosomal dominant retinitis pigmentosa (adRP) and macular dystrophy (adMD), in a Japanese population. Our study was designed to identify mutations in the FSCN2 gene among Spanish persons with adRP or adMD. METHODS: Denaturing gradient gel electrophoresis and direct genomic sequencing were used to evaluate the complete coding region and flanking intronic sequences of the FSCN2 gene for mutations in 150 unrelated adRP and 15 adMD index patients, and in 50 sporadic cases of retinitis pigmentosa, together with 50 controls. Ophthalmic and electrophysiological examination of retinitis pigmentosa patients and their relatives was carried out according to pre-existing protocols. RESULTS: Sixteen nucleotide substitutions were detected in the coding sequence of the index patients. Nine of these, His7Tyr, Ala122Thr, Ser126Phe, His138Tyr, Arg149Gln, Ala240Thr, Ala323Thr, Asn331His, and Phe367Leu are missense mutations, one is a nonsense mutation (Lys302Stop), and six are silent mutations. Co-segregation of the mutations in the families showed no direct relation between mutation and disease. CONCLUSIONS: The photoreceptor-specific FSCN2 gene showed a relatively high number of sequence variations. The mutation 208delG in FSCN2, the only mutation so far associated with adRP or adMD, and which presumably causes a null allele, was not detected in these Spanish families. The nonsense mutation, Lys302Stop, detected in one adRP Spanish family is not the cause of the disease. These findings support the fact that the kind and frequency of the mutations depend on the ethnic population.

Amino Acid Sequence↗

Survival of retinal ganglion cells in vitro: the effect of conditioned medium from retinal cell aggregates.

The time course of degeneration of retinal ganglion cells was studied in vitro. We used the retinae of newborn hooded rats retrogradely labeled with horseradish peroxidase injected bilaterally into the superior colliculus to permit the identification of retinal ganglion cells in culture. We tested the effect of conditioned medium either from aggregates or from explants of retinal cells on the survival of the ganglion cells. Both conditioned media approximately doubled the survival of ganglion cells after 48-72 h in culture. Our data are consistent with the hypothesis that retinal cells produce soluble trophic factors that influence ganglion cell survival.

Animals↗

Orientation of retinal in bovine rhodopsin determined by cross-linking using a photoactivatable analog of 11-cis-retinal.

A photoactivatable analog of 11-cis-retinal has been used to probe the orientation of retinal in bovine rhodopsin. The analog binds to the opsin to regenerate a chromophore with lambda max at 458 nm. The linkage site of the analog to the opsin was confirmed to be Lys-296 as in 11-cis-retinal rhodopsin. The analog-reconstituted rhodopsin activated transducin and was phosphorylated by rhodopsin kinase on illumination. On photolysis of rhodopsin containing the radioactively labeled analog at 365 nm at -15 degrees C, 20-25% of the analog was covalently linked to the protein. Proteolysis of the labeled protein and characterization of the appropriate peptides showed that cross-linking of the analog was predominantly to helices C or F. When analog reconstituted rhodopsin in rod outer segments was photolyzed, cross-linking was predominantly to helix C. However, when analog-reconstituted rhodopsin, purified in lauryl maltoside, was photolyzed, labeling occurred mainly in helix F. Sequence analysis showed major sites of cross-linking to be Phe-115, Ala-117, Glu-122, Trp-126, and Ser-127 in helix C while Trp-265 was the major site in helix F. The results suggest that the beta-ionone ring of retinal orients toward helices C and F.

Amino Acid Sequence↗

[Destruction of anionic sites in blood-retinal barrier after retinal photocoagulation].

The retinal pigment epithelial cells (RPE) have "tight junctions" at the apical side of the lateral wall between neighbouring cells and form physiological blood-retinal barriers. Recently, in addition to physiological barriers, charged barriers, consisting of anionic sites of cell membrane and its basement membrane, have been discussed. We performed weak retinal photocoagulation in rabbit eyes in order to break their charged barriers, and examined the repair process using a cationic probe, polyethyleneimine (PEI). Two days after photocoagulation, RPE cells were broken down and choriocapillaries were occluded with thrombi, and their anionic sites were lost. At one week after photocoagulation, structural reconstruction started from the edge of the photocoagulation area. In this area, proliferated RPE cells covered Bruch's membrane, but their charged barrier did not recover. Two weeks after photocoagulation, proliferated RPE cells covered Bruch's membrane over the entire photocoagulated area, and they obtained anionic charge. The present study revealed that retinal damage induced by weak laser photocoagulation was repaired within two weeks after photocoagulation with respect to the charged barrier.

Animals↗

Altered proteoglycans in cultured human retinitis pigmentosa retinal pigment epithelium.

Proteoglycans are involved in a variety of cell-cell and cell-matrix interactions. These include cell adhesion, growth regulation and a number of developmental processes. Their involvement in such interactions may be of particular importance in retinitis pigmentosa (RP) because of the detachment and migration of retinal pigment epithelial (RPE) cells often associated with this condition. Because of these important functions in cell behavior, we have been studying the proteoglycans produced by human RPE and how these may be altered in RP. Confluent cultures of RPE from normal donors and from two donors with dominantly inherited RP were labeled with 3H-glucosamine and 35SO4 and the proteoglycans isolated from the medium, substratum and two cell membrane-associated compartments, designated "EDTA-released" and "cell-associated." The proteoglycans were analyzed for size distribution by Sepharose CL-4B chromatography and for glycosaminoglycan (GAG) composition based on enzymatic and chemical susceptibilities. Differences in size distribution and GAG composition were found between the two cell-associated compartments on normal cells. Retinitis pigmentosa proteoglycans differed from their normal counterparts in corresponding compartments both in size distribution and GAG composition. Most affected were those proteoglycans released from the cell surface by EDTA. These findings may be of importance in retinitis pigmentosa since alterations in these molecules could influence the way RPE cells interact with their microenvironment.

Adult↗

Retinitis pigmentosa and retinal neovascularization: a case report.

A 21-year-old white man with retinitis pigmentosa was found to have an isolated patch of retinal neovascularization. Ocular and systemic evaluation failed to reveal a recognized cause for the neovascularization. This case is felt to represent the unusual association of retinitis pigmentosa and retinal neovascularization.

Adult↗

[Effect of hemodilution on retinal hemodynamics in retinal branch vein occlusion].

The aim of hemodilution therapy in branch retinal vein occlusion is to lower the hematocrit (HCT) and plasma viscosity and thus to ameliorate perfusion of the affected areas. In this study we compared the influence of hemodilution therapy on the retinal hemodynamics of affected areas with unaffected areas. Thirty patients with branch vein occlusion (duration of symptoms less than 14 days) aged 40-84 years (mean 63 +/- 11 years) were examined. All patients received iso- (HCT > or = 42%) or hypervolemic (HCT < 42%) hemodilution with hydroxyethyl-starch (MW 200,000/0.5 10%, HAES-steril) for 10 days. Retinal hemodynamics were quantified by means of video fluorescein angiography assessing arteriovenous passage time (AVP) of the affected and unaffected branches. Hemodilution resulted in a significant decrease in hematocrit, plasma viscosity and erythrocyte aggregation. The arteriovenous passage time of the affected area improved significantly (before therapy 4.91 +/- 2.2 s, after therapy 3.9 +/- 1.6 s). The unaffected branch showed no significant change in the arteriovenous passage time (1.85 +/- 0.7 s before and 1.79 +/- 0.7 s after therapy). The decrease in AVP in the affected branch indicates ameliorated perfusion in the affected branch area without changing the retinal hemodynamics in unaffected areas.

Adult↗