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At least 649 records · Page 36Linked to original sources
PubMed2004

[Perfluorohexyloctane as internal tamponade in patients with complicated retinal detachment. Results after 6 months].

BACKGROUND: Perfluorohexyloctane (F6H8) is the first medium that can be transiently used as postoperative heavy vitreous substitute expanding the technique of intraocular tamponade by the principle of an inferiorly acting medium. Legally it can be used for up to 3 months. So far very few clinical reports are available on the efficacy and possible complications of F6H8. It was the aim to analyze this in a group of patients with retinal redetachment after one or several previous retinal/vitreoretinal interventions. PATIENTS AND METHODS: This study included 17 patients (10 male, 7 female, median age 66 years, range 34-88 years) with a complicated retinal redetachment (at least inferior quadrants). Median duration of intraocular F6H8 use was 25 days. Follow-up was limited to 6 months. RESULTS: Primary retinal reattachment could be achieved in 16/17 eyes. 8/17 developed retinal redetachment during follow-up. After additional surgery 12/17 presented complete retinal attachment, 4/17 subtotal attachment and 1/17 total retinal detachment. The latter was enucleated as a consequence of several further complications such as chronic hypotony, severe keratopathy and painful atrophy. The spectrum of complications during and after F6H8 tamponade included dispersion 17/17 (10/17 clinical, 7/17 minor), hypotony (endpoint) 14/17, massive cell precipitation on lens/IOL or in the anterior segment 7/17, severe progression of capsular fibrosis (8/17), and keratopathy 6/17. CONCLUSIONS: The spectrum of postoperative complications after F6H8 use, especially the high proportion of eyes with chronic hypotony, indicates that F6H8 may not be a recommendable option in eyes with a complicated surgical history.

Adult↗
PubMedDate not supplied

Voltage-gated calcium and sodium currents of starburst amacrine cells in the rabbit retina.

The voltage-gated calcium and sodium currents of starburst amacrine cells were examined in slices of the adult rabbit retina. ON-center starburst amacrine cells were targeted for whole-cell recording by prelabeling the retina with the nuclear dye 4'-6-diamidino-2-phenylindole hydrochloride (DAPI). Calcium currents were isolated using an external Ringer that contained tetrodotoxin to block sodium currents and barium to block potassium channels. When starburst amacrine cells were stepped to holding potentials positive to -50 mV, a series of voltage-dependent calcium currents were activated. The calcium current peaked at -10 mV. The calcium currents kinetics were mainly sustained in nature, showing only a small amount of slow inactivation. Nickel (100 microM), a T-type channel blocker, had no effect on the calcium current. Application of the L-type channel agonist BAY K8644 (1-2.5 microM) had small variable effects on the calcium current while the L-type channel antagonist nifedipine (10 microM) had no effect. However, addition of a reported N-type calcium channel antagonist, omega-conotoxin G6A (1 microM), blocked a large portion of the calcium current, as did a more nonselective antagonist, omega-conotoxin M7C (200 nM). Agatoxin 4A (500 nM) reduced a smaller sustained calcium current component, implying a P/Q-type calcium channel was present on these neurons. In addition to the calcium currents, a fast voltage-gated sodium current was observed in many starburst cells. This current could be blocked by tetrodotoxin (200-500 nM). The differing kinetics and durations of the sodium and calcium currents could play important roles in the regulation of synaptic release and in the coordination of spiking by starburst amacrine cell dendrites during retinal development and in the encoding of motion across the retinal surface.

Action Potentials↗
PubMed1997

Expression of Sonic hedgehog and its putative role as a precursor cell mitogen in the developing mouse retina.

We show that Sonic hedgehog and patched are expressed in adjacent domains in the developing mouse retina. Treatment of cultures of perinatal mouse retinal cells with the amino-terminal fragment of Sonic hedgehog protein results in an increase in the proportion of cells that incorporate bromodeoxuridine, in total cell numbers, and in rod photoreceptors, amacrine cells and Muller glial cells, suggesting that Sonic hedgehog promotes the proliferation of retinal precursor cells. These findings suggest that hedgehog and patched are part of a conserved signalling pathway in retinal development in mammals and insects.

Aging↗
PubMed1998

Time-specific action of N-methyl-N-nitrosourea in the occurrence of retinal dysplasia and retinal degeneration in neonatal mice.

The morphologic response of neonatal mouse retina to the alkylating agent N-methyl-N-nitrosourea (MNU) was examined at different periods of retinal development. A dose of 60 mg/kg N-methyl-N-nitrosourea was injected intraperitoneally to neonatal C57BL mice at 0, 3, 5, 8, 11, 14, 17, and 20 days of age and to C3H mice at 0 days of age, and the retinas were examined sequentially. In the C57BL mice, MNU evoked a time-dependent occurrence of retinal dysplasia and retinal degeneration. With MNU treatment at day 0 and day 3 (the stage of retinal cell proliferation), retinal dysplasia characterized by the progressive disorganization of neuroblasts, which led to the formation of rosettes, was found in the outer neuroblastic/nuclear layer above the normal pigment epithelial cells during days 8-20, but decreased at day 50. The rosettes were surrounded by photoreceptor segments and Müller cell processes, and by photoreceptor nuclei. The MNU response was related to retinal differentiation; following MNU treatment at day 5 or 8 (the stage of retinal cell differentiation) the cells were much less sensitive (i.e. no retinal response was found). However, with MNU treatment at days 11, 14, 17, and 20 (after cellular differentiation), retinal degeneration characterized by selective photoreceptor apoptosis was seen. These results suggest that there is a critical period for the time of MNU administration in the development of mouse retinal lesions. In C3H (rd/rd) mice, MNU treatment at day 0 resulted in retinal degeneration with only slight rosette formation at the peripheral retina.

Animals↗
PubMed1990

Retinal vasculitis as a complication of rheumatoid arthritis.

Two middle-aged women developed retinal vasculitis in the moderately active phase of classical rheumatoid arthritis. Fluorescein angiography disclosed diffuse leakage from the retinal capillaries and cystoid macular edema, which subsided in response to oral steroid. They did not show any clinical signs of vasculitis in other parts of the body. Retinal vasculitis should be included in the list of complications observed in rheumatoid arthritis.

Adrenal Cortex Hormones↗
PubMed1992

Cellular interactions determine neuronal phenotypes in rodent retinal cultures.

Progenitor cells isolated from early rat embryo retinas differentiate into phenotypes normally generated early in retinal development (e.g., ganglion cells), whereas progenitors isolated from postnatal retinas differentiate into later-generated retinal cell types (e.g., rod photoreceptors; Reh and Kljavin, J. Neurosci. 9:4179-4189; 1989; Adler and Hatlee, 1989; Science 243:391-393; Sparrow, Hicks, and Barnstable, 1990, Dev. Brain Res. 51:69-84). To determine whether this change in committment is intrinsic to the progenitor cells, or alternatively can be modified by interactions with their developing environment, I co-cultured mouse and rat retinal cells, from different developmental stages, and identified the resulting phenotypes with species-specific and cell class-specific antibodies. I found that the phenotypes into which mouse neuroepithelial cells differentiate depends on the phenotypes of the rat cells that surround them. Retinal precursor cells from embryonic day (E) 10-12 will adopt the rod photoreceptor phenotype only when close to cells expressing this phenotype. By contrast, when the E10-12 retinal progenitor cells are cultured with cells from the cerebral cortex, they differentiate primarily into large multipolar neurons, similar in their morphology and antigen expression to retinal ganglion cells. These results indicate that interactions among the cells of the developing retina are important in the determination of cell fate.

Animals↗
PubMed1997

Correction of retinal abnormalities found in albinism by introduction of a functional tyrosinase gene in transgenic mice and rabbits.

The factors that regulate normal retinal development remain obscure. However, it is known that elements in the retinal pigment epithelium are critical. When melanin is absent there is a reduction in rods, the central retina fails to develop fully and there is a systematic distortion in the chiasmatic projection to the brain. It has been demonstrated using transgenic mice that the chiasmatic abnormality is controlled by the tyrosinase gene, which is the key enzyme in melanin synthesis. Here we examine whether the two retinal deficits are regulated by this gene. We have examined the distribution of photoreceptors in an albino mouse strain in which a functional tyrosinase gene has been inserted and compared these transgenics with albino and wild type mice. In albinos, rod photoreceptors were reduced by approximately 30%, but were normal in the transgenics. Cone numbers were unchanged. Cell density in the ganglion cell layer was examined in transgenic rabbits, in which albinism had also been rescued with the tyrosinase gene. Normal rabbits have a steep gradient in cell density between central and peripheral retina. Cell density was abnormally low in the central retina in albinos, but normal in the transgenics. Hence, the tyrosinase gene is responsible for each of the retinal deficits associated with albinism. However, it is not clear whether this is due to the absence of melanin or whether the key agent is an associated cell product.

Albinism, Ocular↗
PubMed1999

Retinal manifestations of HIV-1 and HIV-2 infections among hospital patients in The Gambia, west Africa.

BACKGROUND: In developed countries, 50-75% of AIDS patients develop retinal complications and about 20-40% acquire cytomegalavirus (CMV) retinitis. We conducted a cross-sectional survey to determine prevalence of these in The Gambia where both HIV-1 and HIV-2 infection are present and the prevalence of HIV-1 is rising. METHOD: All patients attending hospital whose percentage CD4+ cells (CD4%) was below 14, the level associated typically with an AIDS diagnosis, and one half of those whose CD4% was 14 or above were asked to join the study. Fifty-six HIV-1, 52 HIV-2 and 12 dually infected patients were recruited. Photographs of the fundi were taken and interpreted independently. The findings were related to the patients' percentage CD4+ cells. RESULTS: The CD4% was < 14 in 40 patients and < 7 in 17 patients. Thirty-six patients were male. No cases of CMV retinitis were found. Four patients whose CD4% were 4, 5, 11 and 23 had cotton wool spots ranging in number from 1 to 14 for any one patient. The prevalence of cotton wool spots was 8% (95% CI, 0-16%) among patients with CD4% below 14 and 12% (95% CI, 0-27) among patients with CD4% below 7. One of the 4 patients had associated microaneurysm and blot haemorrhages typical of more advanced HIV microvasculopathy. CONCLUSION: CMV retinitis is less common in The Gambia than in developed countries. Non-infectious retinopathy may also be less common.

AIDS-Related Opportunistic Infections↗
PubMed2004

The winged helix transcription factor Foxg1 facilitates retinal ganglion cell axon crossing of the ventral midline in the mouse.

During normal development, retinal ganglion cells (RGCs) project axons along the optic nerve to the optic chiasm on the ventral surface of the hypothalamus. In rodents, most RGC growth cones then cross the ventral midline to join the contralateral optic tract; those that do not cross join the ipsilateral optic tract. Contralaterally projecting RGCs are distributed across the retina whereas ipsilaterally projecting RGCs are concentrated in temporal retina. The transcription factor Foxg1 (also known as BF1) is expressed at several key locations along this pathway. Analysis of Foxg1 expression using lacZ reporter transgenes shows that Foxg1 is normally expressed in most, if not all, nasal RGCs but not in most temporal RGCs, neither at the time they project nor earlier in their lineage. Foxg1 is also expressed at the optic chiasm. Mice that lack Foxg1 die at birth and, although the shape of their eyes is abnormal, their retinas still project axons to the brain via the optic chiasm. Using anterograde and retrograde tract tracing, we show that there is an eightfold increase in the ipsilateral projection in Foxg1-/- embryos. The distributions of cells expressing the transcription factors Foxg1 and Nkx2.2, and cell-surface molecules Ephb2, ephrin B2 and SSEA-1 (Fut4) have been correlated to the normally developing retinothalamic projection and we show they are not much altered in the developing Foxg1-/- retina and optic chiasm. As much of the increased ipsilateral projection in Foxg1-/- embryos arises from temporal RGCs that are unlikely to have an autonomous requirement for Foxg1, we propose that the phenotype reflects at least in part a requirement for Foxg1 outwith the RGCs themselves, most likely at the optic chiasm.

Animals↗
PubMed2001

Development of the primate retinal vasculature.

Human and macaque retinae have similar retinal vascular anatomy. The general features of the retinal vascular anatomy of these two primates have much in common with more widely studied animal models such as rat and cat. However, primates are unique amongst mammals in having a region in temporal retina specialized for high visual acuity, which includes the fovea centralis (or 'fovea'). Several features distinguish the fovea from other parts of the retina, including a very high local density of cone photoreceptors, a high density of inner retinal cells during development, and an absence of retinal blood vessels. The retinal vascular complex comprises a number of cell types, in addition to vascular endothelial cells, including pericytes, microglia, astrocytes-none of which is intrinsic to the retina. In addition, amacrine-like cells make bouton-like associations with retinal vessels and may be involved in the autoregulation of blood flow. During development endothelial cells 'invade' the retina, accompanied by a population of microglial cells; glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes are also seen associated with the developing vasculature, and are in advance of the vascular front by a few hundred microns. Recent findings indicate that astrocytes at the vascular front proliferate in response to factors released by endothelial cells, including leukemia inhibitory factor. Better understood is the role of GFAP-immunoreactive astrocytes just in advance of the developing vessels. These astrocytes are sensitive to hypoxia and in response release vascular endothelial growth factor (VEGF) which in turn promotes the migration, differentiation and proliferation of vascular endothelial cells. This hypoxia/VEGF-mediated process of migration, proliferation and differentiation appears common to the retinae of a variety of species, including human. However, in human and macaque retina, different mechanisms appear to govern the development of the retinal vessels growing along the horizontal meridian of the retina towards the central area, which contains the fovea. Despite the relatively advanced state of differentiation and maturation of cells in the central area compared with the periphery, the growth of retinal vessels into the central area has been described as 'retarded', and the incidence of cell proliferation associated with these vessels is lower than in peripheral vessels. Furthermore, neither retinal vessels nor their accompanying astrocytes grow into a circumscribed region which, at a later stage, develops into the foveal depression. These observations suggest that molecular markers define the foveal region and inhibit cell proliferation and vascular growth at the fovea and, perhaps, along the horizontal meridian. The findings also suggest that at the fovea, the retina is adapted morphologically to its blood supply, since in the vicinity of the fovea, the development of retinal vessels is retarded or inhibited. The limitations on vascularization of central retina has implications for its vulnerability to degenerative changes, as seen in age-related macular degeneration.

Animals↗
PubMed1997

Developmental expression of nitric oxide synthase isoform I and III in chick retina.

During our studies on the multiple possible functions of nitric oxide (NO) in chick retinal development and physiology, we have demonstrated the presence and the activity of NO synthase (NOS-I and III) in certain neuronal populations (photoreceptors, amacrine cells in the inner nuclear and ganglion cells) and also in synaptic-rich regions in the developing chick retina. Both enzymes, detected by nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase, immunohistochemistry and Western blotting, appeared between embryonic days 6 and 12, and followed a spatial and temporal pattern of expression which correlated with the differentiation of the neuronal layers. Evaluation of the conversion of [3H]-labeled arginine to [3H]-citrulline, confirmed the presence of a calcium-dependent NOS activity in the cytosolic and particulate retinal extracts during the development. This pattern of NOS expression suggests that the regulated release of NO during key phases of development might be one mechanism involved in the regulation of retinal differentiation.

Animals↗
PubMed2002

Combining phacoemulsification with vitrectomy for treatment of macular holes.

AIM: To describe the results of combined phacoemulsification, insertion of posterior chamber intraocular lens (PCIOL), and pars plana vitrectomy for patients with macular hole. METHODS: A case series of 89 consecutive patients with macular hole who underwent combined phacoemulsification, insertion of PCIOL, posterior capsulectomy, and pars plana vitrectomy. RESULTS: 80 of 89 patients (89%) had their holes closed with the combined surgery. Four of the nine patients who failed had their holes closed with one further procedure. Of the 89 patients operated on, 61 (65%) had vision of 20/40 or better. Three patients (3%) had Snellen acuity of less than 20/400 postoperatively. Three patients (3%) developed retinal detachments, one with proliferative vitreoretinopathy (PVR). Eight patients (9%) developed CMO. Three patients developed late reopening of their macular holes after remaining closed for 9 months or more. CONCLUSION: Combined phacoemulsification, insertion of PCIOL, and pars plana vitrectomy surgery can be used to treat macular holes. Combining cataract surgery with vitrectomy surgery may prevent a later second operation for post-vitrectomy cataract formation.

Aged↗
PubMed1993

Survival prognosis of patients with retinal artery occlusion and associated carotid artery disease.

The records of 151 patients who developed retinal arterial obstruction were reviewed to evaluate the survival prognosis of these patients. Survival rates were calculated to expected rates of an age- and sex-matched control group of patients without retinal arterial obstruction. The presence of visible embolus and a branch retinal artery occlusion were found to be significant factors for worse survival prognosis (P = 0.0001 and P = 0.001, respectively). The survival rate of the entire group of 151 patients with retinal artery occlusion was not significantly different from that of the age- and sex-matched group (P = 0.29). Among the patients evaluated with continuous-wave Doppler sonography, the presence or the absence of the atheromatous carotid disease did not significantly affect the survival.

Adolescent↗
PubMed1981

Retinal arterial obstruction in children and young adults.

The records of 27 patients who developed retinal arterial obstruction (RAO) prior to the age of 30 years were studied to ascertain associated systemic and ocular findings as possible etiologic factors. A history of migraine was found in approximately one third of the patients, and coagulation abnormalities wer also common. Trauma, sickle cell hemoglobinopathies, cardiac disorders, use of oral contraceptives, pregnancy, systemic lupus erythematosus and intravenous drug abuse were less frequently encountered. Ocular abnormalities included increased intraocular pressure, subtle buried drusen of the optic nerve head and a congenital prepapillary arterial loop. In contrast to older patients with RAO, there was no clinical evidence of atheromatous disease. In most patients, one or more systemic or ocular etiologic factors could be discerned. Whereas etiologic relationships may be multifactorial and generally differ from those commonly found in older patients with RAO, the visual prognosis in younger and older patients appears to be similar.

Adolescent↗
PubMed1991

Clinicopathologic correlation of retinal to choroidal venous collaterals of the optic nerve head.

An optic nerve meningioma developed in an elderly woman and was followed for 13 years until her death. The optic nerve was initially normal. Over time it became swollen and then atrophic and developed retinal venous to choroidal venous collaterals. Five hundred serial sections were prepared through the optic nerve and for approximately 1.5 mm superiorly and inferiorly to the optic nerve to trace the course of the collaterals that were seen ophthalmoscopically and angiographically in the optic nerve head. This clinicopathologic study shows clearly that the abnormal channels are, in fact, retinal venous to choroidal venous collaterals (bypass channels). Four collaterals extended around the end of Bruch's membrane at the optic nerve head. Two more collaterals extended through the retinal pigment epithelium to become continuous with a subretinal pigment epithelial neovascular membrane, the vessels of which connected with the choroidal vessels through a defect in Bruch's membrane.

Aged↗
PubMed1993

Secondary retinitis pigmentosa and cerebral demyelination in Lyme borreliosis.

A 15-year-old girl developed retinitis pigmentosa-like fundus changes in the left eye and optic neuropathy in the right eye as well as cerebral demyelination as a result of late Lyme borreliosis (LB). The diagnosis was confirmed by polymerase chain reaction, which detected a Borrelia burgdorferi specific segment of a gene coding for 41 kD endoflagellin, both in the vitreous and the cerebrospinal fluid. The diagnosis was delayed because testing for Borrelia antibodies in serum and cerebrospinal fluid yielded negative results. However, later on, another laboratory reported the antibodies of the patient's pretreatment serum to be positive for LB.

Adolescent↗
PubMed1989

Retinal periphlebitis after hormonal treatment.

Two cases, those of a man and a woman, developed retinal periphlebitis after hormonal treatment for infertility and contraceptives, respectively. Both had a unilateral severe decrease in visual acuity, and a central scotoma and defect in color vision were also present. The fundus had retinal edema, especially of the macula, a hyperemic disc with blurred margins, normal arteries, congested veins, and marked sheathing along the main veins, with retinal hemorrhages in the inferior half of the retina. Fluorescein angiography showed a delayed filling of the veins in the affected retina and late staining of these veins. Since there was severe visual impairment in each case, systemic adrenocorticosteroids were administered, and a rapid improvement in visual acuity occurred. In one patient, a trace Marcus-Gunn sign, a few small paracentral scotomas, and a defect in color vision were permanent sequelae.

Adult↗
PubMed2001

The perplexed and confused mutations affect distinct stages during the transition from proliferating to post-mitotic cells within the zebrafish retina.

To identify and study genes essential for vertebrate retinal development, we are screening zebrafish embryos for mutations that disrupt retinal histogenesis. Key steps in retinogenesis include withdrawal from mitosis by multipotent neuroepithelial cells, specification to particular cell types, migration to the appropriate laminar positions, and molecular and morphological differentiation. In this study, we have identified two recessive mutations that affect the transition of proliferating neuroepithelial cells to postmitotic retinal cells. Both the perplexed and confused mutant phenotypes were initially detectable when the first retinal neuroepithelial cells began to leave the cell cycle. At this time, each mutant retina showed increased cell death and a lack of morphological differentiation. Cell death was found to be apoptotic in both perplexed and confused retinas based on TUNEL analysis and activation of caspase-3. TUNEL-phosphoRb-BrdU colocalization studies indicated that the perplexed mutation caused death in cells transitioning from a proliferative to postmitotic state. For the confused mutation, TUNEL-phosphoRb-BrdU analysis revealed that only a subset of postmitotic cells were induced to activate apoptosis. Mosaic analysis demonstrated that within the retina the perplexed mutation functions noncell-autonomously. Furthermore, whole lens or eye cup transplantations indicated that the retinal defect was intrinsic to the retina. Mosaic analysis with confused embryos showed this mutation acts cell-autonomously. From these studies, we conclude that the perplexed and confused genes are essential at distinct stages during the transition from proliferating to postmitotic cells within the zebrafish retina.

Animals↗