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At least 1,621 records · Page 90Linked to original sources
PubMedDate not supplied

Choroidopathy with serous retinal detachment in a patient with polymyositis.

PURPOSE: The authors report a unique case of multifocal choroidopathy in association with polymyositis. METHODS: The clinical presentation, laser treatment, and subsequent change in ocular findings are described. RESULTS: A 65-year-old Japanese man with polymyositis experienced mid acute vision impairment in both eyes during systemic corticosteroid treatment for interstitial pneumonia. Fundus examination revealed a gray-white subretinal exudate with serous retinal detachment. Angiographic examination disclosed partial dilatation of the choroidal vein at the posterior pole and dye leakage points in the retinal pigment epithelium. The patient's left eye developed bullous retinal detachment and multi focal choroidal nodules at the posterior pole during the period of tapering of oral corticosteroid administration. Retinal burns were applied to the dye leakage points in the right eye using an argon laser. Vision in the right eye showed rapid recovery due to regression of the serous retinal detachment. However, in the left eye without retinal burns visual acuity decreased to light perception only even after regression of the bullous retinal detachment and choroidopathy. CONCLUSIONS: In serous retinal detachment with choroidopathy associated with polymyositis, laser photocoagulation at leakage points may be useful for rapid restoration of vision and for the prevention of permanent severe vision loss.

Aged↗
PubMed2005

Signaling circuitries in development: insights from the retinal determination gene network.

Context-specific integration of information received from the Notch, Transforming growth factor beta, Wingless/Wnt, Hedgehog and Epidermal growth factor receptor signaling pathways sets the stage for deployment of the retinal determination gene network (RDGN), a group of transcription factors that collectively directs the formation of the eye and other tissues. Recent investigations have revealed how these transcription factors are regulated by their interactions with each other and with effectors of the above signaling pathways. Further study of the RDGN may provide insights into how common cues can generate context-specific responses, a key aspect of developmental regulation that remains poorly understood.

Animals↗
PubMed1986

Relationships between growth factors (somatomedin-C and growth hormone) and body development, metabolic control, and retinal changes in children and adolescents with IDDM.

We used the radioimmunoassay (RIA) method to determine somatomedin-C (SmC) basal values in 59 diabetic children and adolescents (20 prepubertal and 39 pubertal subjects; age range 2.75-20.16 yr; duration of diabetes 0.08-15.83 yr) and in 274 control subjects. In comparing diabetic subjects with controls, we considered only those 50 diabetic subjects who were age matched with the controls, i.e., those not over 16 yr chronological age. SmC basal levels in pubertal diabetic patients were no different from those of pubertal age-matched control children, whereas in prepubertal diabetic patients SmC was significantly lower than in the respective control children (P less than .001). No correlation was found between the z score for SmC (i.e., the number of standard deviations each SmC level is from the age- and sex-normalized mean) and duration of disease, velocity standard deviation score, severity of fluoroangiographic retinal changes, basal C-peptide values and HbA1 levels. No differences were encountered in mean SmC and SmC z-score values in the separate groups of poorly, fairly, and well-controlled diabetic children, in the groups with and without residual pancreatic activity, and in the group with and without retinal changes. In 16 of the pubertal diabetics and in 15 pubertal controls, serum glucose, growth hormone (GH), and SmC concentrations were determined during the night. The integrated nocturnal secretion of SmC was no different in diabetics than in controls, whereas the integrated nocturnal secretion of GH was significantly (P less than .025) higher in diabetics than in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Surgical techniques for giant retinal tears with retinal tacks.

In order to repair an inverted retinal flap on the choroid in case of retinal detachment with giant tears, the authors have developed a retinal tack made of acetalcopolymerisate. The tack is very durable and should remain inactive in the human body, owing to its stability under conditions of heat, alkali and acid. Manipulating the tack is adequately easy; the procedure and the tacks themselves appear to be well tolerated by the eye. The detailed design of the tack and its method of use are described in this report.

Adolescent↗
PubMed1993

[The use of domestic silicone oil in the treatment of complicated retinal detachment].

Vitrectomy and domestic silicone oil were used in the treatment of 42 eyes with complicated retinal detachment, and the retina was reattached in 34 cases or a rate of 80%, which dropped to 54% in 4-24 months postoperative. Among 7 eyes with successful retinal attachment and silicone oil removal, 1 eye developed recurrent retinal detachment. The therapeutic effect of silicone oil and operative complications were discussed. Removal of intravitreal silicone oil 3-6 months after injection was necessary to avoid adverse consequences. The study indicated that pars plana vitrectomy with silicone oil injection was an effective procedure in the management of complicated retinal detachment.

Eye Diseases↗
PubMed1993

Late recurrences after successful surgery for retinal detachment with macular hole.

Six myopic eyes affected by retinal detachment with macular hole which had been successfully reattached developed recurrent retinal detachment 7-78 months postoperatively. The mean interval between surgery and the recurrent retinal detachment was 13.4 months in five eyes managed with gas tamponade and no choroidal irritation. In an eye managed by scleral buckling with choroidal irritation, the recurrent retinal detachment occurred 78 months postoperatively. The retina was reattached following reoperation in all eyes. However, an eye successfully reattached without choroidal irritation developed four recurrences during the follow-up period. The pathogenesis of late recurrences after successful surgery for retinal detachment with macular hole remains speculative. A number of clinical findings suggest that vitreous traction plays a decisive role.

Adult↗
PubMed1991

Comparative study of clinical factors that predispose patients to proliferative vitreoretinopathy in aphakia.

To clarify the risk factors of proliferative vitreoretinopathy (PVR) in aphakia, the clinical features of 25 aphakic eyes with PVR were statistically analyzed and compared with a control group of 157 aphakic eyes with non-PVR rhegmatogenous retinal detachment. The statistically significant (P less than 0.05) factors that predisposed patients to PVR in aphakia were as follows: a history of vitreous loss on cataract surgery, retinal detachment developing within 3 months after cataract extraction, duration of retinal detachment longer than 3 months, break larger than three disc diameters, and choroidal detachment. Vitreous loss is believed to play the most important role in the development of PVR in aphakia.

Adolescent↗
PubMed2006

Müller cells in the healthy and diseased retina.

Müller glial cells span the entire thickness of the tissue, and ensheath all retinal neurons, in vertebrate retinae of all species. This morphological relationship is reflected by a multitude of functional interactions between neurons and Müller cells, including a 'metabolic symbiosis' and the processing of visual information. Müller cells are also responsible for the maintenance of the homeostasis of the retinal extracellular milieu (ions, water, neurotransmitter molecules, and pH). In vascularized retinae, Müller cells may also be involved in the control of angiogenesis, and the regulation of retinal blood flow. Virtually every disease of the retina is associated with a reactive Müller cell gliosis which, on the one hand, supports the survival of retinal neurons but, on the other hand, may accelerate the progress of neuronal degeneration: Müller cells protect neurons via a release of neurotrophic factors, the uptake and degradation of the excitotoxin, glutamate, and the secretion of the antioxidant, glutathione. However, gliotic Müller cells display a dysregulation of various neuron-supportive functions. This contributes to a disturbance of retinal glutamate metabolism and ion homeostasis, and causes the development of retinal edema and neuronal cell death. Moreover, there are diseases evoking a primary Müller cell insufficiency, such as hepatic retinopathy and certain forms of glaucoma. Any impairment of supportive functions of Müller cells, primary or secondary, must cause and/or aggravate a dysfunction and loss of neurons, by increasing the susceptibility of neurons to stressful stimuli in the diseased retina. On the contrary, Müller cells may be used in the future for novel therapeutic strategies to protect neurons against apoptosis (somatic gene therapy), or to differentiate retinal neurons from Müller/stem cells. Meanwhile, a proper understanding of the gliotic responses of Müller cells in the diseased retina, and of their protective vs. detrimental effects, is essential for the development of efficient therapeutic strategies that use and stimulate the neuron-supportive/protective-and prevent the destructive-mechanisms of gliosis.

Animals↗
PubMed2005

A case of immune recovery vitritis induced by donor leukocyte infusion for the treatment of cytomegalovirus retinitis.

Donor leukocyte infusion (DLI) has been successfully used for some life-threatening viral infections after stem cell transplantation (SCT). We describe here the first case of DLI treatment for cytomegalovirus (CMV) retinitis. A 49-year-old female patient with AML, M1 underwent SCT with a reduced-intensity conditioning regimen from HLA-haploidentical son. On day +140, the patient developed CMV retinitis of her left eye despite the continuing antiviral therapy. DLI at a dose of 1 x 10(5) CD3+ cells/kg was added to ganciclovir and foscarnet therapy. Eighteen days after the DLI, the funduscopic findings revealed improvement of the retinitis and the development of vitreous inflammation. Simultaneously, the number of CD4+ cells in the peripheral blood rapidly increased. Thus, we consider it likely that DLI induced a local immune response against CMV antigens, which resulted in the immune recovery vitritis. This case suggested the potentiality of DLI for the treatment of CMV retinitis.

Acute Disease↗
PubMed1998

Disruption of the retinal basal lamina during early embryonic development leads to a retraction of vitreal end feet, an increased number of ganglion cells, and aberrant axonal outgrowth.

Bacterial collagenase was injected into the vitreous of the eye of chick and quail embryos. Immunocytochemical and ultrastructural studies revealed that the collagenase dissolved the retinal basal lamina of the injected eye. The basal lamina disruption was first detectable 1 hour after enzyme injection and was complete within 3 hours. With further development, the retinal basal lamina was not reestablished; newly developing neuroepithelium in the peripheral retina, however, generated an intact basal lamina. Western blot analysis showed that Clostridial collagenase degraded various collagens but spared noncollagenous proteins. Basal lamina disruption of embryonic day 3 to 6 retinae led to the retraction of the end feet of the neuroepithelial cells, caused an increase in the number of Islet-1+ cells (most likely ganglion cells), an increase in the thickness of the optic fiber layer, and aberrant growth of optic axons on their way toward the optic disc. None of these changes were observed when retinal basal laminae were disrupted at later stages of development. The present data demonstrate that the retinal basal lamina, by anchoring the neuroepithelial cells to the pial surface of the retina, has an important function in the development of the normal cytoarchitecture of this structure. It is proposed that the altered extracellular environment in the vitreal part of the retina, resulting in the retraction of the neuroepithelial end feet, is responsible for the increased number of Islet-1+ cells and the aberrant axonal navigation.

Animals↗
PubMed1999

Domains of regulatory gene expression and the developing optic chiasm: correspondence with retinal axon paths and candidate signaling cells.

In mammals, some axons from each retina cross at the optic chiasm, whereas others do not. Although several loci have been identified within the chiasmatic region that appear to provide guidance cues to the retinal axons, the underlying molecular mechanisms that regulate this process are poorly understood. Here we investigate whether the earliest retinal axon trajectories and a cellular population (CD44 and stage-specific embryonic antigen 1 [SSEA] neurons), previously implicated in directing axon growth in the developing chiasm (reviewed in Mason and Sretavan [1997] Curr. Op. Neurobiol. 7:647-653), correlate with the expression patterns of several regulatory genes (BF-1, BF-2, Dlx-2, Nkx-2.1, Nkx-2.2, and Shh). These studies demonstrate that gene expression patterns in the chiasmatic region reflect the longitudinal subdivisions of the forebrain in that axon tracts in this region generally are aligned parallel to these subdivisions. Moreover, zones defined by overlapping domains of regulatory gene expression coincide with sites implicated in providing guidance information for retinal axon growth in the developing optic chiasm. Together, these data support the hypothesis that molecularly distinct, longitudinally aligned domains in the forebrain regulate the pattern of retinal axon projections in the developing hypothalamus.

Animals↗
PubMed1989

Postnatal development of the ipsilaterally projecting retinal ganglion cells in normal rats and rats with neonatal lesions.

The postnatal development of normal and anomalous uncrossed retinofugal projections in albino rats was studied using horseradish peroxidase and lectin-conjugated horseradish peroxidase as retrograde neuronal tracers. In normal rats, the number of ipsilaterally projecting retinal ganglion cells (IPRGCs) decreased continuously from more than 3000 cells on the day of birth (day 0) to slightly more than 1000 on postnatal day 5. In contrast, the number of IPRGCs in rats which received either unilateral eye enucleation or thalamectomy at birth increased abruptly to more than 4000 after 24 h on postnatal day 1, thereafter the number decreased rapidly reaching an adult level of slightly more than 2000 on postnatal day 5. The overall pattern of changes of the number, density and distribution of the IPRGCs was similar in rats which received eye enucleation or thalamectomy, although minor differences regarding the number of cells labelled in the temporal and nasal parts of retinas in rats with different lesions were detected. These findings imply that a neonatal lesion such as monocular enucleation or unilateral thalamectomy may not only result in retention of normally transient IPRGCs but also cause an increased number of IPRGCs by misrouting, rerouting or collateral sprouting of optic axons at the optic chiasma that could significantly affect the developing optic pathway. Furthermore, the differential effects of the two types of neonatal lesions upon the IPRGCs provide further evidence to previous findings that different mechanisms might be involved in generating the anomalously enlarged uncrossed retinofugal projections in rodents.

Aging↗
PubMedDate not supplied

Development of the primate area of high acuity, 3: temporal relationships between pit formation, retinal elongation and cone packing.

By establishing an avascular, highly elastic, region within the fetal area of high acuity (AHA), the developing primate eye has created a unique substrate on which the mechanical forces of intraocular pressure (IOP) and growth-induced retinal stretch (stretch) can act. We proposed (Springer & Hendrickson, 2004b) that these forces generate both the pit and high cone density found in the adult AHA. In this paper, we use quantitative measures to determine the temporal relationships between nasal and temporal retinal elongation, changes in pit depth, cone packing, and cone morphology over M. nemestrina retinal development. Retinal length increased rapidly to about 105 days postconception (dpc; Phase 1) and then elongation virtually ceased (Phase 2) until just after birth (180 dpc). Retinal elongation due to stretch resumed during Phase 3 until approximately 315 dpc (4-5 months), after which time the retina appeared mature (Phase 4). The pit appeared during the quiescent Phase 2, suggesting that IOP acts, in conjunction with molecular changes in the inner retina, on the highly elastic, avascular, AHA to generate a deep, narrow pit and causes inner retinal cellular displacements. Subsequently (Phase 3), the pit widened, became 50% shallower and central inner retinal lamina thinned slightly due to a small amount of retinal stretch occurring in the AHA. Centripetal movement of cones was minimal until just after birth when the pit reached 88% of its maximal depth. Accelerated cone packing during Phase 3 was temporally correlated with increased stretch.

Animals↗
PubMed1989

Correlation of fibrosis and transforming growth factor-beta type 2 levels in the eye.

Approximately 1 out of every 10 eyes undergoing surgery for retinal detachment develops excessive intraocular fibrosis that can lead to traction retinal detachment and ultimate blindness. This disease process has been termed proliferative vitreoretinopathy (PVR). The ability to monitor and grade this fibrotic response accurately within the eye as well as the ability to aspirate vitreous cavity fluid bathing the fibrotic tissue makes this an ideal setting in which to investigate the development of fibrosis. Although laboratory studies have recently shown that transforming growth factor-beta (TGF-beta) can enhance fibrosis, little clinical evidence is yet available correlating the level of this or other growth factors with the degree of fibrosis in a clinical setting. We have found that vitreous aspirates from eyes with intraocular fibrosis associated with PVR have more than three times the amount of TGF-beta (1,200 +/- 300 pM [SEM]) found in eyes with uncomplicated retinal detachments without intraocular fibrosis (360 +/- 91 pM [SEM]). Using an in vitro assay, 84-100% of the TGF-beta activity could be blocked with specific antibodies against TGF-beta 2, whereas only 10-21% could be blocked by specific antibodies against TGF-beta 1. TGF-beta 1 was used in an animal model of traction retinal detachment. Since beta 1 and beta 2 have essentially identical biologic effects and only human beta 1 was available in quantities required, beta 1 was chosen for these in vivo studies. The injection of TGF-beta1 plus fibronectin (FN) but not TGF-beta1 alone into the vitreous cavity of rabbits resulted in the increased formation of intraocular fibrosis and traction retinal detachments as compared to control eyes. In previous studies, intravitreal FN levels were also found to be elevated in eyes with intraocular fibrosis.

Adolescent↗