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At least 613 records · Page 34Linked to original sources
PubMed2001

The ganciclovir implant plus oral ganciclovir versus parenteral cidofovir for the treatment of cytomegalovirus retinitis in patients with acquired immunodeficiency syndrome: The Ganciclovir Cidofovir Cytomegalovirus Retinitis Trial.

PURPOSE: To compare the regimen of the ganciclovir implant plus oral ganciclovir to one of intravenous cidofovir for the treatment of cytomegalovirus retinitis. METHODS: Sixty-one patients with acquired immunodeficiency syndrome and cytomegalovirus retinitis were randomized either to the regimen of the ganciclovir implant plus oral ganciclovir, 1 gm three times daily, or intravenous cidofovir, 5 mg/kg once weekly for two doses, followed by 5 mg/kg every other week. RESULTS: Mortality was similar between the two treatment groups. Mortality rates were 0.41 per person-year in patients assigned to the ganciclovir regimen and 0.49 per person-year in patients assigned to cidofovir (P =.59). Ocular outcomes were similar between the two groups. Retinitis progression occurred at a rate of 0.67 per person-year in the ganciclovir group and 0.71 per person-year in the cidofovir group (P =.72). A loss of visual acuity of 15 letters or more occurred at a rate of 0.78 per person-year in the ganciclovir group and 0.47 per person-year in the cidofovir group (P =.28). The rate of loss of visual field was 7 degrees per month in the ganciclovir group and 2 degrees per month in the cidofovir group (P =.048). Vitreous hemorrhage was more common in the ganciclovir implant group (0.13 per person-year) than in the cidofovir group (no cases, P =.014), whereas uveitis appeared to be more common in the cidofovir group (0.35 per person-year) than in the ganciclovir group (0.09 per person-year, P =.066). Nephrotoxicity (serum creatinine 1.6 mg/dL or greater) occurred at a rate of 0.18 per person-year in the ganciclovir group and 0.48 per person-year in the cidofovir group (P =.10). CONCLUSIONS: Although the small number of patients in this study limits definitive interpretation, these data suggest that in the era of highly active antiretroviral therapy, the regimens of the ganciclovir implant plus oral ganciclovir and of intravenous cidofovir are similar for controlling cytomegalovirus retinitis and preventing visual loss but have different side effects.

AIDS-Related Opportunistic Infections↗
PubMed1999

Limiting the proliferation and reactivity of retinal Müller cells during experimental retinal detachment: the value of oxygen supplementation.

PURPOSE: To assess the role of hypoxia in inducing the proliferation, hypertrophy, and dysfunction of Muller cells in detached retina and the effectiveness of supplemental oxygen in limiting these reactions. METHODS: Retinal detachments were produced in the right eye of each of 13 cats; the cats survived surgery for 3 days, during which six were kept in normoxia (room air, 21%) and seven in hyperoxia (70% oxygen). Retinas were labeled for proliferation with an antibody (MIB-1) to a cell cycle protein (Ki-67), for evidence of hypertrophy employing antibodies to the intermediate filament protein glial fibrillary acidic protein (GFAP) and to beta-tubulin and for disturbance of glutamate neurochemistry employing antibodies to glutamate to a glutamate receptor (GluR-2) and to glutamine synthetase. RESULTS: Results from the two animals kept in normoxia after retinal detachment confirmed previous reports that detachment caused the proliferation of Muller cells, the hypertrophy of Muller cell processes, and the disruption of glutamate recycling by Muller cells. Oxygen supplementation during detachment reduced Muller cell proliferation and hypertrophy and reduced the abnormalities in the distributions of glutamate, GluR-2, and glutamine synthetase. CONCLUSIONS: Oxygen supplementation reduced the reaction of retinal Muller cells to retinal detachment, limiting their proliferation and helping to maintain their normal structure and function. In the clinical setting, oxygen supplementation between diagnosis and reattachment surgery may reduce the incidence and severity of glial-based complications, such as proliferative vitreoretinopathy.

Animals↗
PubMed1998

Renal-retinal syndromes: association of retinal anomalies and recessive nephronophthisis in patients with homozygous deletion of the NPH1 locus.

Tapeto-retinal degeneration is frequent in patients with nephronophthisis. Association of the most severe forms of tapeto-retinal dystrophy with NPH identifies a syndrome described first by Senior et al and Loken et al. This syndrome is distinct on molecular grounds from pure renal nephronophthisis (NPH1), which has its gene locus mapped on chromosome 2q13. We describe three families with large homozygous deletion of the NPH1 locus in which mild to moderate ocular lesions due to tapeto-retinal degeneration coexisted and were correlated to renal defects. This new association of NPH1 with retinal dystrophy is characterized by focal lesions of retina and is pauci-symptomatic in clinical presentation. For this reason it may remain unrecognized in most NPH1 patients.

Adult↗
PubMed2002

Retinal ganglion cell differentiation in cultured mouse retinal explants.

The availability of genetically engineered mice harboring specific mutations in genes affecting one or more retinal cell types affords new opportunities for investigating the genetic regulatory mechanisms of vertebrate retina formation. When identifying critical regulatory genes involved in retina development it is often advantageous to complement in vivo analysis with in vitro characterization. In particular, by combining classical techniques of retinal explant culturing with gene transfer procedures relying on herpes simple virus (HSV) amplicon vectors, gain-of-function analysis with genes of interest can be performed quickly and efficiently. Here, details are provided for isolating and culturing explants containing retinal progenitor cells and for infecting the explants with HSV expression vectors that perturb or rescue retinal ganglion cells, the first cell type to differentiate in the retina. In addition, the availability of sensitive techniques to monitor gene expression, including detection of reporter gene expression using antibodies and detection of endogenous marker gene expression using quantitative RT-PCR, provides an effective means for comparing wild-type and mutant retinas from genetically engineered mice.

Animals↗
PubMedDate not supplied

Does hyperbaric oxygen (HBO) delivery rescue retinal photoreceptors in retinitis pigmentosa?

As previously reported in the literature, hyperbaric oxygen delivery seems to modify the natural course of retinitis pigmentosa. In order to evaluate these first encouraging data, 48 affected subjects were separately studied in two subgroups (cases and controls). All patients underwent yearly an ophthalmological examination completed by a maximum amplitude electroretinogram, conducted according to our 'differential derivation' system, a new recording technique specifically designed to enhance the signal-to-noise ratio. Oxygen delivery was provided regularly for 90 min daily (2.2 Absolute Atmosphere) in three cycles according to a standard protocol. In the cases, electroretinographic mean values were as follows: at T0 (basal) 4.68 +/- 3.81 microV; after one year (T1) 8.46 +/- 5.71 microV; at two years (T2) 10.7 +/- 7.6 microV; at the end of the study (T3) 14.4 +/- 11.7 microV. In the controls, electroretinographic mean values were as follows: at T0 4.92 +/- 3.05 microV; at T1 5.04 +/- 3.07 microV; at T2 3.46 +/- 2.77 microV: at T3 2.97 +/- 3.61 microV. Amplitudes showed a remarkable (p<0.001) increase in the cases, while a slightly significant (p<0.02) decrease was evident at the end of the study in the controls. In our opinion, retinal oxygen availability may be critical in retinal degeneration and hyperbaric oxygen delivery, inducing hyperoxia, seems to be able to bring about the rescue of the retinal photoreceptors helping them in their metabolic requirements. Unfortunately, our study demonstrates an increase in electroretinographic responses only, which may not necessarily also mean an evident change in visual acuity.

Adolescent↗
PubMed2000

Concentration of astrocytic filaments at the retinal optic nerve junction is coincident with the absence of intra-retinal myelination: comparative and developmental evidence.

The structure of the lamina cribrosa (LC) and astrocytic density were examined in various species with and without intra-retinal myelination. Sections of optic nerve from various species were stained with Milligan's trichrome or antibodies to glial fibrillary acidic protein, myelin basic protein (MBP) and antibody O4. Marmoset, flying fox, cat, and sheep, which lack intraretinal myelination, were shown to possess a well-developed LC as well as a marked concentration of astrocytic filaments distal to the LC. Rat and mouse, which lack intraretinal myelination, lacked a well-developed LC but exhibited a marked concentration of astrocytic filaments in this region. Rabbit and chicken, which exhibit intraretinal myelination, lacked both a well-developed LC and a concentration of astrocytes at the retinal optic nerve junction (ROJ). A marked concentration of astrocytes at the ROJ of human fetuses was also apparent at 13 weeks of gestation, prior to myelination of the optic nerve; in contrast, the LC was not fully developed even at birth. This concentration of astrocytes was located distal to O4 and MBP immunoreactivity in human optic nerve, and coincided with the site of initial myelination of ganglion cell axons in marmoset and rat. Myelination proceeded from the chiasm towards the retinal end of the human optic nerve. Moreover, the outer limit of oligodendrocyte precursor cells (OPC) migration into the rabbit retina was restricted by the outer limit of astrocyte spread. These observations indicate that a concentration of astrocytic filaments at the ROJ is coincident with the absence of intraretinal myelination. Differential expression of tenascin-C by astrocytes at the ROJ appears to contribute to the molecular barrier to OPC migration (see Bartsch et al., 1994), while expression of the homedomain protein Vax 1 by glial cells at the optic nerve head appears to inhibit migration of retinal pigment epithelial cells into the optic nerve (see Bertuzzi et al., 1999). These observations combined with our present comparative and developmental data lead us to suggest that the astrocytes at the ROJ serve to regulate cellular traffic into and out of the retina.

Aging↗
PubMed2003

Identification and characterisation of the retinitis pigmentosa 1-like1 gene (RP1L1): a novel candidate for retinal degenerations.

Retinitis pigmentosa (RP) is the most common form of inherited retinopathy, with an approximate incidence of 1 in 3700 individuals worldwide. Mutations in the retinitis pigmentosa 1 (RP1) gene are responsible for about 5-10% cases of autosomal dominant RP. The RP1 gene is specifically expressed in the photoreceptor layers of the postnatal retina and encodes a predicted protein characterised by the presence of two doublecortin (DC) domains, known to be implicated in microtubule binding. We identified and characterised, both in human and in mouse, a novel mammalian gene, termed Retinitis Pigmentosa1-like1 (RP1L1), because of its significant sequence similarity to the RP1 gene product. The sequence homology between RP1 and RP1L1 was found to be mostly restricted to the DC domains and to the N-terminal region, including the first 350 amino acids. The RP1L1 gene was also found to be conserved in distant vertebrates, since we identified a homologue in Fugu rubripes (pufferfish). Similar to RP1, RP1L1 expression is restricted to the postnatal retina, as determined by semiquantitative reverse transcriptase-PCR and Northern analysis. The retina-specific expression and the sequence similarity to RP1 render RP1L1 a potential candidate for inherited retinal disorders.

Amino Acid Motifs↗
PubMed2005

Long-term preservation of retinal function in the RCS rat model of retinitis pigmentosa following lentivirus-mediated gene therapy.

The Royal College of Surgeons (RCS) rat is a well-characterized model of autosomal recessive retinitis pigmentosa (RP) due to a defect in the retinal pigment epithelium (RPE). It is homozygous for a null mutation in the gene encoding , a receptor tyrosine kinase found in RPE cells, that is required for phagocytosis of shed photoreceptor outer segments. The absence of Mertk results in accumulation of outer segment debris. This subsequently leads to progressive loss of photoreceptor cells. In order to evaluate the efficacy of lentiviral-mediated gene replacement therapy in the RCS rat, we produced recombinant VSV-G pseudotyped HIV-1-based lentiviruses containing a murine Mertk cDNA driven by a spleen focus forming virus (SFFV) promoter. The vector was subretinally injected into the right eye of 10-day-old RCS rats; the left eye was left untreated as an internal control. Here, we present a detailed assessment of the duration and extent of the morphological rescue and the resulting functional benefits. We examined animals at various time points over a period of 7 months by light and electron microscopy, and electroretinography. We observed correction of the phagocytic defect, slowing of photoreceptor cell loss and preservation of retinal function for up to 7 months. This study demonstrates the potential of gene therapy approaches for the treatment of retinal degenerations caused by defects specific to the RPE and supports the use of lentiviral vectors for the treatment of such disorders.

Animals↗
PubMed2000

Mapping of X-linked progressive retinal atrophy (XLPRA), the canine homolog of retinitis pigmentosa 3 (RP3).

X-linked progressive retinal atrophy (XLPRA) in the Siberian husky dog is a naturally occurring X-linked retinopathy closely resembling X-linked retinitis pigmentosa (XLRP) in humans. In affected males, initial degeneration of rods is followed by cone degeneration and complete retinal atrophy; carrier females have random patches of rod degeneration consistent with random X chromosome inactivation. By typing the XLPRA pedigree with five intragenic markers [dystrophin, retinitis pigmentosa GTPase regulator ( RPGR ), tissue inhibitor of metalloproteinases 1, androgen receptor and factor IX], we established a linkage map of the canine X chromosome, and confirmed that the order of these five genes is identical to that on the human X. XLPRA was tightly linked to an intragenic RPGR polymorphism (LOD 11.7, zero recombination), thus confirming locus homology with RP3. We cloned the full-length canine RPGR cDNA and three additional splice variants. No disease-causing mutation was found in the RPGR-coding sequence of the four splice variants characterized, a finding similar to approximately 80% of human XLRP patients whose disease maps to the RP3 locus. In addition, there were no significant differences in the proportional expression of each splice variant in normal and pre-degenerate XLPRA-affected retina. Expression of all RPGR splice variants increased later in the disease, when retinas were undergoing active degeneration. The results provide further evidence of cross-species retention of a complex splicing pattern in the 3' portion of RPGR, the functional significance of which is unknown. In addition, the possibility of another disease locus in the RP3 region is supported.

Alternative Splicing↗
PubMed2005

Abnormal maturation of the retinal vasculature in type XVIII collagen/endostatin deficient mice and changes in retinal glial cells due to lack of collagen types XV and XVIII.

Type XVIII collagen is important in the early phase of retinal vascular development and for the regression of the primary vasculature in the vitreous body after birth. We show here that the retina in Col18a1-/- mice becomes densely vascularized by anomalous anastomoses from the persistent hyaloid vasculature by day 10 after birth. In situ hybridizations revealed normal VEGF mRNA expression, but the phenotype of collagen XVIII deficient mice closely resembled that of mice expressing VEGF120 and VEGF188 isoforms only, suggesting that type XVIII collagen may be involved in VEGF function. Type XVIII collagen was found to be indispensable for angiogenesis in the eye, as also oxygen-induced neovascularization was less intense than normal in the Col18a1-/- mice. We observed a marked increase in the amount of retinal astrocytes in the Col18a1-/- mice. Whereas the retinal vessels of wild-type mice are covered by astrocytes and the regressing, thin hyaloid vessels are devoid of astrocytes, the retinal vessels in the Col18a1-/- mice were similarly covered by astrocytes but not the persistent hyaloid vessels in the vitreous body. Interestingly, double null mice lacking type XVIII collagen and its homologue type XV collagen had the persistent hyaloid vessels covered by astrocytes, including the parts located in the vitreous body. We thus hypothesize that type XV collagen is a regulator of glial cell recruitment around vessels and that type XVIII collagen regulates their proliferation.

Animals↗
PubMedDate not supplied

Experimental retinal detachment in the rabbit. Penetrating ocular injury with retinal laceration.

Retinal detachment was studied in a rabbit model of penetrating ocular injury with retinal laceration. The injury was an 8 mm perforation through the sclera, choroid, and retina with vitreous loss and incarceration. When the injury was located at the equator of the globe, the rate of retinal detachment was 16%, but if located at the ora serrata, the rate was 78%. The higher rate of retinal detachment following injuries located at the ora serrata is probably due to the involvement of the vitreous base.

Animals↗
PubMed1990

Surgical intervention for combined retinal-retinal pigment epithelial hamartoma.

A young woman was followed for over 20 years with a macular combined hamartoma of the retina and retinal pigment epithelium. When vision deteriorated due to contracture of an overlying epiretinal membrane, a pars plana vitrectomy with removal of the membrane was performed. Decreased vascular tortuosity and retinal vascular leakage resulted in postoperative improvement of visual acuity. Selected patients with combined retinal and retinal pigment epithelial hamartomas may benefit from removal of epiretinal membranes.

Child↗
PubMed1993

Retinal calcifications in cytomegalovirus retinitis.

Cytomegalovirus (CMV) retinitis has been well documented in the literature, both in patients with acquired immune deficiency syndrome (AIDS) and in other immunocompromised hosts. The clinical and histopathologic findings in three patients with AIDS and CMV retinitis are presented. In areas of healed retinitis, focal, yellow-white, plaque-like lesions and small refractile retinal lesions were noted clinically. Histopathologic studies confirmed the plaque-like lesions to be intraretinal calcifications. Detailed clinical pathologic correlation between fundus photographs and histologic material is made and its clinical importance discussed.

AIDS-Related Opportunistic Infections↗
PubMed1998

Incidence of foscarnet resistance and cidofovir resistance in patients treated for cytomegalovirus retinitis. The Cytomegalovirus Retinitis and Viral Resistance Study Group.

Cytomegalovirus (CMV) retinitis is a common opportunistic infection in patients with AIDS. With long-term therapy for CMV retinitis, resistant CMV may develop. In a prospective study of 122 patients with CMV retinitis, 2.4 and 0.8% of patients had foscarnet-resistant blood culture isolates (50% inhibitory concentration [IC50], >400 microM) and urine culture isolates, respectively, at diagnosis of CMV retinitis prior to treatment, whereas 4.1 and 6.6% had cidofovir-resistant (IC50, >2 microM) blood and urine culture isolates, respectively. Patients were treated according to best medical judgement. Of 44 foscarnet-treated patients, 26% had a resistant blood or urine culture isolate by 6 months of treatment and 37% had a resistant isolate by 9 months; of 13 cidofovir-treated patients, 29% had a resistant blood or urine culture isolate by 3 months of therapy. The probabilities of developing foscarnet resistance while on foscarnet and developing cidofovir resistance while on cidofovir were not significantly different from that for developing ganciclovir resistance while on ganciclovir (odds ratios, 1.87 [P = 0.19] and 2.28 [P = 0.15], respectively).

Adult↗
PubMed2006

Impaired retinal autoregulation in small retinal arterioles before and after focal laser treatment for diabetic maculopathy.

AIMS: To study the effect of an acute increase in the arterial blood pressure on the diameter response of retinal arterioles supplying areas with focal diabetic macular oedema before and after laser photocoagulation, and control arterioles supplying areas without oedema. METHODS: In 17 diabetic patients the diameter response of arterioles after an increase in the arterial blood pressure induced by isometric exercise was studied using the retinal vessel analyser (RVA). In each patient a study arteriole supplying a focal area of macular oedema as well as a control arteriole supplying a retinal area without retinopathy lesions was selected, and the diameter response of these vessels was performed immediately before, and 1 hour and 3 months after focal laser photocoagulation of the focal oedema area. RESULTS: The diameter response was impaired in both study arterioles and control arterioles before focal laser photocoagulation. The treatment induced regression of the focal retinal oedema, but did not affect the diameter response in the arteriole supplying this area (p = 0.85). CONCLUSION: Impairment of the diameter response in small arterioles from diabetic patients does not parallel the regional distribution of retinopathy lesions. Other factors than disturbed autoregulation are probably involved in generating flow disturbances and oedema in diabetic maculopathy.

Adult↗
PubMed1982

Preserved para-arteriole retinal pigment epithelium (PPRPE) in retinitis pigmentosa.

Five patients with retinitis pigmentosa (RP) with probable autosomal recessive inheritance have been identified in whom there is relative preservation of retinal pigment epithelium adjacent to and under retinal arterioles despite a panretinal degenerative process. All the patients were hypermetropic, though patients with RP tend to be myopic. This implies that there is a factor associated with retinal arterioles which locally retards the RP process in these patients. It may be appropriate to look for the PPRPE pattern in hypermetropic RP patients.

Adolescent↗
PubMed1989

Retinal sensitivity in hereditary retinal degeneration in Abyssinian cats: electrophysiological similarities between man and cat.

The functional and electrophysiological similarities in the changes in the electroretinogram (ERG) of man and cat affected by hereditary retinal degenerative disease were studied. The results of a series of log intensity-amplitude studies in a group of young affected Abyssinian cats were fitted to the Naka-Rushton relationship by means of a mathematical package on the University of London mainframe. The analysis showed that the amplitude of the maximum dark-adapted b-wave was significantly reduced by the end of the period studied but that the value of k, a variable inversely equivalent to retinal sensitivity, was only slightly reduced by the retinal degenerative process. The electrophysiological findings thus are similar to those found in cases of human diffuse dominantly inherited retinitis pigmentosa.

Animals↗
PubMed1990

Localised blood-retinal barrier leakage and retinal light sensitivity in diabetic retinopathy.

Twenty patients with insulin dependent diabetes mellitus were selected on the basis of morphological signs of blood-retinal barrier leakage--namely, hard exudates seen on fundus photographs and/or localised leakage of fluorescein seen on fluorescein angiograms. Computerised perimetry was carried out in visual field areas that corresponded to the morphological lesions, and the visual field data were accurately correlated with the morphology as seen on fundus photographs and fluorescein angiograms. In addition, in seven of the patients who represented the range of leakage among the patients studied, the blood-retinal barrier leakage was quantitated by vitreous fluorophotometry. In 16 cases normal light sensitivity was found in retinal areas showing localised leakage as studied on fluorescein angiograms. In four cases with pronounced maculopathy, where scotomata occurred, there was no topographical correlation between the scotomata and barrier leakage. Furthermore hard exudates often, but not consistently, caused localised scotomata when arranged in dense conglomerates. The permeability values correlated with angiographically observed hyperfluorescence in the macular area. On the basis of the techniques employed in the present study it seems that breakdown of the blood-retinal barrier is an earlier event than disturbance of neurosensory function in the development of diabetic retinopathy. However, the findings give no evidence of a causal relationship between barrier leakage and damage to sensory cell function.

Blood-Retinal Barrier↗