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Intraocular Injections (intraocular + injection)

Distribution by Scientific Domains

Medical Sciences	57%
Life Sciences	42%

Selected Abstracts

Intraocular injection of tamoxifen-loaded nanoparticles: a new treatment of experimental autoimmune uveoretinitis

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 12 2004
Yvonne de Kozak
Abstract In this study, we tested the efficiency of an intravitreal injection of tamoxifen, a non-steroidal estrogen receptor modulator, in retinal soluble antigen (S-Ag)-induced experimental autoimmune uveoretinitis (EAU). To increase the bioavailability of tamoxifen, we incorporated tamoxifen into polyethylene glycol (PEG)-coated nanoparticles (NP-PEG-TAM). The localization of the nanoparticles within the eye was investigated using fluorescent-labeled PEG-coated nanoparticles after injection into the vitreous cavity of rats with EAU. Some nanoparticles were distributed extracellularly throughout the ocular tissues, others were concentrated in resident ocular cells and in infiltrating macrophages. Whereas the injection of free tamoxifen did not alter the course of EAU, injection of NP-PEG-TAM performed 1,2,days before the expected onset of the disease in controls resulted in significant inhibition of EAU. NP-PEG-TAM injection significantly reduced EAU compared to injection of NP-PEG-TAM with 17,-estradiol (E2), suggesting that tamoxifen is acting as a partial antagonist to E2. Diminished infiltration by MHC class,II+ inflammatory cells and low expression of TNF-,, IL-1,, and RANTES mRNA were noted in eyes of NP-PEG-TAM-treated rats. Intravitreal injection of NP-PEG-TAM decreased S-Ag lymphocyte proliferation, IFN-, production by inguinal lymph node cells, and specific delayed-type hypersensitivity indicative of a reduced Th1-type response. It increased the anti-S-Ag IgG1 isotype indicating an antibody class switch to Th2 response. These data suggest that NP-PEG-TAM inhibition of EAU could result from a form of immune deviation. Tamoxifen-loaded nanoparticles may represent a new option for the treatment of experimental uveitis. [source]

3412: Anti-VEGF and corticosteroids therapy in macular edema secondary to venous occlusions

ACTA OPHTHALMOLOGICA, Issue 2010
JAC POURNARAS
Purpose To assess the evidence on interventions to improve visual acuity (VA) and to treat macular edema (ME) secondary to central (CRVO) and branch retinal vein occlusion (BRVO) Methods Recent randomized studies have evaluated the safety and efficacy of corticosteroids (triamcinolone, dexamethasone) and anti-VEGF therapies (ranibizumab). Score study evaluates preservative-free intravitreal triamcinolone with standard care in BRVO and CRVO. In Geneva study, dexamethasone (DEX) intravitreal implant is compared with sham in BRVO and CRVO. BRAVO and Cruise studies evaluate intraocular injections of ranibizumab in patients with ME following BRVO and CRVO, respectively. Results In SCORE study, there was no difference identified in visual acuity at 12 months for the standard care group compared with the triamcinolone groups in BRVO patients. Intravitreal triamcinolone is superior to observation for treating vision loss associated with ME secondary to CRVO. Improvements in BCVA with DEX implant were seen in patients with BRVO and CRVO, although the patterns of response differed. Intraocular injections of 0.3 mg or 0.5 mg ranibizumab provided rapid, effective treatment for ME following BRVO and CRVO Conclusion Grid photocoagulation remains the standard care for patients with vision loss associated with ME secondary to BRVO. Intravitreal triamcinolone is superior to observation for treating vision loss associated with ME secondary to CRVO. Dexamethasone intravitreal implant can both reduce the risk of vision loss and improve the speed and incidence of visual improvement in eyes with ME secondary to BRVO or CRVO. Anti-VEGF therapies represent new therapeutical option in the treatment of ME secondary to BRVO and CRVO. Further randomized studies are needed [source]

Injecting 1000 Centistoke Liquid Silicone With Ease and Precision

DERMATOLOGIC SURGERY, Issue 3 2003
Anthony V. Benedetto DO, FACP
BACKGROUND Since the Food and Drug Administration approved the use of the 1000 centistoke liquid silicone, Silikon 1000, for intraocular injection, the off-label use of this injectable silicone oil as a permanent soft-tissue filler for facial rejuvenation has increased in the United States. Injecting liquid silicone by the microdroplet technique is the most important preventive measure that one can use to avoid the adverse sequelae of silicone migration and granuloma formation, especially when injecting silicone to improve small facial defects resulting from acne scars, surgical procedures, or photoaging. OBJECTIVE To introduce an easy method for injecting a viscous silicone oil by the microdroplet technique, using an inexpensive syringe and needle that currently is available from distributors of medical supplies in the United States. METHOD We suggest the use of a Becton Dickinson 3/10 cc insulin U-100 syringe to inject Silikon 1000. This syringe contains up to 0.3 mL of fluid, and its barrel is clearly marked with an easy-to-read scale of large cross-hatches. Each cross-hatch marking represents either a unit value of 0.01 mL or a half-unit value of 0.005 mL of fluid, which is the approximate volume preferred when injecting liquid silicone into facial defects. Because not enough negative pressure can be generated in this needle and syringe to draw up the viscous silicone oil, we describe a convenient and easy method for filling this 3/10 cc diabetic syringe with Silikon 1000. RESULTS We have found that by using the Becton Dickinson 3/10 cc insulin U-100 syringe, our technique of injecting minute amounts of Silikon 1000 is facilitated because each widely spaced cross-hatch on the side of the syringe barrel is easy to read and measures exact amounts of the silicone oil. These lines of the scale on the syringe barrel are so large and clearly marked that it is virtually impossible to overinject the most minute amount of silicone. CONCLUSION Sequential microdroplets of 0.01 cc or less of Silikon 1000 can be measured and injected with the greatest ease and precision so that inadvertent overdosing and complications can be avoided. [source]

Ganglion cell regeneration following whole-retina destruction in zebrafish

DEVELOPMENTAL NEUROBIOLOGY, Issue 2 2008
Tshering Sherpa
Abstract The retinas of adult teleost fish can regenerate neurons following injury. The current study provides the first documentation of functional whole retina regeneration in the zebrafish, Danio rerio, following intraocular injection of the cytotoxin, ouabain. Loss and replacement of laminated retinal tissue was monitored by analysis of cell death and cell proliferation, and by analysis of retina-specific gene expression patterns. The spatiotemporal process of retinal ganglion cell (RGC) regeneration was followed through the use of selective markers, and was found to largely recapitulate the spatiotemporal process of embryonic ganglion cell neurogenesis, over a more protracted time frame. However, the re-expression of some ganglion cell markers was not observed. The growth and pathfinding of ganglion cell axons was evaluated by measurement of the optic nerve head (ONH), and the restoration of normal ONH size was found to correspond to the time of recovery of two visually-mediated behaviors. However, some abnormalities were noted, including overproduction of RGCs, and progressive and excessive growth of the ONH at longer recovery times. This model system for whole-retina regeneration has provided an informative view of the regenerative process. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2008 [source]

Low sensitivity of retina to AMPA-induced calcification

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2003
Noemí Andrés
Abstract Glutamate is involved in most CNS neurodegenerative diseases. In particular, retinal diseases such as retinal ischemia, retinitis pigmentosa, and diabetic retinopathy are associated with an excessive synaptic concentration of this neurotransmitter. To gain more insight into retinal excitotoxicity, we carried out a dose,response study in adult rats using ,-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), a glutamate analogue. AMPA intraocular injections (between 0.27 and 10.8 nmol) caused no morphologic modification, but a 10.8 + 21 nmol double injection in a 10-day interval produced a lesion characterized by discrete neuronal loss, astroglial and microglial reactions, and calcium precipitation. Abundant calcium deposits similar to those present in rat and human brain excitotoxicity or hypoxia-ischemia neurodegeneration were detected by alizarin red staining within the retinal surface and the optic nerve. Glial reactivity, associated normally with astrocytes in the nerve fiber, was assessed in Müller cells. GABA immunoreactivity was detected not only in neuronal elements but also in Müller cells. In contrast to the high vulnerability of the brain to excitotoxin microinjection, AMPA-induced retinal neurodegeneration may provide a useful model of low central nervous system sensitivity to excitotoxicity. © 2003 Wiley-Liss, Inc. [source]

Transitin, a nestin-related intermediate filament, is expressed by neural progenitors and can be induced in Müller glia in the chicken retina

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2005
Andy J. Fischer
Abstract The purpose of this study was to test whether transitin, the avian homologue of nestin, is expressed by retinal progenitors in the developing and postnatal chicken. Because nestin has been widely used as a cell-distinguishing marker of neural progenitors in the mammalian nervous system, we expected to find transitin expressed specifically by the neural progenitors of the retina. In early stages of development, transitin is expressed by neural progenitors in the retina and by cells in the developing ciliary body. During later stages of development, transitin expression persists in differentiating Müller glia but is down-regulated by these cells as maturation proceeds. In the postnatal chick, transitin expression is restricted to neural progenitors at the peripheral edge of the retina. We found that the expression of transitin in mature Müller glia was induced by intraocular injections of insulin and fibroblast growth factor-2 (FGF2) but not by ciliary neurotrophic factor. In response to insulin and FGF2, the expression of transitin was induced in the nonpigmented epithelium (NPE) of the ciliary body. In the postnatal retina, acute retinal damage transiently induces transitin expression in Müller glia. We propose that the expression of transitin by retinal Müller glia and NPE cells in the postnatal animal represents a state of de-differentiation and a step toward becoming neurogenic progenitor cells. Taken together, our findings indicate that transitin is expressed by neural progenitors in the embryonic and postnatal chicken retina. However, transitin is not exclusively expressed by neural progenitors and is also expressed by non-neurogenic cells. J. Comp. Neurol. 484:1,14, 2005. © 2005 Wiley-Liss, Inc. [source]