Home About us Contact
|
Home About us Contact | ||
|
|
||
Retinal Damage (retinal + damage)
Selected AbstractsRetinal Evaluation After 810 nm Dioderm Laser Removal of EyelashesDERMATOLOGIC SURGERY, Issue 9 2002Randal T. H. Pham MD background. When operating hair removal lasers on the face or in the periorbital region, even with an ocular shield in place, patients often report seeing "flashing lights" each time the laser is fired. This phenomenon suggests stimulation of retinal photoreceptors and raises laser safety issues. objective. To perform retinal electrophysiologic studies to evaluate the safety of hair removal lasers in the periorbital region. methods. Five patients with severe trichiasis secondary to trachoma were studied. The 810 nm Dioderm laser (Cynosure, Inc., Chelmsford, MA) was used to treat the eyelash follicles on the lower eyelid of each patient. Cox III metal eye shields (Oculo-Plastik, Inc., Montreal, Canada) were placed behind the eyelids of both eyes during the laser procedure. Prior to irradiation, a comprehensive ophthalmic evaluation including pupillary and slit-lamp examination, funduscopy, and full-field electroretinograms (ERGs) was performed. A comprehensive ophthalmic evaluation including ERG testing was repeated 30 minutes and 3,6 months after completion of treatment. An independent blinded assessor evaluated the ERG studies. Subjective reports of laser light sensation, pain, and discomfort during and after the laser procedure were also assessed. results. There was no detectable change in slit-lamp, pupillary, or funduscopic evaluations after periorbital laser irradiation. Similarly the pre- and posttreatment ERGs were unchanged. Three patients reported seeing flashing lights during the procedure. conclusion. We found no ERG evidence of retinal damage after laser hair removal in the periorbital region, with Cox III-type ocular shields over the eyes, even when patients subjectively reported "flashing lights" during laser irradiation. [source] Brain-derived neurotrophic factor shows a protective effect and improves recovery of the ERG b-wave response in light-damageJOURNAL OF NEUROCHEMISTRY, Issue 2 2003Kazuhito Ikeda Abstract We investigated the neuroprotective effects of brain-derived neurotrophic factor (BDNF) and its influence on the functional recovery of the retina following light-induced retinal damage by electroretinogram (ERG). Rats were exposed to constant fluorescent light for 2, 5, 7, or 14 days, then returned to a cyclic light environment for 14 days. The result indicated that BDNF had few effects on the a-wave amplitude, but there was a statistically significant difference in the b-wave amplitudes between BDNF-treated and control eyes from day 0,14 of the recovery period following 2 days of light exposure (p < 0.05). Our findings suggest that BDNF not only protects the retinal neuronal function but also enhances the recovery from retinal light damage. [source] Astaxanthin, a dietary carotenoid, protects retinal cells against oxidative stress in-vitro and in mice in-vivoJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 10 2008Yoshimi Nakajima We have investigated whether astaxanthin exerted neuroprotective effects in retinal ganglion cells in-vitro and in-vivo. In-vitro, retinal damage was induced by 24-h hydrogen peroxide (H2O2) exposure or serum deprivation, and cell viability was measured using a WST assay. In cultured retinal ganglion cells (RGC-5, a rat ganglion cell-line transformed using E1A virus), astaxanthin inhibited the neurotoxicity induced by H2O2 or serum deprivation, and reduced the intracellular oxidation induced by various reactive oxygen species (ROS). Furthermore, astaxanthin decreased the radical generation induced by serum deprivation in RGC-5. In mice in-vivo, astaxanthin (100 mg kg,1, p.o., four times) reduced the retinal damage (a decrease in retinal ganglion cells and in thickness of inner plexiform layer) induced by intravitreal N -methyl- d -aspartate (NMDA) injection. Furthermore, astaxanthin reduced the expressions of 4-hydroxy-2-nonenal (4-HNE)-modified protein (indicator of lipid peroxidation) and 8-hydroxy-deoxyguanosine (8-OHdG; indicator of oxidative DNA damage). These findings indicated that astaxanthin had neuroprotective effects against retinal damage in-vitro and in-vivo, and that its protective effects may have been partly mediated via its antioxidant effects. [source] Effect of Visible Light on Normal and P23H-3 Transgenic Rat Retinas: Characterization of a Novel Retinoic Acid Derivative Present in the P23H-3 RetinaPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2006Todd Duncan ABSTRACT Transgenic rats with the P23H mutation in rhodopsin exhibit increased susceptibility to light damage, compared with normal animals. It is known that light-induced retinal damage requires repetitive bleaching of rhodopsin and that photoreceptor cell loss is by apoptosis; however, the underlying molecular mechanism(s) leading to photoreceptor cell death are still unknown. Photoproducts, such as all- trans retinal or other retinoid metabolites, released by the extensive bleaching of rhodopsin could lead to activation of degenerative processes, especially in animals genetically predisposed to retinal degenerations. Using wild-type and transgenic rats carrying the P23H opsin mutation, we evaluated the effects of acute intense visible light on retinoid content, type and distribution in ocular tissues. Rats were exposed to green light (480,590 nm) for 0, 5, 10, 30 and 120 min. Following light treatment, rats were sacrificed and neural retinas were dissected free of the retinal pigment epithelium. Retinoids were extracted from retinal tissues and then subjected to HPLC and mass spectral analysis. We found that the light exposure affected relative levels of retinoids in the neural retina and retinal pigment epithelium of wild-type and P23H rat eyes similarly. In the P23H rat retina but not the wild-type rat retina, we found a retinoic acid-like compound with an absorbance maximum of 357 nm and a mass of 304 daltons. Production of this retinoic acid-like compound in transgenic rats is influenced by the age of the animals and the duration of light exposure. It is possible that this unique retinoid may be involved in the process of light-induced retinal degeneration. [source] Transitin, a nestin-related intermediate filament, is expressed by neural progenitors and can be induced in Müller glia in the chicken retinaTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2005Andy 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] Protective effects of triamcinolone acetonide upon the upregulation and phosphorylation of GAP 43 in an animal model of retinopathy of prematurityACTA OPHTHALMOLOGICA, Issue 6 2010In Y. Chung Acta Ophthalmol. 2010: 88: e217,e221 Abstract. Purpose:, The aim of the current study was to investigate the effects of triamcinolone acetonide (TA) upon the expression and phosphorylation of growth-associated protein 43 (GAP 43) in the retinas of oxygen-induced retinopathy (OIR) rats. Methods:, Oxygen-induced retinopathy was induced by exposing Sprague-Dawley rats to hyperoxia (80% oxygen) from postnatal (P) days 2,14 and then returning the rats to normoxic conditions. Triamcinolone acetonide or a conditioned saline (control) was injected intravitreally into the right or left eye, respectively, of OIR rats at P15. We then assessed the molecular and histological changes in the expression of GAP 43 and phospho-GAP 43 in OIR and control rat retinas, and also after treatment with TA by RT-PCR, Western blotting and immunohistochemistry. Results:, Growth-associated protein 43 mRNA levels were found to be increased by 1.6-fold (p = 0.001, n = 5) in the retinas of P18 OIR rats compared with the control rats. The protein levels of GAP 43 and phospho-GAP43 were found to be elevated in the retina of P18 OIR rats (2.40- and 2.39-fold greater than each control, p<0.001, n = 5, respectively). Immunoreactivities of GAP 43 and phospho-GAP 43 were stronger in the inner plexiform layer in OIR rat retinas compared with the control. However, treatment with TA attenuated GAP 43 and phospho-GAP 43 upregulation in the OIR retinas. Conclusion:, Our results indicate that GAP 43 and phospho-GAP 43 participate in retinal (potentially pathologic) changes following oxygen-induced damage. Triamcinolone acetonide protects the retinal damage in relatively hypoxic retinas of OIR rats. Therefore, TA treatment does not induce the expression and phosphorylation of GAP 43 in OIR rat retinas. [source] 4412: Immunohistochemistry and Western blot methodologies to evaluate neuroprotective agents in models of retinopathiesACTA OPHTHALMOLOGICA, Issue 2010K THERMOS Purpose Many retinopathies that lead to visual loss and blindness are characterized by neovascularization and neural retinal defects, such as a marked loss in retinal neurons and an increase in apoptosis. There are no therapeutic agents for the treatment of the neurodegenerative component of retinal disease. Immunohistochemistry and western blot methodologies were employed to determine retinal viability and to elucidate the putative neuroprotective properties of new therapeutic targets, in animal models of retinopathy (chemical ischemia, excitotoxicity, STZ). Methods To assay retinal viability, the following antibodies for retinal markers were employed in immunohistochemical assays: PKC (rod bipolar cells), ChAT, bNOS, TH (cholinergic-, nitric oxide synthetase-, and dopamine- containing amacrine cells, respectively), calbindin-containing horizontal, amacrine and cone bipolar cells, NFL and MAP1 (ganglion axons and cells, respectively). Antibodies against various pro-survival or pro-death molecules (western blots), as well as the TUNEL-assay, were employed to examine retinal apoptosis and neuroprotection. Results Loss of retinal marker immunoreactivity was differentially observed according to the animal model employed. The neuroprotection of specific retinal neurons by the new therapeutic targets examined (somatostatin and neurosteroids) reflect the existence of protein substrates involved in the mechanism of action of these molecules. Conclusion Immunohistochemical and western blot analysis techniques provide important information on the retinal damage induced by ischemic insults and the neuroprotection afforded by new targets of retinal therapeutics. [source] Nitric oxide and inflammationACTA OPHTHALMOLOGICA, Issue 2009AD DICK Purpose The talk will discuss the dichomatous role of nitric oxide in inflammation as a result of macrophage activation and also its role in controlling T cell responses. Methods We have used both microglial cell cultures, bone marrow derived macrophages and finally animal models of uveitis to dissect the role of macrophage activation and nitric oxide production in both tissue damage and limiting the extent of the inflammatory response. Results Macrophages when activated via T cell responses secreting interferon gamma, elicit a TNF-dependent nitrite response. Inhibiting nitric oxide activity by either suppressing NOS2 or via inhibiting TNF activity results in marked suppression of macrophage activation and reduction in retinal damage observed during experimental autoimmune uveoretinitis (EAU). Macrophages regulate T cell responses, in part via nitric oxide production, but is dependent upon IFN-gamma and autocrine TNF signalling via TNFReceptor1. Conclusion TNF and Interferon play essential roles in generating macrophage activation that elaborates in turn nitric oxide production. The nitric oxide, whilst damaging to cell membranes thus contributing to tissue damage during autoimmunity, also assists in regulating T cell responses by down regulating of T cell proliferation within the target tissue. [source] Clinical and Histological Aspects of CNV Formation: Studies in an Animal ModelACTA OPHTHALMOLOGICA, Issue thesis2 2008Nathan Lassota MD Abstract. The purpose of the present thesis was to develop an animal model of CNV in order to study the early formation of CNV and to test the effects of an anti-angiogenic treatment. Porcine eyes were chosen as a substrate for CNV induction, since they are similar to human eyes in terms of both macroscopic and microscopic morphology. However, a major difference is that pigs lack a fovea; instead they have a visual streak, with a relatively stable and high concentration of cones. By surgical perforation of Bruch's membrane we were able to induce formation of CNV membranes. The morphology and cellular composition of these membranes varied with the surgical technique employed. When RPE cells were locally removed at the time of perforation, the resulting CNV was thinner, contained fewer blood vessels and was less prone to leak on fluorescein angiography than when RPE cells were left intact at induction. The neuroretina overlying the perforation site was not damaged by any of the surgical techniques, thus allowing the subsequent retinal damage to be ascribed to the actual process of CNV formation. Using this animal model allowed us to directly map histological findings onto fluorescein angiograms and thereby perform meaningful correlations between histopathologic and photographic features. Such correlations have been hampered in human subjects, since human eyes are not enucleated as a consequence of CNV and are therefore only available for post-mortem studies. In such studies there often is a considerable time-gap between the death of the patient and the latest available fluorescein angiogram, thereby allowing macular pathology to evolve in the interim. Histological examination of the porcine membranes demonstrated that they were composed of RPE cells, glial cells, macrophages, endothelial cells, collagen and smooth muscle fibres, which are the same cellular and fibrillar elements that dominate human CNV membranes. The porcine model was applied to test the effects, in a randomized and masked fashion, of intravitreally injected bevacizumab. Bevacizumab, a pan VEGF A antibody, was found to reduce both the proliferation of endothelial cells in CNV membranes and the propensity to leak in fluorescein angiograms. Immunohistochemically, bevacizumab was detected in the inner limiting membrane, in retinal blood vessels and binding uniformly to the entire CNV membrane without any cellular predisposition. Based on the above findings we believe that the porcine CNV model shows a bearing to human disease and therefore might be used as a tool to obtain improved treatments for this debilitating condition. [source] Association between serum levels of soluble CD40/CD40 ligand and organ damage in hypertensive patientsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2010Ming Yuan Summary 1.,CD40 and CD40 ligand (CD40L) have a critical role in the pathophysiology and risk prediction of coronary artery syndrome, including atherothrombosis and atherosclerosis. However, the contribution of the CD40/CD40L dyad, especially the soluble form of CD40L (sCD40L), to the pathophysiology of hypertension and associated organ damage remains unknown. 2.,In the present study, serum levels of CD40 and sCD40L were measured in 328 hypertensive patients with varying degrees of organ damage. The data revealed that serum levels of CD40 were significantly greater in patients with severe, but not mild, organ damage compared with patients without any organ damage. There were no significant differences in serum concentrations of sCD40L between patients with no, mild and severe organ damage. Concentrations of soluble CD40 were comparable in patients with mild organ damage that included left ventricular hypertrophy, retinal damage, renal dysfunction and proteinuria. In contrast, concentrations of soluble CD40 were increased significantly in patients with certain forms of severe organ damage, specifically stroke, but not coronary and peripheral artery disease. 3.,Collectively, our data indicate that upregulation of the CD40 system in hypertensive patients with certain forms of severe end-organ damage may contribute to the pro-inflammatory, pro-atherogenic and prothrombotic milieu in hypertension. [source] Reactive Oxygen Species, Aging, and Antioxidative NutraceuticalsCOMPREHENSIVE REVIEWS IN FOOD SCIENCE AND FOOD SAFETY, Issue 1 2004J. Lee ABSTRACT The important roles of reactive oxygen species in diseases related to aging and the necessity and benefits of antioxidative nutraceuticals in the prevention of diseases and promotion of healthy aging have been extensively reported in recent years. Oxygen is an essential component of living organisms. The generation of reactive oxygen species such as superoxide anion, hydrogen peroxide, hydroxyl radicals, and singlet oxygen is inevitable in aerobic metabolism of the body. Reactive oxygen species cause lipid oxidation, protein oxidation, DNA strand break and base modification, and modulation of gene expression. In the past several years, unprecedented progress has been made in the recognition and understanding of roles of reactive oxygen species in many diseases. These include atherosclerosis, vasospasms, cancers, trauma, stroke, asthma, hyperoxia, arthritis, heart attack, age pigments, dermatitis, cataractogenesis, retinal damage, hepatitis, liver injury, and periodontis, which are age-related. The body protects itself from the potential damages of reactive oxygen species. Its first line of defense is superoxide dismutases, glutathione peroxidases, and catalase. Scientists have indicated that antioxidant nutraceuticals supplied from daily diets quench the reactive oxygen species or are required as cofactors for antioxidant enzymes. Nutraceuticals play significant roles in the prevention of a number of age-related diseases and are essential for healthy aging. Epidemiological studies also reported the relevance of antioxidative nutraceuticals to health issues and the prevention of age-related diseases. Health-conscious consumers have made antioxidative nutraceuticals the leading trend in the food industry worldwide in recent years. [source] Telangiectasia evaluated with adaptive optics and HR-OCTACTA OPHTHALMOLOGICA, Issue 2009K ATMANI Purpose Type 2 Macular Telangiectasia is a progressive disease starting in the fifth to seventh decade and characterized by a progressive damage of the neurosensory retina.. The purpose of this study is to compare the images obtained using two non-invasive techniques, High-Resolution Optical Coherence Tomography (HR-OCT) and Adaptive Optics (AO), in Type 2 Macular Telangiectasia. Methods Nine eyes of 5 patients affected by Type 2 Macular Telangiectasia underwent examination including visual acuity measurement with ETDRS (Early Treatment of Diabetic Retinopathy Study) chart, color photographs, monochromatic photographs, Spectral-Domain Optical Coherence Tomography with Heidelberg SpectralisÔ OCT and Adaptive Optics assessment with Imagine EyesÔ System. The neurosensory retina and the photoreceptor layer were analyzed using both HR-OCT and AO imaging. Results The disruptions of the photoreceptor layer on HR-OCT correspond to a cellular loss on Adaptive Optics Imaging. On the other hand, Adaptive optics Imaging allows the measurement of cellular density in areas which have a normal aspect on HR-OCT. Conclusion The diagnosis of Macular Telangiecctasia is based on biomicroscopy and fluorescein angiography. Adaptive Optics Imaging is helpful to analyze the retinal damages, especially the cone abnormalities. This technique will certainly allow a better understanding of this rare disease. Author Disclosure Information: K. Atmani, None; N. Leveziel, None G. Soubrane, None. [source] | |||||||||||||