Thematische Bibliographien / Bruch's membrane

Auswahl der wissenschaftlichen Literatur zum Thema „Bruch's membrane“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 20. Februar 2023

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Zeitschriftenartikel zum Thema "Bruch's membrane"

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Pauleikhoff, Daniel, C. Alex Harper, John Marshall und Alan C. Bird. „Aging Changes in Bruch's Membrane“. Ophthalmology 97, Nr. 2 (Februar 1990): 171–78. http://dx.doi.org/10.1016/s0161-6420(90)32619-2.

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Bird, A. C. „Bruch's membrane change with age.“ British Journal of Ophthalmology 76, Nr. 3 (01.03.1992): 166–68. http://dx.doi.org/10.1136/bjo.76.3.166.

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KARWATOWSKI, WOJCIECH S. S., TRACY E. JEFFRIES, VICTOR C. DUANCE, JULIE ALBON, ALAN J. BAILEY und DAVID L. EASTY. „Collagen and ageing in Bruch's Membrane“. Biochemical Society Transactions 19, Nr. 4 (01.11.1991): 349S. http://dx.doi.org/10.1042/bst019349s.

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Afshari, F. T., und J. W. Fawcett. „Improving RPE adhesion to Bruch's membrane“. Eye 23, Nr. 10 (16.01.2009): 1890–93. http://dx.doi.org/10.1038/eye.2008.411.

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Pino, R. P., und E. Essner. „On the components of Bruch's membrane.“ Journal of Histochemistry & Cytochemistry 34, Nr. 3 (März 1986): 413. http://dx.doi.org/10.1177/34.3.3950388.

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Booij, J. C., D. C. Baas, J. Beisekeeva, T. G. M. F. Gorgels und A. A. B. Bergen. „The dynamic nature of Bruch's membrane“. Progress in Retinal and Eye Research 29, Nr. 1 (Januar 2010): 1–18. http://dx.doi.org/10.1016/j.preteyeres.2009.08.003.

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JONAS, J., Q. YOU, XY PENG, L. XU, WB WEI, Y. WANG und CX CHEN. „Macular Bruch's membrane defects in Hi“. Acta Ophthalmologica 92 (20.08.2014): 0. http://dx.doi.org/10.1111/j.1755-3768.2014.f028.x.

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Korte, Gary E. „The Elastic Tissue of Bruch's Membrane“. Archives of Ophthalmology 107, Nr. 11 (01.11.1989): 1654. http://dx.doi.org/10.1001/archopht.1989.01070020732037.

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Hirabayashi, Yoshifumi, Osamu Fujimori und Satoru Shimizu. „Bruch's membrane of the brachymorphic mouse“. Medical Electron Microscopy 36, Nr. 3 (01.09.2003): 139–46. http://dx.doi.org/10.1007/s00795-003-0218-z.

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10

Rizzolo, L. J. „Basement membrane stimulates the polarized distribution of integrins but not the Na,K-ATPase in the retinal pigment epithelium.“ Cell Regulation 2, Nr. 11 (November 1991): 939–49. http://dx.doi.org/10.1091/mbc.2.11.939.

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The basement membrane stimulates the differentiation and polarity of simple transporting epithelia. We demonstrated for the retinal pigment epithelium (RPE) of chicken embryos that polarity develops gradually. Although the RPE and an immature basement membrane are established on embryonic day 4 (E4), the distribution of the Na,K-ATPase and a family of basement membrane receptors containing the beta 1 subunit of integrin is nonpolarized. The percentage of polarized cells increases gradually until cells in all regions of the epithelium are polarized on E11. During this time, the basement membrane increases in size and complexity to form Bruch's membrane. To study the ability of the basement membrane to stimulate the polarized distribution of the beta 1 integrins or the Na,K-ATPase, RPE was harvested from E7, E9, or E14 embryos and cultured on Bruch's membrane isolated (in association with the choroid) from E14 embryos. As a control, the RPE was plated on the side of the choroid lacking a Bruch's membrane. The distribution of the beta 1 integrins and the Na,K-ATPase was determined by indirect immunofluorescence. Bruch's membrane stimulated the polarized distribution of the beta 1 integrins regardless of the developmental age of the RPE even though E7 RPE is nonpolarized in vivo. To examine the role of individual matrix components, RPE was plated on matrix-coated filters. The polarized distribution of the beta 1 integrins was stimulated by laminin, collagen IV, and Matrigel but not by fibronectin. Interestingly, laminin and collagen IV are present in the basement membrane on E4 when RPE is not polarized in vivo. Under no circumstances was the distribution of the Na,K-ATPase polarized. These data indicate that the basement membrane influences the distribution of a subset of plasma membrane proteins but that other factors are required for full polarity.
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Dissertationen zum Thema "Bruch's membrane"

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Karwatowski, Wojciech Stefan Stanislaw. „Bruch's membrane and its collagen“. Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361162.

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Lee, Yunhee. „Characterisation and modulation of the gelatinase system of human Bruch's membrane“. Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/characterisation-and-modulation-of-the-gelatinase-system-of-human-bruchs-membrane(013f751e-04af-44a8-a866-2eec03998309).html.

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Ageing of Bruch’s membrane is associated with structural and functional deterioration. Accumulation of normal and abnormal collagen in ageing Bruch’s has led to the hypothesis of diminished matrix degradation mediated normally by a family of protease enzymes called the matrix metalloproteinases (MMPs). Underlying mechanisms leading to diminished MMP activity in ageing Bruch’s remain unknown but functional changes of diminished transport are well documented. Ageing remains the biggest risk factor in AMD with nearly 30% of all individuals reaching the age of 85 years showing some loss of central vision. In the present thesis, the gelatinase system (constituting MMPs 2&9) has been examined resulting in the identification and characterisation of three additional high molecular weight species termed HMW 1&2 and a large macromolecular weight MMP complex (LMMC). HMW1&2 were shown to be covalently bonded homo-and/or hetero- polymers of pro-MMPs 2&9. HMW species in effect sequester pro-MMPs 2&9 reducing the pool available for activation and the age-related increase in HMW species is expected to augment this reduction. In Bruch’s membrane from donors with AMD, levels of HMW1&2 were considerably elevated (p<0.05) with a concomitant reduction in the amount of active MMPs 2&9 (p<0.05). The reduction in activated MMP species therefore underlies the reduced degradative capacity of Bruch’s in these patients. Elution studies demonstrated the existence of a free-bound equilibrium for the gelatinases with the bound forms being retained by hydrophobic, ionic or metal mediated interactions. Since divalent metal ions are deposited in Bruch’s of AMD donors, metal chelation was assessed as a possible means of inducing MMP release. Metal chelation with EGTA resulted in the release of active forms of MMP2 and significantly improved the fluid transport properties of the membrane (p<0.005).
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Zayas-Santiago, Astrid, Samuel D. Cross, James B. Stanton, Alan D. Marmorstein und Lihua Y. Marmorstein. „Mutant Fibulin-3 Causes Proteoglycan Accumulation and Impaired Diffusion Across Bruch's Membrane“. ASSOC RESEARCH VISION OPHTHALMOLOGY INC, 2017. http://hdl.handle.net/10150/624956.

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PURPOSE. The mutation R345W in EFEMP1 (fibulin-3) causes macular degeneration. This study sought to determine whether proteoglycan content and diffusion across Bruch's membrane are altered in Efemp1(ki/ki) mice carrying this mutation or in Efemp1(-/-) mice. METHODS. Proteoglycans in mouse Bruch's membranes were stained with Cupromeronic Blue (CB). Heparan sulfated proteoglycan (HSPG) and chondroitin/dermatan sulfate proteoglycan (C/DSPG) distributions were visualized following treatments with chondroitinase ABC (C-ABC) or nitrous acid. Total sulfated glycosaminoglycans (sGAGs) in Bruch's membrane/choroid (BrM/Ch) were measured with dimethylmethylene blue (DMMB). Matrix metalloprotease (MMP)-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-3 were examined by immunofluorescence and quantified using Image J. Molecules with different Stokes radius (R-s) were allowed simultaneously to diffuse through mouse BrM/Ch mounted in a modified Ussing chamber. Samples were quantified using gel exclusion chromatography. RESULTS. HSPGs and C/DSPGs were markedly increased in Efemp1(ki/ki) Bruch's membrane, and MMP-2 and MMP-9 were decreased, but TIMP-3 was increased. Diffusion across Efemp1(ki/ki) Bruch's membrane was impaired. In contrast, the proteoglycan amount in Efemp1(-/-) Bruch's membrane was not significantly different, but the size of proteoglycans was much larger. MMP-2, MMP-3, and TIMP-3 levels were similar to that of Efemp1(+/+) mice, but they were localized diffusely in retinal pigment epithelium (RPE) cells instead of Bruch's membrane. Diffusion across Efemp1(-/-) Bruch's membrane was enhanced. CONCLUSIONS. Mutant fibulin-3 causes proteoglycan accumulation, reduction of MMP-2 and MMP-9, but increase of TIMP-3, and impairs diffusion across Bruch's membrane. Fibulin-3 ablation results in altered sizes of proteoglycans, altered distributions of MMP-2, MMP-9, and TIMP-3, and enhances diffusion across Bruch's membrane.
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Moore, David Jonathan. „An investigation of the permeability of Bruch's membrane and its variation with age“. Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338867.

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Haneef, Atikah Shahid. „Fabrication of novel cytocompatible membranes for ocular application, concentrating in particular on age-related macular degeneration (AMD)“. Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/fabrication-of-novel-cytocompatible-membranes-for-ocular-application-concentrating-in-particular-on-agerelated-macular-degeneration-amd(7d1ace68-09d8-4c64-83e7-3ede1e2f52e1).html.

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The aims of this research were to investigate polymer fibre morphology, overall mat morphology, mechanical properties and general handling of the mats, and ideal mat thickness in order to fabricate a suitable substrate for potential use in cell transplantation for application as a permanent substrate for the treatment of dry age-related macular degeneration (AMD). Polystyrene (PS), poly(ethylene terephthalate) (PET) and polyurethane (PU) were electrospun to ascertain the ideal electrospinning parameters to reproducibly obtain fibres to construct a mat as a potential candidate for a replacement Bruch’s membrane (BM). After identifying the ideal spinning parameters, mats were fabricated, their fibre morphology, overall mat morphology, and handling during processing were examined. This allowed the shortlisting of PS and PET substrates, which were suitable to be taken forward for further testing and cell culture. PU was found to be unsuitable as it had a tendency to become entwined and stick to itself, which would destroy the gross mat morphology. Therefore PU was excluded from further testing. Further handling, both quantitative and qualitative, and thickness and porosity were tested for PS and PET mats. Electrospun PET demonstrated greater handling and durability properties compared to PS mats, which were more fragile. PET was able to withstand twisting, folding, and rolling, whereas PS could not undergo twisting and fell apart. PS mats were thicker and more porous compared to PET mats, which was attributed to the widely spaced placement of the larger PS fibres and the fluffy gross morphology of the PS mats, in comparison to the closer fibre placement of the smaller PET mats which had a smooth gross mat morphology. Considering this, PS mats were compressed and thickness and porosity was reduced, while maintaining its fibrous structure. However the compressed PS mats became extremely fragile and could not withstand much handling. Although PET mats were thinner than PS mats, it did not match the native BM thickness and so experiments in varying collection time during electrospinning to match the native BM thickness were undertaken. Tensile tests, thickness and porosity measurements showed that PET tensile properties, thickness, and porosity reduced with reduced collection time. For the purposes of surface treatment and cell culture, uncompressed mats collected for 60 minutes were used since sufficient PS fibres were able to be collected to form a mat that was able to withstand processing at this collection time. Effect of UV/ozone surface treatment was tested for both PS and PET mats. Treatment of both substrate types affected protein adsorption, with evidence of aminolysis observed on PET substrates. Short-term initial growth and survival of retinal pigment epithelial cells (RPE cells) on electrospun, surface oxidised PS and PET was investigated. Untreated PS did not support cell proliferation and although treated PS did, the resultant RPE cell morphology was undesirable, therefore was not taken forward to long term cell culture. Treated and untreated PET supported cell proliferation, and was taken forward to the long term culture study, where cells exhibited the desired monolayer morphology. In this work it has been demonstrated that electrospun PET may potentially be a suitable candidate as cell carrier substrate for subsequent implantation in application towards AMD treatment.
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Duvall-Young, Josephine. „New concepts in the pathophysiology of macular disease : morphological responses in the choriocapillaris and Bruch's membrane“. Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/18853.

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Starita, Carla. „An investigation of the site of resistance to fluid transport within Bruch's membrane and changes with age“. Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250686.

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Ahir, Alpa. „An investigation of matrix metalloproteinases derived from retinal pigment epithelial cells and their influence on fluid movement through Bruch's membrane“. Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274921.

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Hodgetts, Andrea. „An investigation of the changes in fibre and matrix components of human Bruch's membrane as a function of age and their implications for movement of fluids“. Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246304.

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Shadforth, Audra M. „Development of a cultured tissue substitute to repair the ageing retina“. Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/90058/12/Audra_Shadforth_Thesis.pdf.

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This project provides a foundation for the use of silk membranes in a tissue engineered therapy for the treatment of devastating retinal diseases such as age-related macular degeneration. The three-dimensional tissue model described in this thesis has great potential for use in basic research of retinal pathologies, and the potential to be implemented into clinical approaches after appropriate refinement.
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Buchteile zum Thema "Bruch's membrane"

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Sugino, Ilene K., Qian Sun, Noounanong Cheewatrakoolpong, Christopher Malcuit und Marco A. Zarbin. „Biochemical Restoration of Aged Human Bruch's Membrane: Experimental Studies to Improve Retinal Pigment Epithelium Transplant Survival and Differentiation“. In Developments in Ophthalmology, 133–42. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000358531.

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Carroll, Joseph J. „Bruch’s Membrane“. In Encyclopedia of Ophthalmology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-35951-4_144-4.

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Carroll, Joseph J. „Bruch’s Membrane“. In Encyclopedia of Ophthalmology, 282. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_144.

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Drack, Arlene V. „Heritable Disorders of RPE, Bruch’s Membrane, and the Choriocapillaris“. In Pediatric Ophthalmology and Strabismus, 523–38. New York, NY: Springer New York, 2003. http://dx.doi.org/10.1007/978-0-387-21753-6_30.

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Sears, Jonathan E. „Macular Choroidal Neovascularization and Defects in Bruch’s Membrane in Children“. In Pediatric Retina, 345–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12041-1_14.

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Edwards, Malia, und Gerard A. Lutty. „Bruch’s Membrane and the Choroid in Age-Related Macular Degeneration“. In Age-related Macular Degeneration, 89–119. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66014-7_4.

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Jonas, Jost B., Kyoko Ohno-Matsui und Songhomitra Panda-Jonas. „Theories of Myopization: Potential Role of a Posteriorly Expanding Bruch’s Membrane“. In Pathologic Myopia, 161–66. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-74334-5_11.

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Ho, Tzyy-Chang, Yung-Feng Shih, Luke L.-K. Lin, Muh-Shy Chen, I.-Jong Wang, Ping-Kang Hou und Por-Tying Hung. „Degenerative Changes of Retinal Pigment Epithelium-Bruch’s membrane-Choriocapillaris Complex in Form-deprivation Myopia in Chicks“. In Myopia Updates II, 47–49. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66917-3_10.

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Kamei, Motohiro, Suneel S. Apte, Mary E. Rayborn, Hilel Lewis und Joe G. Hollyfield. „TIMP-3 Accumulation in Bruch’s Membrane and Drusen in Eyes From Normal and Age-Related Macular Degeneration Donors“. In Degenerative Retinal Diseases, 11–15. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5933-7_2.

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Fernandez-Godino, Rosario. „Alterations in Extracellular Matrix/Bruch’s Membrane Can Cause the Activation of the Alternative Complement Pathway via Tick-Over“. In Retinal Degenerative Diseases, 29–35. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_4.

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Konferenzberichte zum Thema "Bruch's membrane"

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Lu, Bo, Zhao Liu, Laura Liu, Danhong Zhu, David Hinton, Biju Thomas, Mark S. Humayun und Yu-Chong Tai. „Semipermeable parylene membrane as an artificial Bruch's membrane“. In TRANSDUCERS 2011 - 2011 16th International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2011. http://dx.doi.org/10.1109/transducers.2011.5969376.

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Zhang, Tingwei, Aaron Kho, Vyas Akondi, Alfredo Dubra und Vivek Srinivasan. „In vivo quantification of Bruch's membrane in humans with visible light OCT (Conference Presentation)“. In Ophthalmic Technologies XXX, herausgegeben von Fabrice Manns, Per G. Söderberg und Arthur Ho. SPIE, 2020. http://dx.doi.org/10.1117/12.2546437.

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Wang, Jui-Kai, Patrick A. Sibony, Randy H. Kardon, Mark J. Kupersmith und Mona K. Garvin. „Semi-automated 2D Bruch's membrane shape analysis in papilledema using spectral-domain optical coherence tomography“. In SPIE Medical Imaging, herausgegeben von Barjor Gimi und Robert C. Molthen. SPIE, 2015. http://dx.doi.org/10.1117/12.2077797.

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Shen, Yuhe, Liling Guan, Kai Yu und Xinjian Chen. „A CNN based retinal regression model for Bruch’s membrane opening detection“. In Image Processing, herausgegeben von Elsa D. Angelini und Bennett A. Landman. SPIE, 2019. http://dx.doi.org/10.1117/12.2511727.

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Zhang, Tingwei, Aaron Kho, Robert Zawadzki, Ravi S. Jonnal, Glenn C. Yiu und Vivek Srinivasan. „Optical physics-based methodology for quantifying Bruch’s membrane with visible light OCT“. In Ophthalmic Technologies XXXI, herausgegeben von Daniel X. Hammer, Karen M. Joos und Daniel V. Palanker. SPIE, 2021. http://dx.doi.org/10.1117/12.2577851.

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Goren, O. „E-254 Evaluation of Bruch’s membrane in the management of idiopathic intracranial hypertension“. In SNIS 19th Annual Meeting Abstracts. BMA House, Tavistock Square, London, WC1H 9JR: BMJ Publishing Group Ltd., 2022. http://dx.doi.org/10.1136/neurintsurg-2022-snis.365.

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Burns, Stephen A., Ann E. Elsner, John J. Weiter und Mark R. Kreitz. „Cone Photopigment Density in Aging and AMD“. In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/navs.1991.wa3.

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Age-related Macular Degeneration (AMD) is the leading cause of vision loss in the elderly. Histopathologically AMD is characterized by diffuse changes in Bruch’s membrane and in many cases by the development of drusen. The pathogenesis of AMD is thought to derive from abnormalities of the Retinal Pigment Epithelium (RPE). The RPE is critically important for the nourishment and health of the photoreceptors. For this reason we are using a psychophysical measure of photoreceptor function to examine patients with AMD. The measure used is the change in the color-match with retinal illuminance which provides information on the optical density and regeneration of the cone photopigments.
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Elsner, Ann E., Stephen A. Burns, Mark R. Kreitz und John J. Weiter. „New Views of the Retina/ RPE Complex: Quantifying Sub-retinal Pathology“. In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/navs.1991.tua1.

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The early stages of sub-retinal pathology are often difficult to observe and quantify in vivo. One important example is age-related macular degeneration (AMD), which is one of the chief causes of visual loss in the United States. Histopathological studies of human eyes indicate that there is a deposition of material in the layers beneath the retina, particularly in Bruch’s membrane prior to clinical detection of the disease. (Fig 1, as in Ref 1). These changes are not visible clinically when the deposits are diffuse or small (e.g. <25 urn). We are currently attempting to determine if these earliest changes can be detected by non-invasive techniques.
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Wang, Jui-Kai, Randy H. Kardon und Mona K. Garvin. „Automated Bruch’s Membrane Opening Segmentation in Cases of Optic Disc Swelling in Combined 2D and 3D SD-OCT Images Using Shape-Prior and Texture Information“. In Ophthalmic Medical Image Analysis Second International Workshop. Iowa City, IA: University of Iowa, 2015. http://dx.doi.org/10.17077/omia.1024.

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