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Готові списки джерел за темами / Geographic atrophy

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Добірка наукової літератури з теми "Geographic atrophy"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 21 лютого 2023

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Статті в журналах з теми "Geographic atrophy"

1

STAURENGHI, G. "Geographic atrophy." Acta Ophthalmologica 90 (August 6, 2012): 0. http://dx.doi.org/10.1111/j.1755-3768.2012.4212.x.

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2

Holz, Frank G., Erich C. Strauss, Steffen Schmitz-Valckenberg, and Menno van Lookeren Campagne. "Geographic Atrophy." Ophthalmology 121, no. 5 (May 2014): 1079–91. http://dx.doi.org/10.1016/j.ophtha.2013.11.023.

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3

Sheikh, Ahmed Bilal, Andrew Lee, Adnan Mallick, and Ronni M. Lieberman. "Geographic Atrophy." Advances in Ophthalmology and Optometry 3, no. 1 (August 2018): 205–15. http://dx.doi.org/10.1016/j.yaoo.2018.04.011.

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4

Schmitz-Valckenberg, Steffen, Srinivas Sadda, Giovanni Staurenghi, Emily Y. Chew, Monika Fleckenstein, and Frank G. Holz. "GEOGRAPHIC ATROPHY." Retina 36, no. 12 (December 2016): 2250–64. http://dx.doi.org/10.1097/iae.0000000000001258.

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5

Bird, Alan C., Rachel L. Phillips, and Gregory S. Hageman. "Geographic Atrophy." JAMA Ophthalmology 132, no. 3 (March 1, 2014): 338. http://dx.doi.org/10.1001/jamaophthalmol.2013.5799.

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6

Takahashi, Ayako, Sotaro Ooto, Kenji Yamashiro, Hiroshi Tamura, Akio Oishi, Manabu Miyata, Masayuki Hata, Munemitsu Yoshikawa, Nagahisa Yoshimura, and Akitaka Tsujikawa. "Pachychoroid Geographic Atrophy." Ophthalmology Retina 2, no. 4 (April 2018): 295–305. http://dx.doi.org/10.1016/j.oret.2017.08.016.

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7

Guymer, Robyn H. "Geographic Atrophy Trials." Ophthalmology Retina 2, no. 6 (June 2018): 515–17. http://dx.doi.org/10.1016/j.oret.2018.03.004.

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8

Ergun, Erdem, Michael Stur, and Wolfgang Drexler. "Geographic Atrophy Margins." Ophthalmology 117, no. 5 (May 2010): 1051. http://dx.doi.org/10.1016/j.ophtha.2010.01.013.

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9

Neroev, Vladimir V., Marina V. Zueva, Natalia V. Neroeva, Ludmila A. Katargina, Oksana A. Losanova, Marina V. Ryabina, and Irina V. Tsapenko. "Clinical and Functional Characteristics of Secondary Geographic Atrophy Against the Background of Exudative Age-Related Macular Degeneration." Annals of the Russian academy of medical sciences 76, no. 4 (October 22, 2021): 384–93. http://dx.doi.org/10.15690/vramn1557.

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Background.Studies demonstrate the need for long-term follow-up of patients with wet age-related macular degeneration (AMD) treated with inhibitors of angiogenesis to monitor long-term vision outcomes and assess the safety of antiangiogenic therapy in relation to the risk of secondary geographic atrophy. Aims to determine the characteristic clinical and functional signs of secondary GA that developed against the background of wet AMD. Methods.In 22 patients (25 eyes) with wet AMD and 18 healthy subjects comparable in age and sex standard ophthalmological and instrumental studies were performed and photopic electroretinograms (ERGs) were recorded according to ISCEV standards, flicker-ERGs, multifocal ERGs and electrooculogram. Results.The appearance of the area of secondary atrophy against the background of wet AMD in eyes treated with inhibitors of angiogenesis is clinically indistinguishable from areas of geographic atrophy that developed as an outcome of dry AMD. The ERG-signs of secondary atrophy are described, which are similar to the biomarkers of primary atrophy and specifically differ from them. Secondary atrophy is characterized by the dependence of the increase in the b/a ratio on the atrophic area, reducing of the 8.3 Hz-flicker-ERG amplitude in the absence of 24 Hz-flicker ERG changes. In eyes with secondary atrophy, a significant decrease in the density of the multifocal ERG P1-peak was shown not only in the first hexagon but also in the parafoveal zone. The electrooculography results showed a sharper dark troughs decrease in with an increase in Ardens ratio in patients with secondary atrophya on the background of wet AMD, in contrast to the previously described changes in primary geographic atrophy. Conclusion.Comparison of the change in the b/a ratio with secondary atrophy area in patients with wet AMD may have clinical implications for assessing retinal dysfunction and predicting visual function. Secondary atrophy is associated with a pronounced inhibition of photoreceptor activity with better preservation of cone bipolar cells. The ERG and electrooculography data taking together indicate a more significant dysfunction of the retinal pigment epithelium in GA against the background of wet AMD and the associated deterioration of photoreceptor function than the changes characterizing primary geographic atrophy.

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10

Sadda, SriniVas R., and David Sarraf. "Therapeutic Margin for Geographic Atrophy." JAMA Ophthalmology 139, no. 7 (July 1, 2021): 751. http://dx.doi.org/10.1001/jamaophthalmol.2021.1414.

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Більше джерел

Дисертації з теми "Geographic atrophy"

1

Takahashi, Ayako. "Photoreceptor Damage and Reduction of Retinal Sensitivity Surrounding Geographic Atrophy in Age-Related Macular Degeneration." Kyoto University, 2018. http://hdl.handle.net/2433/232112.

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2

Biarnés, Pérez Marc 1973. "Increased fundus autofluorescence, a biomarker of lipofuscin content, as a risk factor for the progression of geographic atrophy secondary to age-related macular degeneration." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/318157.

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L’atròfia geogràfica (AG) és la variant avançada de la degeneració macular associada a l’edat seca i es caracteritza per la presència d’àrees d’atròfia de l’epiteli pigmentari de la retina (EPR) que creixen progressivament, amb pèrdua secundària dels fotorreceptors i la coriocapilar adjacents. Actualment és una condició sense tractament. L’acumulació de lipofuscina a l’EPR, visualitzable clínicament mitjançant l’autofluorescència del fons d’ull (AFU) com a zones d’elevada autofluorescència, ha estat vinculada a la progressió de l’AG en alguns estudis. De fet, s’han descrit certs patrons (“fenotips”) en l’AFU basats en la distribució d’hiperautofluorescència que s’han associat amb taxes específiques de progressió de la malaltia. En aquesta Tesi hem fet un estudi clínic prospectiu per simplificar la complexa classificació dels patrons d’AFU i avaluar el paper de la hiperautofluorescència, un biomarcador de la lipofuscina, en la progressió de l’AG.
Geographic atrophy (GA) is the advanced form of dry age-related macular degeneration. It is characterized by large areas of retinal pigment epithelium (RPE) atrophy that grow progressively, with concomitant loss of photoreceptors and choriocapillaris. Currently, there is no treatment for this disorder. Lipofuscin build-up within the RPE, which is identifiable by fundus autofluorescence (FAF) as areas of increased autofluorescence, has been linked to GA progression in some studies. Actually, the distribution of hyperautofluorescence on FAF identified some patterns (“phenotypes”), which have been associated with specific rates of disease growth. We conducted a prospective clinical study to simplify the complex classification of FAF patterns and to determine the role of increased FAF, a biomarker of lipofuscin, in the progression of GA.

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3

Sufian, Elfandi. "CLINICAL AND GENETIC CHARACTERISTICS OF JAPANESE PATIENTS WITH AGE-RELATED MACULAR DEGENERATION AND PSEUDODRUSEN." Kyoto University, 2018. http://hdl.handle.net/2433/232120.

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4

Cherepanoff, Svetlana. "Age-related macular degeneration: histopathological and serum autoantibody studies." University of Sydney, 2008. http://hdl.handle.net/2123/2464.

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Doctor of Philosophy (PhD)
BACKGROUND: The accumulation of abnormal extracellular deposits beneath the retinal pigment epithelium characterises the pathology of early age-related macular degeneration. However, the histopathological threshold at which age-related changes become early AMD is not defined, and the effect of each of the deposits (basal laminar deposit and membranous debris) on disease progression is poorly understood. Evidence suggests that macrophages play a key role in the development of AMD lesions, but the influence of basal laminar deposit (BLamD) and membranous debris on the recruitment and programming of local macrophages has not been explored. Although evidence also suggests that inflammation and innate immunity are involved in AMD, the significance of anti-retinal autoantibodies to disesase pathogenesis is not known. AIMS: (i) To determine the histopathological threshold that distinguishes normal ageing from early AMD; (ii) to determine the influence of BLamD and membranous debris on disease progression; (iii) to examine whether distinct early AMD phenotypes exist based on clinicopathological evidence; (iv) to determine the histopathological context in which Bruch’s membrane macrophages first found; (v) to examine the relationship between Bruch’s membrane macrophages and subclinical neovascularisation; (vi) to determine if the progressive accumulation of BLamD and membranous debris alters the immunophenotype of Bruch’s membrane macrophages and/or resident choroidal macrophages; (vii) to determine if the anti-retinal autoantibody profile differs significantly between normal individuals and those with early AMD, neovascular AMD or geographic atrophy; (viii) to examine whether baseline anti-retinal autoantibodies can predict progression to advanced AMD in individuals with early AMD; and (ix) to examine whether baseline anti-retinal autoantibodies can predict vision loss in individuals with neovascular AMD. METHODS:Clinicopathological studies were performed to correlate progressive accumulation of BLamD and membranous debris to fundus characteristics and visual acuity, as well as to sub-macular Bruch’s membrane macrophage count. Immunohistochemical studies were perfomed to determine whether the presence of BLamD and membranous debris altered the programming of Bruch’s membrane or resident choroidal macrophages. The presence of serum anti-retinal autoantibodies was determined by western blotting, and the association with disease progression examined in early and neovascular AMD. RESULTS: The presence of both basal linear deposit (BLinD) and a continuous layer of BLamD represents threshold early AMD histopathologically, which was seen clinically as a normal fundus in the majority of cases. Membranous debris accumulation appeared to influence the pathway of progression from early AMD to advanced AMD. Bruch’s membrane macrophages were first noted when a continuous layer of BLamD and clinical evidence of early AMD were present, and increased with the amount of membranous debris in eyes with thin BLamD. Eyes with subclinical CNV had high macrophage counts and there was some evidence of altered resident choroidal macrophage programming in the presence of BLamD and membranous debris. Serum anti-retinal autoantibodies were found in a higher proportion of early AMD participants compared with both controls and participants with neovascular AMD, and in a higher proportion of individuals with atrophic AMD compared to those with neovascular AMD. The presence of baseline anti-retinal autoantibodies in participants with early AMD was not associated with progression to advanced AMD. Participants with neovascular AMD lost more vision over 24 months if they had IgG autoantibodies at baseline compared to autoantibody negative participants. CONCLUSIONS: The finding that eyes with threshold early AMD appear clinically normal underscores the need to utilise more sophisticated tests to enable earlier disease detection. Clinicopathological evidence suggests two distinct early AMD phenotypes, which follow two pathways of AMD progression. Macrophage recruitment and programming may be altered by the presence of BLamD and membranous debris, highlighting the need to further characterise the biology of human resident choroidal macropahges. Anti-retinal autoantibodies can be found in both control and AMD sera, and future approaches that allow the examination of subtle changes in complex repertoires will determine whether they are involved in AMD disease pathogenesis.

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5

Cherepanoff, Svetlana. "Age-related macular degeneration: histopathological and serum autoantibody studies." Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/2464.

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BACKGROUND: The accumulation of abnormal extracellular deposits beneath the retinal pigment epithelium characterises the pathology of early age-related macular degeneration. However, the histopathological threshold at which age-related changes become early AMD is not defined, and the effect of each of the deposits (basal laminar deposit and membranous debris) on disease progression is poorly understood. Evidence suggests that macrophages play a key role in the development of AMD lesions, but the influence of basal laminar deposit (BLamD) and membranous debris on the recruitment and programming of local macrophages has not been explored. Although evidence also suggests that inflammation and innate immunity are involved in AMD, the significance of anti-retinal autoantibodies to disesase pathogenesis is not known. AIMS: (i) To determine the histopathological threshold that distinguishes normal ageing from early AMD; (ii) to determine the influence of BLamD and membranous debris on disease progression; (iii) to examine whether distinct early AMD phenotypes exist based on clinicopathological evidence; (iv) to determine the histopathological context in which Bruch’s membrane macrophages first found; (v) to examine the relationship between Bruch’s membrane macrophages and subclinical neovascularisation; (vi) to determine if the progressive accumulation of BLamD and membranous debris alters the immunophenotype of Bruch’s membrane macrophages and/or resident choroidal macrophages; (vii) to determine if the anti-retinal autoantibody profile differs significantly between normal individuals and those with early AMD, neovascular AMD or geographic atrophy; (viii) to examine whether baseline anti-retinal autoantibodies can predict progression to advanced AMD in individuals with early AMD; and (ix) to examine whether baseline anti-retinal autoantibodies can predict vision loss in individuals with neovascular AMD. METHODS:Clinicopathological studies were performed to correlate progressive accumulation of BLamD and membranous debris to fundus characteristics and visual acuity, as well as to sub-macular Bruch’s membrane macrophage count. Immunohistochemical studies were perfomed to determine whether the presence of BLamD and membranous debris altered the programming of Bruch’s membrane or resident choroidal macrophages. The presence of serum anti-retinal autoantibodies was determined by western blotting, and the association with disease progression examined in early and neovascular AMD. RESULTS: The presence of both basal linear deposit (BLinD) and a continuous layer of BLamD represents threshold early AMD histopathologically, which was seen clinically as a normal fundus in the majority of cases. Membranous debris accumulation appeared to influence the pathway of progression from early AMD to advanced AMD. Bruch’s membrane macrophages were first noted when a continuous layer of BLamD and clinical evidence of early AMD were present, and increased with the amount of membranous debris in eyes with thin BLamD. Eyes with subclinical CNV had high macrophage counts and there was some evidence of altered resident choroidal macrophage programming in the presence of BLamD and membranous debris. Serum anti-retinal autoantibodies were found in a higher proportion of early AMD participants compared with both controls and participants with neovascular AMD, and in a higher proportion of individuals with atrophic AMD compared to those with neovascular AMD. The presence of baseline anti-retinal autoantibodies in participants with early AMD was not associated with progression to advanced AMD. Participants with neovascular AMD lost more vision over 24 months if they had IgG autoantibodies at baseline compared to autoantibody negative participants. CONCLUSIONS: The finding that eyes with threshold early AMD appear clinically normal underscores the need to utilise more sophisticated tests to enable earlier disease detection. Clinicopathological evidence suggests two distinct early AMD phenotypes, which follow two pathways of AMD progression. Macrophage recruitment and programming may be altered by the presence of BLamD and membranous debris, highlighting the need to further characterise the biology of human resident choroidal macropahges. Anti-retinal autoantibodies can be found in both control and AMD sera, and future approaches that allow the examination of subtle changes in complex repertoires will determine whether they are involved in AMD disease pathogenesis.

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6

Teixeira, Luís Miguel Xavier Alves de Castro. "Role of Choroidal Tickness and Cataract Surgery in the progression of Geographic Atrophy." Master's thesis, 2014. https://repositorio-aberto.up.pt/handle/10216/72936.

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7

Teixeira, Luís Miguel Xavier Alves de Castro. "Role of Choroidal Tickness and Cataract Surgery in the progression of Geographic Atrophy." Dissertação, 2014. https://repositorio-aberto.up.pt/handle/10216/72936.

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8

Tavares, Samuel Oliveira Ferreira. "Papel dos anti-VEGF na atrofia macular: consequência do tratamento ou progressão natural da Degenerescência Macular da Idade?" Master's thesis, 2021. http://hdl.handle.net/10316/98319.

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Trabalho Final do Mestrado Integrado em Medicina apresentado à Faculdade de Medicina
Desde a introdução dos anti-VEGF como abordagem terapêutica para a DMI neovascular que estes se têm mantido como único tratamento manifestamente eficaz no combate à progressão da doença. A possibilidade de um maior desenvolvimento de atrofia macular nos olhos dos doentes tratados, porém, tem vindo a ser levantada. Atualmente, é ainda difícil estabelecer com segurança se a atrofia macular verificada neste contexto se deve, efetivamente, aos fármacos anti-VEGF, se, por outro lado, traduz somente a progressão natural da DMI atrófica. Com a elaboração deste trabalho, pretendeu-se avaliar os resultados dos principais estudos publicados sobre a temática e perceber a validade das principais hipóteses explicativas para a associação encontrada. Elaborou-se, para tal, uma pesquisa na base de dados online PubMed, selecionando-se os estudos de maior relevância. Posteriormente, procedeu-se a uma análise comparativa dos mesmos. A obtenção de uma resposta inequívoca não foi conseguida. Perceberam-se as limitações ao confronto dos diferentes estudos e exploraram-se os fatores envolvidos em potenciais conclusões discrepantes. Contudo, tornou-se claro que a evidência mais atual atesta a segurança dos fármacos anti-VEGF. A sua utilização é fortemente encorajada no contexto da DMI neovascular, e os potenciais riscos envolvidos são largamente suplantados pelos seus benefícios.
Since the introduction of anti-VEGF drugs as a therapeutical approach for neovascular AMD that this has remained the only clearly effective treatment to fight the progression of the disease. The possibility of a larger development of macular atrophy in the eyes of treated patients, however, has been raised in recent years. Nowadays, it is still difficult to assess clearly if the identified macular atrophy in this context is due, truly, to anti-VEGF drugs, or, on the other hand, if it merely reflects the natural progression of atrophic AMD. With the elaboration of this paper, it was intended for one to evaluate the results of the leading studies published on the subject, and to apprehend the validity of the main hypothesis that try to explain the verified association. To do that, a research using the online database PubMed was made, being selected the studies with the higher relevance. Subsequently, one proceeded to a comparative analysis of said studies.It was not possible to obtain an unequivocal answer on the proposed topic. The limitations in contrasting the different studies were ascertained, and the various factors involved in potentially discrepant conclusions were explored. Nonetheless, it has been made clear that the most recent scientifical evidence attests the safety of anti-VEGF drugs. Its use is strongly encouraged in the context of neovascular AMD, and any potentially existing risk is largely outweighed by its unmistakable benefits.

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Частини книг з теми "Geographic atrophy"

1

Pilotto, Elisabetta, and Francesca Guidolin. "Geographic Atrophy." In Microperimetry and Multimodal Retinal Imaging, 77–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40300-2_8.

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2

Lindner, Moritz, Monika Fleckenstein, Steffen Schmitz-Valckenberg, and Frank G. Holz. "Atrophy, Geographic." In Encyclopedia of Ophthalmology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_1125-1.

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3

Lindner, Moritz, Monika Fleckenstein, Steffen Schmitz-Valckenberg, and Frank G. Holz. "Atrophy, Geographic." In Encyclopedia of Ophthalmology, 207–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_1125.

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4

Fleckenstein, M., S. Schmitz-Valckenberg, J. S. Sunness, and F. G. Holz. "Geographic Atrophy." In Age-related Macular Degeneration, 121–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-22107-1_8.

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5

Lindner, Moritz, Monika Fleckenstein, Julia Steinberg, Steffen Schmitz-Valckenberg, and Frank G. Holz. "Geographic Atrophy Secondary to Age-Related Macular Degeneration." In Spectral Domain Optical Coherence Tomography in Macular Diseases, 169–82. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-3610-8_14.

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6

Yang, Qi, Neha Anegondi, Verena Steffen, Simon S. Gao, Julia Cluceru, Christina Rabe, Jian Dai, and Daniela Ferrara. "Uncertainty-Aware Geographic Atrophy Progression Prediction from Fundus Autofluorescence." In Lecture Notes in Computer Science, 29–38. Cham: Springer Nature Switzerland, 2022. http://dx.doi.org/10.1007/978-3-031-17721-7_4.

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7

Marmor, M. F. "Age-related geographic atrophy and pattern dystrophy of the RPE." In Documenta Ophthalmologica Proceedings Series, 291–96. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5137-5_48.

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8

Bearelly, Srilaxmi, and Scott W. Cousins. "Fundus Autofluorescence Imaging in Age-Related Macular Degeneration and Geographic Atrophy." In Retinal Degenerative Diseases, 395–402. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1399-9_45.

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9

Joussen, Antonia M., Jan van Meurs, and Bernd Kirchhof. "Autologous Translocation of the Choroid and RPE in Patients with Geographic Atrophy." In Essentials in Ophthalmology, 143–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-33670-9_12.

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10

Li, Yuchun, Sijie Niu, Zexuan Ji, and Qiang Chen. "Automated and Robust Geographic Atrophy Segmentation for Time Series SD-OCT Images." In Pattern Recognition and Computer Vision, 249–61. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-03398-9_22.

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Тези доповідей конференцій з теми "Geographic atrophy"

1

Lee, Noah, R. Theodore Smith, and Andrew F. Laine. "Interactive segmentation for geographic atrophy in retinal fundus images." In 2008 42nd Asilomar Conference on Signals, Systems and Computers. IEEE, 2008. http://dx.doi.org/10.1109/acssc.2008.5074488.

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2

Hu, Zhihong, Ziyuan Wang, and SriniVas Sadda. "Automated segmentation of geographic atrophy using deep convolutional neural networks." In Computer-Aided Diagnosis, edited by Kensaku Mori and Nicholas Petrick. SPIE, 2018. http://dx.doi.org/10.1117/12.2287001.

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3

Hu, Zhihong, Gerard G. Medioni, Matthias Hernandez, and SriniVas R. Sadda. "Supervised pixel classification for segmenting geographic atrophy in fundus autofluorescene images." In SPIE Medical Imaging, edited by Stephen Aylward and Lubomir M. Hadjiiski. SPIE, 2014. http://dx.doi.org/10.1117/12.2043178.

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4

Devisetti, K., T. P. Karnowski, L. Giancardo, Y. Li, and E. Chaum. "Geographic atrophy segmentation in infrared and autofluorescent retina images using supervised learning." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090983.

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5

Anegondi, Neha, Qi Yang, Michael Kawczynski, Verena Steffen, and Simon S. Gao. "Predicting geographic atrophy growth rate from fundus autofluorescence images using deep neural networks." In Multimodal Biomedical Imaging XVI, edited by Fred S. Azar, Xavier Intes, and Qianqian Fang. SPIE, 2021. http://dx.doi.org/10.1117/12.2575898.

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6

Peralta-Ildefonso, Martha J., Ernesto Moya-Albor, Jorge Brieva, Esmeralda Lira-Romero, Andric C. Perez-Ortiz, Ramon Coral-Vazquez, and Francisco J. Estrada-Mena. "Nuclear density analysis in microscopic images for the characterization of retinal geographic atrophy." In 15th International Symposium on Medical Information Processing and Analysis, edited by Jorge Brieva, Eduardo Romero, and Natasha Lepore. SPIE, 2020. http://dx.doi.org/10.1117/12.2542061.

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7

Dong, Jiwen, Junting Chen, Xizhan Gao, Rongbin Xu, and Sijie Niu. "Automated geographic atrophy segmentation with multi-loss for SD-OCT images based on patient independent." In Twelfth International Conference on Graphics and Image Processing, edited by Zhigeng Pan and Xinhong Hei. SPIE, 2021. http://dx.doi.org/10.1117/12.2589371.

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Lee, Noah, Andrew F. Laine, and R. Theodore Smith. "A hybrid segmentation approach for geographic atrophy in fundus auto-fluorescence images for diagnosis of age-related macular degeneration." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4353455.

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Zhang, Yuhan, Zexuan Ji, Sijie Niu, Theodore Leng, Daniel L. Rubin, and Qiang Chen. "A Multi-Scale Deep Convolutional Neural Network For Joint Segmentation And Prediction Of Geographic Atrophy In SD-OCT Images." In 2019 IEEE 16th International Symposium on Biomedical Imaging (ISBI). IEEE, 2019. http://dx.doi.org/10.1109/isbi.2019.8759253.

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