Relevant bibliographies by topics / Cone, retinitis pigmentosa

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Cone, retinitis pigmentosa'

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Published: 10 March 2023

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Journal articles on the topic "Cone, retinitis pigmentosa"

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haradhan chowdhury, Partha. "GIST OF RETINITIS PIGMENTOSA." EPH - International Journal of Medical and Health Science 4, no. 1 (January 16, 2018): 18–19. http://dx.doi.org/10.53555/eijmhs.v4i1.15.

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It is a hereditary disease and mainly it is characterized by Night Blindness and visual field constriction. Here, degeneration occurs in rods and cone cells. In case of Retinitis Pigmentosa:Blood vessels became attenuate means it becomes thin. Rods and Cone cells are degenerated. Highest number of rod cells are present at the peripheral part of the retina and the highest number of cone cells are present at foveal part
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Wong, Fulton. "Visual Pigments, Blue Cone Monochromasy, and Retinitis Pigmentosa." Archives of Ophthalmology 108, no. 7 (July 1, 1990): 935. http://dx.doi.org/10.1001/archopht.1990.01070090037033.

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Bovolenta, Paola, and Elsa Cisneros. "Retinitis pigmentosa: cone photoreceptors starving to death." Nature Neuroscience 12, no. 1 (January 2009): 5–6. http://dx.doi.org/10.1038/nn0109-5.

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Elsner, Ann E., Stephen A. Burns, and Louis A. Lobes. "Foveal cone optical density in retinitis pigmentosa." Applied Optics 26, no. 8 (April 15, 1987): 1378. http://dx.doi.org/10.1364/ao.26.001378.

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Jones, Jennifer, Michael Baldinger, and John Sharpe. "Cone-Rod Dystrophy Versus Inverse Retinitis Pigmentosa." Optometry - Journal of the American Optometric Association 81, no. 6 (June 2010): 298. http://dx.doi.org/10.1016/j.optm.2010.04.067.

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Kaplan, HenryJ, Wei Wang, Niloofar Piri, and DouglasC Dean. "Metabolic rescue of cone photoreceptors in retinitis pigmentosa." Taiwan Journal of Ophthalmology 11, no. 4 (2021): 331. http://dx.doi.org/10.4103/tjo.tjo_46_21.

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Murakami, Y., Y. Ikeda, S. Nakatake, J. W. Miller, D. G. Vavvas, K. H. Sonoda, and T. Ishibashi. "Necrotic cone photoreceptor cell death in retinitis pigmentosa." Cell Death & Disease 6, no. 12 (December 2015): e2038-e2038. http://dx.doi.org/10.1038/cddis.2015.385.

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Kaplan, Henry J., Wei Wang, and Douglas C. Dean. "Restoration of Cone Photoreceptor Function in Retinitis Pigmentosa." Translational Vision Science & Technology 6, no. 5 (September 6, 2017): 5. http://dx.doi.org/10.1167/tvst.6.5.5.

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Arsiwalla, Tasneem A., Elisa E. Cornish, Phuc Vuong Nguyen, Maria Korsakova, Haipha Ali, Nonna Saakova, Clare L. Fraser, Robyn V. Jamieson, and John R. Grigg. "Assessing Residual Cone Function in Retinitis Pigmentosa Patients." Translational Vision Science & Technology 9, no. 13 (December 17, 2020): 29. http://dx.doi.org/10.1167/tvst.9.13.29.

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Sahel, José-Alain, Thierry Léveillard, Serge Picaud, Deniz Dalkara, Katia Marazova, Avinoam Safran, Michel Paques, Jens Duebel, Botond Roska, and Saddek Mohand-Said. "Functional rescue of cone photoreceptors in retinitis pigmentosa." Graefe's Archive for Clinical and Experimental Ophthalmology 251, no. 7 (April 11, 2013): 1669–77. http://dx.doi.org/10.1007/s00417-013-2314-7.

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Dissertations / Theses on the topic "Cone, retinitis pigmentosa"

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Lipinski, Daniel Mark. "Neuroprotection of cone photoreceptors in retinitis pigmentosa." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:aee440bc-f990-4216-9d43-63902ff0fc52.

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Retinitis pigmentosa (RP) is a genetically and phenotypically heterogeneous condition that affects approximately 1 in 4000 individuals worldwide. The most common presentation of RP is a rod-cone dystrophy, where the degeneration of cone photoreceptors occurs secondary to advanced rod loss, leading to a significant decline in central vision and a corresponding reduction in patient quality of life. The mechanisms underlying secondary cone loss are poorly understood, particularly in disorders where the gene defect is unknown or manifest only in rod photoreceptors. Consequently, the thesis presented herein proceeds on several fronts. First, in the long term a greater understanding of the causes underlying cone loss in RP is likely to be beneficial, and so in chapter one a dominant cone degeneration is characterized using intrinsically fluorescent cone photoreceptors to track the degenerative process. Second, as we develop a greater understanding of the genetic etiology underlying RP it is likely that the number of large genes identified as being causative will increase. As currently there is no efficient way to deliver large genes to photoreceptors, chapter two explores the use of alternate viral vectors that might be used to deliver a large therapeutic transgene. Lastly, whilst our understanding of cone loss in RP remains incomplete, it is necessary to develop a broadly applicable therapy to slow or attenuate further cone loss in RP patients regardless of the underlying cause. In chapters three and four we examine the use of low molecular weight "growth factors‟, such as ciliary neurotrophic factor (CNTF), to preserve cone photoreceptors long-term using a rhodopsin knockout model of RP.
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Chung, Chung-yee, and 鍾震宇. "Cone photoreceptor degeneration in the rd10 model of retinitis pigmentosa." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48333700.

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Purpose Retinal pigmentosa (RP) is a heterogeneous group of retinal degeneration with a multitude of hereditary genetic defect. Photoreceptor degeneration usually starts with rods but invariably involves cones in later stages, leading to significant visual debilitation. Many animal models, in particular mouse models, have been used for the study of RP. The rd10 mouse, with mutation in the beta subunit of the rod phosphodiesterase gene, has been chosen as a model for an autosomal recessive form of human RP because of its later onset of retinal degeneration. The topographic and morphological patterns of cone photoreceptor degeneration following the loss of rods were studied. Methods The rd10 mice were sacrificed and enucleated at postnatal 14 days, 21 days, 1 month, 2 months and 3 months. The retina was processed with immuno-staining to differentiate different photoreceptor cells and mounted flat for microscopic examination. The topographic pattern of cone photoreceptor loss at different ages was identified. Confocal microscopy was used to examine the morphological changes of cone degeneration. The retina from an adult c35 mouse was chosen as a reference for comparison. Results Following the onset of rod degeneration, the orderly arrangement of cones became disrupted. Remodeling of cone cells was observed as the loss of outer segments, swelling of the somata, and redistribution of opsin. Subsequently the inner segment and part of their axon and pedicles were involved. Some cones then demonstrated neurite sprouting, restoring a new polarized morphology. However, with increasing age, extensive atrophy of cone cells ensued. The topographic pattern of cone degeneration advanced from central to the peripheral retina, with the cones in the superior part of the retina most resistant to degeneration. Conclusion Cone photoreceptors respond to the loss of rods by remodelling and maintain a relatively normal phenotype for a considerable period of time, especially those in the superior part of the retina. This may provide a therapeutic window for cone rescue for patients of RP.
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Venkatesh, Aditya. "Activation of mTORC1 Improves Cone Cell Metabolism and Extends Vision in Retinitis Pigmentosa Mice: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/822.

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Retinitis Pigmentosa (RP) is an inherited photoreceptor degenerative disease that leads to blindness and affects about 1 in 4000 people worldwide. The disease is predominantly caused by mutations in genes expressed exclusively in the night active rod photoreceptors; however, blindness results from the secondary loss of the day active cone photoreceptors, the mechanism of which remains elusive. Here, we show that the mammalian target of rapamycin complex 1 (mTORC1) is required to delay the progression of cone death during disease and that constitutive activation of mTORC1 is sufficient to maintain cone function and promote cone survival in RP. Activation of mTORC1 increased expression of genes that promote glucose uptake, retention and utilization, leading to increased NADPH levels; a key metabolite for cones. This protective effect was conserved in two mouse models of RP, indicating that the secondary loss of cones can be delayed by an approach that is independent of the primary mutation in rods. However, since mTORC1 is a negative regulator of autophagy, its constitutive activation led to an unwarranted secondary effect of shortage of amino acids due to incomplete digestion of autophagic cargo, which reduces the efficiency of cone survival over time. Moderate activation of mTORC1, which promotes expression of glycolytic genes, as well as maintains autophagy, provided more sustained cone survival. Together, our work addresses a long-standing question of non-autonomous cone death in RP and presents a novel, mutation-independent approach to extend vision in a disease that remains incurable.
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Venkatesh, Aditya. "Activation of mTORC1 Improves Cone Cell Metabolism and Extends Vision in Retinitis Pigmentosa Mice: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/822.

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Retinitis Pigmentosa (RP) is an inherited photoreceptor degenerative disease that leads to blindness and affects about 1 in 4000 people worldwide. The disease is predominantly caused by mutations in genes expressed exclusively in the night active rod photoreceptors; however, blindness results from the secondary loss of the day active cone photoreceptors, the mechanism of which remains elusive. Here, we show that the mammalian target of rapamycin complex 1 (mTORC1) is required to delay the progression of cone death during disease and that constitutive activation of mTORC1 is sufficient to maintain cone function and promote cone survival in RP. Activation of mTORC1 increased expression of genes that promote glucose uptake, retention and utilization, leading to increased NADPH levels; a key metabolite for cones. This protective effect was conserved in two mouse models of RP, indicating that the secondary loss of cones can be delayed by an approach that is independent of the primary mutation in rods. However, since mTORC1 is a negative regulator of autophagy, its constitutive activation led to an unwarranted secondary effect of shortage of amino acids due to incomplete digestion of autophagic cargo, which reduces the efficiency of cone survival over time. Moderate activation of mTORC1, which promotes expression of glycolytic genes, as well as maintains autophagy, provided more sustained cone survival. Together, our work addresses a long-standing question of non-autonomous cone death in RP and presents a novel, mutation-independent approach to extend vision in a disease that remains incurable.
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Makiyama, Yukiko. "Macular Cone Abnormalities in Retinitis Pigmentosa with Preserved Central Vision Using Adaptive Optics Scanning Laser Ophthalmoscopy." Kyoto University, 2014. http://hdl.handle.net/2433/189342.

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Dauletbekov, Daniyar. "Adeno-associated virus mediated rhodopsin delivery in preventing secondary cone degeneration in rhodopsin knockout mice." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:041ef367-7ce6-467e-8988-b9735231bdf2.

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Rhodopsin-linked retinitis pigmentosa (RP) is the most common form of autosomal dominant RP, an inherited retinal degeneration, in which rod degeneration is followed by secondary cone loss leading to loss of vision and blindness. The overall objective of this work was to develop an optimized gene replacement therapy, delivering the rhodopsin gene for rhodopsin- linked RP and establish whether secondary cone loss can be delayed. A fast-acting single mutant serotype 8 self-complementary adeno-associated virus vector was produced containing the human rhodopsin promoter and the human rhodopsin coding sequence. In vivo studies in rhodopsin knockout mouse showed that the vector administration led to widespread and robust expression of the transgene. Subretinal injection of the vector into three-week pups of rhodopsin knockout mice with cones expressing green fluorescent protein showed restoration of rod-derived electroretinogram (ERG) responses, and preservation of cone- driven ERG responses three months after injection. Similarly, the longitudinal follow-up with confocal scanning ophthalmoscopy found preservation of fluorescent cones up to three months after injection. Overall, these data provided evidence that the designed vector resulted in significant benefit to rod photoreceptors as well as in delay in secondary cone degeneration and built a basis for future use of this vector on dominant models of RP.
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Köhn, Linda. "Genetic mapping of retinal degenerations in Northern Sweden." Doctoral thesis, Umeå universitet, Medicinsk och klinisk genetik, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-27004.

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Inherited retinal degenerations are a group of disorders characterised by great genetic heterogeneity. Clinically, they can be divided into two large groups of diseases, those associated with night blindness, e.g. retinitis pigmentosa (RP), and those with macular malfunction, e.g. cone/cone-rod dystrophy (COD/CORD). This thesis is focused on finding the genetic basis of disease in families with autosomal dominant COD, autosomal dominant RP, and Bothnia dystrophy (BD), a regional variant of RP.   A variant of COD was previously mapped to 17p12-p13 in a family from northern Sweden. One additional family originating from the same geographical area was included in fine mapping of this chromosome region. Using 12 microsatellite markers in linkage and haplotype analysis, the region was refined from 26.9 to 14.3 cM. A missense mutation, Q626H, in an evolutionarily conserved region of PITPNM3, phosphatidylinositol transfer membrane-associated protein, was identified. The mutation segregated with the disease in both families and was absent from normal control chromosomes. PITPNM3 is a human homologue of the Drosophila retinal degeneration (rdgB) protein, which is highly expressed in the retina and has been proposed to be required for membrane turnover of photoreceptor cells. With the intention of establishing the global impact that PITPNM3 has on retinal degenerations 165 DNA samples from COD and CORD patients were obtained from Denmark, Germany, the UK, and USA and screened for mutations. The Q626H mutation found in the Swedish families was also found in one British family and a novel Q342P variant was detected in a German patient. In addition, two intronic variants were identified: c.900+60C>T and c.901-45G>A. Thus, we concluded that mutations in PITPNM3 represent a rare cause of COD worldwide. In two large families from northern Sweden showing autosomal dominant RP with reduced penetrance, the disease locus was mapped using genome-wide linkage analysis to 19q13.42 (RP11). Since mutation screening of eight genes on 19q13.42 revealed no mutations, multiplex ligation-dependent probe amplification (MLPA) was used to screen for large genomic abnormalities in PRPF31, RHO, RP1, RPE65, and IMPDH1. A large deletion spanning 11 exons of PRPF31 and three genes upstream was identified. Using long-range PCR, the breakpoints of the deletion were identified and the size of the deletion was determined to encompass almost 59 kb. BD is an autosomal recessive type of RP with high prevalence in northern Sweden. The disease is associated with a c.700C>T mutation in RLBP1. In a screening of recessive RP in northern Sweden, 67 patients were found to be homozygous for c.700C>T and 10 patients were heterozygous. An evaluation with arrayed primer extension (APEX) technology revealed a second mutation, c.677T>A, in RLBP1 giving rise to compound heterozygosity in these patients. In addition, a c.40C>T exchange in CAIV was detected in a patient with BD and in 143 healthy blood donors. The c.40C>T substitution in CAIV has been reported to cause autosomal dominant RP in South African families with European ancestry. However, in the population of northern Sweden it appears to be a benign polymorphism. In summary, a first mutation in PITPNM3, encoding a human homologue of the Drosophila retinal degeneration protein, was detected in two large families with COD. A large deletion in PRPF31 was discovered in two families with autosomal dominant RP showing reduced penetrance and in 10 patients BD was shown to be caused by two allelic mutations in RLBP1.
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Köhn, Linda. "Genetic mapping of retinal degenerations in Northern Sweden." Umeå : Umeå university, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-27004.

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BIAGIONI, MARTINA. "Fighting inflammation to save cones: anti-inflammatory approaches to slow down cone degeneration in a mouse model of retinitis pigmentosa." Doctoral thesis, 2019. http://hdl.handle.net/2158/1151621.

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The term Retinitis Pigmentosa (RP) defines a group of inherited dystrophies characterized by progressive degeneration of photoreceptors (PRs) and abnormalities in retinal pigment epithelium (RPE). In typical RP, primary degeneration of rods is followed by secondary death of cones. Affected individuals exhibit initial night blindness and constricted visual field, while central vision is eventually lost later, as cone cells degenerate. Unfortunately, there is no cure for RP. An important concept of RP pathophysiology is the biological link(s) between rod and cone death in this disease, where mutations are usually rod-specific and cones, genetically intact, degenerate as a consequence of a bystander effect. To note, the main cause of clinically significant vision loss is associated with cone, rather than with rod death. Although cones represent less than 5% of all PRs in the retina of most mammals, their role on human vision is crucial and their degeneration leads to a condition of irreversible vision loss. Survival of still-functioning cones following rod death enables patients with a night-blindness disease to lead normal lives for some time (Shelley et al., 2009). Previous studies of our laboratory and based on the rd10 mouse model of human RP demonstrated with molecular tools that inflammation emerges as a relevant component of RP, overcoming any other biological process expected to occur in this pathology. Here, we hypothesized that cones, non-primarily affected by the disease-causing mutation and long lasting with respect to rods, may suffer from side effects of such inflammatory process and finally die out. In this study, we employed a protocol of synthetic steroid administration to test the hypothesis that counteracting retinal inflammation concomitantly to the acute phase of PR degeneration may improve cone fate. Indeed, we demonstrated that systemic Dexamethasone treatment resulted in decreased inflammatory response at retinal level and this event was associated to improved cone survival and preservation of visual acuity in rd10 mice. Subsequently, we postulated that different classes of Mononuclear Phagocytes (MPs, such as microglia and monocytes-derived macrophages, primarily involved in the inflammatory response) played different roles in the chronic, noxious inflammatory response found at retinal level. The particular role of the CCL2 chemokine was assessed. Altogether, our findings suggest a link between local retinal inflammation and worsening of cone fate, opening the perspective of slowing down retinal decay and vision loss in RP by using anti-inflammatory strategies.
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Pimentel, Miguel Ângelo Apóstolo. "Genomic profile and genotype-phenotype correlations in patients with non-syndromic retinitis pigmentosa in a tertiary care centre in portugal." Master's thesis, 2020. http://hdl.handle.net/10316/97749.

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Trabalho Final do Mestrado Integrado em Medicina apresentado à Faculdade de Medicina
Introduction: Retinitis Pigmentosa (RP) is the most frequent inherited retinal dystrophy and a major cause of visual impairment and blindness worldwide. In Portugal, the genomic profile of patients with non-syndromic RP has never been reported. This study aimed to characterize the genomic landscape of Portuguese patients with non-syndromic RP and to establish possible genotype-phenotype correlations.Methods: Cross-sectional, single-centre study conducted in 50 consecutive patients (from 39 families) with a clinical diagnosis of non-syndromic-RP, followed at a tertiary care hospital in Portugal. Patients underwent genetic testing through Sanger sequencing of a suspected gene, next generation sequencing panels, whole exome sequencing (WES)-based next generation sequencing panels or WES. Results: We found disease-causing mutations in 25/39 patients (64.10%), totalizing 22 pathogenic variants identified in 10 genes. EYS, IMPG2, RPGR and RHO were the most frequently implicated genes, explaining 72% of the solved cases. Within autosomal recessive cases, EYS was the most frequently identified gene, while RPGR and RHO were the most common among X-linked and autosomal dominant cases, respectively. Conclusion: This preliminary study is the first study to characterize the genomic profile of non-syndromic RP in Portugal. Achieving strong population-based data is the first step towards better genetic and prognostic counselling as well as guidance for future therapeutic interventions.
Introdução: A retinopatia pigmentar (RP) é a distrofia hereditária da retina mais prevalente e uma das principais causas irreversíveis de comprometimento visual e cegueira em todo o mundo. Em Portugal, o perfil genético dos doentes com RP não sindrómica é ainda desconhecido. Este estudo tem como objetivos caracterizar a etiologia genética de uma série de casos de RP não sindrómica, bem como estabelecer eventuais correlações genótipo-fenótipo.Métodos: Estudo unicêntrico, transversal, que incluiu 50 doentes consecutivos (de 39 famílias) com o diagnóstico clínico de RP não sindrómica, seguidos num centro hospitalar terciário em Portugal. Todos os doentes realizaram estudo molecular, seja através de sequenciação Sanger, painéis de sequenciação de nova geração ou sequenciação do exoma completo.Resultados: Encontrámos variantes causadoras de doença (clinicamente relevantes) em 25/39 famílias (64.10%), totalizando 22 variantes causadoras de doença em 10 genes diferentes. Os genes EYS, IMPG2, RPGR e RHO foram os mais frequentemente implicados, explicando 72% dos casos resolvidos. Na RP com hereditariedade autossómica recessiva, o gene EYS foi o mais frequente, enquanto que os genes RPGR e RHO foram os mais frequentes na RP ligada ao cromossoma X e na RP autossómica dominante, respetivamente.Conclusão: Este estudo preliminar é o primeiro estudo a reportar o perfil genético de doentes portugueses com RP não sindrómica. A obtenção de dados robustos baseados em estudos populacionais é o primeiro passo para um melhor aconselhamento genético e prognóstico, bem como para uma melhor orientação para futuras intervenções terapêuticas.
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Book chapters on the topic "Cone, retinitis pigmentosa"

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Oishi, Akio, Maho Oishi, Ken Ogino, Satoshi Morooka, and Nagahisa Yoshimura. "Wide-Field Fundus Autofluorescence for Retinitis Pigmentosa and Cone/Cone-Rod Dystrophy." In Retinal Degenerative Diseases, 307–13. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_41.

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Nusinowitz, Steven, and David G. Birch. "Topography of Rod and Cone Sensitivity Loss in Retinitis Pigmentosa." In Documenta Ophthalmologica Proceedings Series, 227–30. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5698-1_38.

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Rajala, Ammaji, Yuhong Wang, and Raju V. S. Rajala. "Constitutive Activation Mutant mTOR Promote Cone Survival in Retinitis Pigmentosa Mice." In Retinal Degenerative Diseases, 491–97. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_61.

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Robson, Anthony G., Catherine Egan, Graham E. Holder, Alan C. Bird, and Fred W. Fitzke. "Comparing Rod and Cone Function with Fundus Autofluorescence Images in Retinitis Pigmentosa." In Advances in Experimental Medicine and Biology, 41–47. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0067-4_6.

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Kaplan, Henry J., Wei Wang, and Douglas C. Dean. "Restoration of Cone Photoreceptor Function in Retinitis Pigmentosa (RP): Retinal Cell-Based Therapy." In Stem Cell Biology and Regenerative Medicine, 157–66. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-05222-5_9.

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Greenstein, Vivienne C., Donald C. Hood, and Ronald E. Carr. "A Comparison of S Cone Pathway Sensitivity Loss in Patients with Diabetes and Retinitis Pigmentosa." In Colour Vision Deficiencies IX, 233–41. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2695-0_28.

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Grossman, N., K. Nikolic, P. Degenaar, C. Toumazou, H. Yang, and E. Drakakis. "A Non-Invasive Approach to the Bionic Eye." In Encyclopedia of Healthcare Information Systems, 998–1003. IGI Global, 2008. http://dx.doi.org/10.4018/978-1-59904-889-5.ch124.

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According to the World Health Organisation definition for blindness, that is, visual acuity bellow 3/60 for the best eye on the Snellen scale, there are thought to be 38 million blind people worldwide (Delbeke et al., 2004). This figure is expected to double over the next 25 years due to combination of an increasing population and aging worldwide. There are additionally 110 million people who have severely impaired vision and are high risk of becoming blind. The most common causes of blindness are: cataract, trachoma, glaucoma, diabetic retinopathy, age related macular degeneration (AMD) and retinitis pigmentosa (RP). In the west countries, cataract and glaucoma make up only 11% of the total causes of blindness. In these regions AMD and RP are prevalent eye diseases. AMD increases dramatically with age, so that (with about 2million cases in the USA) it is the leading cause of blindness among Americans of European descent (Friedman et al., 2004). The AMD and RP result in the loss of photosensitivity primarily due to destruction of the rod and cone photoreceptors. Medical intervention to date has been disappointing. There is no known mechanism by which the eye can self-repair. Anti-angiogenesis drugs can significantly slow down the progression of wet type AMD, but in most cases there is very little treatment. Even more significantly, none of the drugs are capable of restoring lost vision. The idea of using stem cells in therapies is still complex and may be many decades away from potential treatment. Prosthetic implants are therefore the only method at present by which we can offer a return of some of the lost vision. Here we present a special type of vision restoration based on the optical stimulation of retinal ganglion cells (RGCs), which remain operational.
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Conference papers on the topic "Cone, retinitis pigmentosa"

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Elsner, Ann E., Stephen A. Burns, and Louis A. Lobes. "Cone Optical Density in Retinitis Pigmentosa." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1986. http://dx.doi.org/10.1364/navs.1986.tub1.

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We use two noninvasive, psychophysical techniques to study the foveal cones of patients with retinitis pigmentosa. The techniques, steady-state color matching and dynamic color matching, are based on the fact that a color match depends on the optical density of the photopigment contained in the cones1-4. Reduction of the number of cones or neural deficits will not affect the color match so long as the observer can do the task. These techniques provide estimates of 1) the optical density of the cones at a given retinal illuminance, 2) the illuminance that reduces optical density by half (the half-bleach illuminance or IO), and 3) the rate of change in optical density3-4. To examine patients with minimal cone damage, we recruit patients in the early phases of disease with good visual acuity, 20/20-20/50. Patients, aged 14-46, vary as to the inheritance pattern and age of onset of night vision problems. All have reduced amplitude or extinguished photopic and scotopic ERG responses.
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Birch, David G., and Jane L. Anderson. "Yearly Rates of Rod and Cone Functional Loss in Retinitis Pigmentosa and Cone-Rod Degeneration." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1993. http://dx.doi.org/10.1364/navs.1993.ntua.3.

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Although night-blindness is typically the earliest symptom, little is known about the progression of rod loss in retinitis pigmentosa. Since detectable rod ERGs are unusual in adults with retinitis pigmentosa, despite detectable cone ERGs, it seems likely that the rate of progression is faster for rods than for cones. The ability to assess therapeutic intervention in young patients with measures that show rapid progression should enhance attempts to alter the natural history of this potentially blinding disease. We are presently conducting a prospective natural history study utilizing psychophysical and electrophysiological measures of rod function in a large sample of patients with either retinitis pigmentosa or cone-rod degeneration. The present report contains a preliminary analysis of relative rates of rod and cone ERG loss in these diseases and a summary of yearly changes in parameters of full-field rod ERGs and rod visual fields.
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Hood, Donald C., and David G. Birch. "Retinitis pigmentosa affects cone phototransduction as well as post-synaptic cone activity." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/vsia.1995.ma4.

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Numerous reports have documented delays in the implicit times of the b-wave of the cone ERG in patients with retinitis pigmentosa (RP) (see ref 1 for review). Abnormalities of the cone a-wave combined with anatomical evidence have lead to the proposal that the cone ERG abnormalities are due, at least in part, to cone photoreceptor abnormalities, specifically to shortened outer segmentse.g.1-3. Other ERG evidencee.g.4-7 is more difficult to explain by a cone receptor defect.
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4

Birch, David G., and Jane L. Anderson. "Rod Visual Fields in Cone-Rod Degeneration: Comparisons To Retinitis Pigmentosa." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/navs.1990.mb3.

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Cone-rod degeneration is characterized by atrophic macular degeneration with progressive decline in visual acuity and peripheral pigmentary disturbances with associated field loss1. The mode of inheritance is typically autosomal recessive2. Besides fundus appearance, patients with cone-rod degeneration can be distinguished from patients with retinitis pigmentosa on the basis of full-field electroretinography (ERG). Patients with cone-rod degeneration show markedly reduced cone ERG amplitudes with relative preservation of rod ERG amplitude. Rod b-wave implicit times are typically shorter than in patients with retinitis pigmentosa1,3-5. Rod sensitivity, as indexed by the semi-saturation constant (log k) of the Naka-Rushton function, is often only slightly elevated above normal4-5. These differences in rod ERG function suggest that the pattern of rod loss across the retina may differ between patients with cone-rod degeneration and patients with retinitis pigmentosa.
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5

Swanson, William H., David G. Birch, and Jane L. Anderson. "S-cone ERGs and S-cone acuity in patients with retinitis pigmentosa (RP)." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/oam.1992.tull1.

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Increment thresh old studies have reported selective S-cone damage within the macula in RP. To evaluate widespread S-cone damage, we obtained S-cone ERGs with a 50° field from 11 patients with RP who had detectable full field 30-Hz flicker ERGs. To evaluate peak macular S-cone density, we also measured S-cone acuity. S-cone amplitudes ranged from 0.6 to 1.4 log units below normal, while amplitudes for L- and M-cones ranged from 0.0 to 0.9 log unit below nor mal. Full intensity-response functions could only be measured in five patients; four had normal semisaturation constants, and all five functions were consistent with the primary loss being decreased number of photoreceptors rather than decreased photoreceptor sensitivity. S-cone acuity was normal for eight patients, including four with extinguished S-cone ERGs. These data suggest that peak macular S-cone density may be normal despite widespread loss of S-cones across the posterior pole. In patients with RP, S-cone loss seems to follow the pattern previously seen for L- and M-cones, with foveal sparing despite widespread degeneration.
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6

Swanson, William H., Marilyn Fiedelman, and Gary E. Fish. "Flicker Sensitivity in Patients with Retinitis Pigmentosa and Good Acuity." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/vsia.1995.tua1.

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Retinitis pigmentosa (RP) is a retinal degeneration which can be produced by a large number of different genetic mutations. In the early stages rod photoreceptor function is more severely impaired than cone photoreceptor function, and the rate of degeneration is faster for rods than for cones. Although the end stage can be complete loss of light perception, visual acuity often remains relatively unaffected despite severe loss of peripheral visual function.
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7

Lassoued, Ayoub, Furu Zhang, Kazuhiro Kurokawa, Yan Liu, James A. Crowell, and Donald T. Miller. "Measuring dysfunction of cone photoreceptors in retinitis pigmentosa with phase-sensitive AO-OCT." In Ophthalmic Technologies XXX, edited by Fabrice Manns, Per G. Söderberg, and Arthur Ho. SPIE, 2020. http://dx.doi.org/10.1117/12.2550216.

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8

Birch, David G. "Diurnal Rhythm in the ROD ERG in Retinitis Pigmentosa and CONE-ROD Degeneration." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/navs.1987.mc4.

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Systematic variations in full-field ERG threshold have been reported in eyes of normal human subjects entrained to a 14 hour light: 10 hour dark daily cycle. Rod ERG thresholds were 0.13 log unit higher following light-onset than at other times of day (1). This threshold elevation is believed to reflect rod outer segment (ROS) shedding since the time course is similar to that documented in anatomical studies of shedding (2-4) and since neither rod responses of fellow eyes (1) nor rod responses in unentrained subjects (5) vary with time of day. The entrainment process takes 3 days, that is, by the third day of entrainment, the magnitude of the diurnal variation in rod ERG threshold is similar to that obtained following 7 or more days of entrainment (5). Light-onset is necessary to synchronize the rhythm since no increase in threshold is detectable at 9:30 am without light exposure at 8:00 am (5).
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9

Sunness, Janet S. "Visual Function Evaluation of a Patient with Congenital Nightblindness and White Spots in the Fundus." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/navs.1992.tub1.

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A patient with congenital nightblindness and white spots in the fundus was evaluated in 1985 and again in 1990. This patient appeared to represent an intermediate state between fundus albipunctatus, a congenital stationary nightblindness with the special features of white spots in the fundus and prolonged dark adaptation of several hours leading to normal absolute thresholds(1,2,3), and retinitis punctata albescens, a form of retinitis pigmentosa characterized by white spots in the retina and by the functional features of retinitis pigmentosa (ring scotomas, diminished ERGs, progressive decrease of function, etc)(5). The patient was fascinating particularly in terms of 1) her dark adaptation abnormalities and the critical importance of prior recent light exposure in interpreting her visual function, 2) her evidence of cone involvement, and 3) her ERG abnormalities. The visual function tests in this patient provide diagnostic information, are critical in following her course, and provide fascinating insight into the mechanism of her disease.
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10

Massof, Robert W. "Theoretical Evaluation of S-Cone Pathway Sensitivity Losses In Diseases of The Visual System." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/navs.1990.tub4.

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Several recent studies have focused on the vulnerability of the S-cone pathway to visual system diseases. Selective or preferential S-cone pathway defects have been reported in diabetic retinopathy, age-related macular degeneration, retinitis pigmentosa, and glaucoma, to name but a few. Conclusions about Scone pathway defects in these disorders have been drawn from threshold versus wavelength measures (i.e., increment threshold spectral sensitivity), heterochromatic threshold versus radiance functions (ala Stiles pi mechanisms), heterochromatic visual acuity under conditions where contrast favors S-cones, and flicker versus flashed heterochromatic increment thresholds. These various methods rely on the presumed high chromatic gain and coarse spacetime resolution of the S-cone pathway.1-2
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