Relevant bibliographies by topics / Pigmented epithelium

Academic literature on the topic 'Pigmented epithelium'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Pigmented epithelium"

1

Pittack, C., G. B. Grunwald, and T. A. Reh. "Fibroblast growth factors are necessary for neural retina but not pigmented epithelium differentiation in chick embryos." Development 124, no. 4 (February 15, 1997): 805–16. http://dx.doi.org/10.1242/dev.124.4.805.

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During eye development, optic vesicles evaginate laterally from the neural tube and develop into two bilayered eye cups that are composed of an outer pigment epithelium layer and an inner neural retina layer. Despite their similar embryonic origin, the pigment epithelium and neural retina differentiate into two very distinct tissues. Previous studies have demonstrated that the developmental potential of the pigmented epithelial cells is not completely restricted; until embryonic day 4.5 in chick embryos, the cells are able to switch their phenotype and differentiate into neural retina when treated with fibroblast growth factors (FGF) (Park, C. M., and Hollenberg, M. J. (1989). Dev. Biol. 134, 201–205; Pittack, C., Jones, M., and Reh, T. A. 1991). Development 113, 577–588; Guillemot, F. and Cepko, C. L. (1992). Development 114, 743–754). These studies motivated us to test whether FGF is necessary for neural retina differentiation during the initial stages of eye cup development. Optic vesicles from embryonic day 1.5 chick were cultured for 24 hours as explants in the presence of FGF or neutralizing antibodies to FGF2. The cultured optic vesicles formed eye cups that contained a lens vesicle, neural retina and pigmented epithelium, based on morphology and expression of neural and pigmented epithelium-specific antigens. Addition of FGF to the optic vesicles caused the presumptive pigmented epithelium to undergo neuronal differentiation and, as a consequence, a double retina was formed. By contrast, neutralizing antibodies to FGF2 blocked neural differentiation in the presumptive neural retina, without affecting pigmented epithelial cell differentiation. These data, along with evidence for expression of several FGF family members and their receptors in the developing eye, indicate that members of the FGF family may be required for establishing the distinction between the neural retina and pigmented epithelium in the optic vesicle.
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AbdullGaffar, Badr. "Pilar Cyst Pigmented Epithelial Remnants: A Potential Diagnostic Pitfall." International Journal of Surgical Pathology 27, no. 6 (April 30, 2019): 639–42. http://dx.doi.org/10.1177/1066896919846376.

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Pilar cysts are common cutaneous cysts of follicular origin. They are easy to diagnose clinically and pathologically. Histologic diagnostic difficulties might arise in certain situations, however. Acute inflammation with total destruction of the cyst wall due to rupture with replacement by an abscess formation, foreign body giant cell reaction, and fibrosis could obscure their recognition. Cysts with hybrid lining epithelium could be confused with other cutaneous cysts. Epithelial remnants of the basal layer with loss of the squamous epithelium and shelled out cyst contents might mimic other epithelial cysts and vascular lesions. Few studies focused on the phenomenon of epithelial remnants or epithelial separation of pilar cysts. We report a case of a scalp cyst composed of a single layer of pigmented cuboidal lining epithelium. The initial differential diagnosis was hidrocystoma, solid-cystic hidradenoma, arteriovenous malformation, and lymphangioma. The intraepithelial pigment was melanin. The lining epithelium was positive for cytokeratin cocktail, CK5/6, CK8, CK19, p63, and D2-40 with scattered S-100 protein and melan-A positive melanocytes. Being unaware of the phenomenon of epithelial split in pilar cysts, it was mislabeled as a melanin-pigmented eccrine hidrocystoma. Surgical pathologists should be aware of pilar cysts’ epithelial remnants to avoid potential diagnostic pitfalls. An attention to certain histologic hints and knowledge of the immunoprofile of the basal layer should help pathologists avoid this pitfall.
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Ly, Angelica, Lisa Nivison-Smith, Michael Hennessy, and Michael Kalloniatis. "Pigmented Lesions of the Retinal Pigment Epithelium." Optometry and Vision Science 92, no. 8 (August 2015): 844–57. http://dx.doi.org/10.1097/opx.0000000000000640.

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Jensen, A. M., C. Walker, and M. Westerfield. "mosaic eyes: a zebrafish gene required in pigmented epithelium for apical localization of retinal cell division and lamination." Development 128, no. 1 (January 1, 2001): 95–105. http://dx.doi.org/10.1242/dev.128.1.95.

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For proper function of the retina, the correct proportions of retinal cell types must be generated, they must be organized into cell-specific laminae, and appropriate synaptic connections must be made. To understand the genetic regulation of retinal development, we have analyzed mutations in the mosaic eyes gene that disrupt retinal lamination, the localization of retinal cell divisions to the retinal pigmented epithelial surface and retinal pigmented epithelial development. Although retinal organization is severely disrupted in mosaic eyes mutants, surprisingly, retinal cell differentiation occurs. The positions of dividing cells and neurons in the brain appear normal in mosaic eyes mutants, suggesting that wild-type mosaic eyes function is specifically required for normal retinal development. We demonstrate that mosaic eyes function is required within the retinal pigmented epithelium, rather than in dividing retinal cells. This analysis reveals an interaction between the retinal pigmented epithelium and the retina that is required for retinal patterning. We suggest that wild-type mosaic eyes function is required for the retinal pigmented epithelium to signal properly to the retina.
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Nguyen, M., and H. Arnheiter. "Signaling and transcriptional regulation in early mammalian eye development: a link between FGF and MITF." Development 127, no. 16 (August 15, 2000): 3581–91. http://dx.doi.org/10.1242/dev.127.16.3581.

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During vertebrate eye development, the optic vesicle is partitioned into a domain at its distal tip that will give rise to the neuroretina, and another at its proximal base that will give rise to the pigmented epithelium. Both domains are initially bipotential, each capable of giving rise to either neuroretina or pigmented epithelium. The partitioning depends on extrinsic signals, notably fibroblast growth factors, which emanate from the overlying surface ectoderm and induce the adjacent neuroepithelium to assume the neuroretinal fate. Using explant cultures of mouse optic vesicles, we demonstrate that bipotentiality of the optic neuroepithelium is associated with the initial coexpression of the basic-helix-loop-helix-zipper transcription factor MITF, which is later needed solely in the pigmented epithelium, and a set of distinct transcription factors that become restricted to the neuroretina. Implantation of fibroblast growth factor-coated beads close to the base of the optic vesicle leads to a rapid downregulation of MITF and the development of an epithelium that, by morphology, gene expression, and lack of pigmentation, resembles the future neuroretina. Conversely, the removal of the surface ectoderm results in the maintenance of MITF in the distal optic epithelium, lack of expression of the neuroretinal-specific CHX10 transcription factor, and conversion of this epithelium into a pigmented monolayer. This phenomenon can be prevented by the application of fibroblast growth factor alone. In Mitf mutant embryos, parts of the future pigment epithelium become thickened, lose expression of a number of pigment epithelium transcription factors, gain expression of neuroretinal transcription factors, and eventually transdifferentiate into a laminated second retina. The results support the view that the bipotential optic neuroepithelium is characterized by overlapping gene expression patterns and that selective gene repression, brought about by local extrinsic signals, leads to the separation into discrete expression domains and, hence, to domain specification.
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Moszczynska, Anna, and Michal Opas. "Regulation of adhesion-related protein tyrosine kinases during in vitro differentiation of retinal pigment epithelial cells: translocation of pp60c-src to the nucleus is accompanied by downregulation of pp125FAK." Biochemistry and Cell Biology 72, no. 1-2 (January 1, 1994): 43–48. http://dx.doi.org/10.1139/o94-007.

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In the present report we show that induction of expression of a differentiated phenotype in cultured retinal pigmented epithelium of chick embryo is accompanied by coordinate regulation of expression and distribution of two adhesion-related nonreceptor protein tyrosine kinases, pp60c-src and pp125FAK∙pp60c-src translocates from the cell surface in flat undifferentiated cells to the nucleus in the packed differentiated cells. In contrast, pp125FAK, abundant in focal adhesions of flat undifferentiated cells, is downregulated in cells that have differentiated and packed into an epithelial sheet.Key words: retinal pigment epithelium, retina, tyrosine kinases, adhesion, differentiation.
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Kharitonov, A. E., A. V. Surdina, O. S. Lebedeva, A. N. Bogomazova, and M. A. Lagarkova. "Possibilities for Using Pluripotent Stem Cells for Restoring Damaged Eye Retinal Pigment Epithelium." Acta Naturae 10, no. 3 (September 15, 2018): 30–39. http://dx.doi.org/10.32607/20758251-2018-10-3-30-39.

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The retinal pigment epithelium is a monolayer of pigmented, hexagonal cells connected by tight junctions. These cells compose part of the outer blood-retina barrier, protect the eye from excessive light, have important secretory functions, and support the function of photoreceptors, ensuring the coordination of a variety of regulatory mechanisms. It is the degeneration of the pigment epithelium that is the root cause of many retinal degenerative diseases. The search for reliable cell sources for the transplantation of retinal pigment epithelium is of extreme urgency. Pluripotent stem cells (embryonic stem or induced pluripotent) can be differentiated with high efficiency into the pigment epithelium of the retina, which opens up possibilities for cellular therapy in macular degeneration and can slow down the development of pathology and, perhaps, restore a patient's vision. Pioneering clinical trials on transplantation of retinal pigment epithelial cells differentiated from pluripotent stem cells in the United States and Japan confirmed the need for developing and optimizing such approaches to cell therapy. For effective use, pigment epithelial cells differentiated from pluripotent stem cells should have a set of functional properties characteristic of such cells in vivo. This review summarizes the current state of preclinical and clinical studies in the field of retinal pigment epithelial transplantation therapy. We also discuss different differentiation protocols based on data in the literature and our own data, and the problems holding back the widespread therapeutic application of retinal pigment epithelium differentiated from pluripotent stem cells.
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Hyer, J., T. Mima, and T. Mikawa. "FGF1 patterns the optic vesicle by directing the placement of the neural retina domain." Development 125, no. 5 (March 1, 1998): 869–77. http://dx.doi.org/10.1242/dev.125.5.869.

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Patterning of the bipotential retinal primordia (the optic vesicles) into neural retina and retinal pigmented epithelium depends on its interaction with overlaying surface ectoderm. The surface ectoderm expresses FGFs and the optic vesicles express FGF receptors. Previous FGF-expression data and in vitro analyses support the hypothesis that FGF signaling plays a significant role in patterning the optic vesicle. To test this hypothesis in vivo we removed surface ectoderm, a rich source of FGFs. This ablation generated retinas in which neural and pigmented cell phenotypes were co-mingled. Two in vivo protocols were used to replace FGF secretion by surface ectoderm: (1) implantation of FGF-secreting fibroblasts, and (2) injection of replication-incompetent FGF retroviral expression vectors. The retinas in such embryos exhibited segregated neural and pigmented epithelial domains. The neural retina domains were always close to a source of FGF secretion. These results indicate that, in the absense of surface ectoderm, cells of the optic vesicles display both neural and pigmented retinal phenotypes, and that positional cues provided by FGF organize the bipotential optic vesicle into specific neural retina and pigmented epithelium domains. We conclude that FGF can mimic one of the earliest functions of surface ectoderm during eye development, namely the demarcation of neural retina from pigmented epithelium.
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Cherney, Edward. "Congenital hypertrophy of the retinal pigment epithelium." Ophthalmology journal 6, no. 4 (December 15, 2013): 55–59. http://dx.doi.org/10.17816/ov2013455-59.

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Congenital hypertrophy of the retinal pigment epithelium is a benign pigmented lesion of the posterior pole with a unique clinical appearance. It is flat, round, and has sharp edges. While it is usually black, it may have internal lacunae without pigment. The lesion may also be all hypopigmented. Over many years, the lesions may grow slightly and change their pigmentation. Even though malignant transformation is extremely rare, annual examinations should be performed.
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Soares, Andresa Borges, Vera Cavalcanti de Araújo, Fabricio Passador-Santos, Luiz Alexandre Thomaz, Andre Luis Santana de Freitas, Mario Claudio Mautoni, Rafael Fantelli Stelini, and Maria Leticia Cintra. "Uncommon Pigmented Carcinoma In Situ: Case Report and Brief Review." Clinical Pathology 14 (January 2021): 2632010X2110098. http://dx.doi.org/10.1177/2632010x211009819.

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Pigmented lesions of the oral mucosa encompass several benign and malignant conditions that may be a matter of concern under both clinical and histopathological views. We reported a case of a 62-year-old woman, presenting with an asymptomatic, deeply pigmented lesion on the soft palate. On examination, it appeared asymmetrical, with irregular borders and an area of ulceration. A biopsy, taken to rule out melanoma, revealed a pigmented carcinoma in situ. Throughout the tumor thickness, numerous interspersed melanocytes were found that did not extend to neighboring epithelium. These were large, richly dendritic, and presented abundance of melanin granules and small nuclei. Mild melanin incontinence was found. Scanty transfer of pigment to dysplastic epithelial cells was found through Fontana Masson staining. On immunohistochemical analyses, there were pancytokeratin-stained tumor epithelial cells; increased cell proliferation throughout the entire thickness of the tumor was emphasized by Ki-67 immunomarking. P16 was negative. The dendritic cells were selectively stained for S-100, HMB45 and Melan A. Wide spectrum in situ hybridization for human papillomavirus (HPV) was negative. Unfortunately, following diagnosis, the patient refused any treatment option. Pigmented squamous cell carcinoma with melanocyte colonization must be taken into account in the differential diagnosis of pigmented lesions of the oral cavity.
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Dissertations / Theses on the topic "Pigmented epithelium"

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Mehat, M. S. "Investigation of stem cell-derived retinal pigmented epithelium transplantation." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1540121/.

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Retinal pigment epithelium (RPE) cells perform a variety of roles that are principally directed at maintaining retinal function and homeostasis and their loss causes conditions such as age-related macular degeneration (AMD) and Stargardt disease (STGD). Regeneration of the loss or dystrophic RPE cells with stem cell-derived RPE may provide a potential therapeutic option. STGD is the commonest form of juvenile-onset, inherited macular degeneration. In order to determine the safety and efficacy of embryonic stem (ES) cell-derived RPE transplantation for the treatment of STGD, twelve subjects with STGD received a suspension of hES-derived RPE cells in escalating dose cohorts. Following the intervention, areas of sub retinal pigmentation were noted in all participants, suggestive of engraftment and survival. Transplanted hES-derived RPE cells were often observed overlying regions of atrophic Bruch's membrane (BrM). There was no evidence of tumorigenicity, immune adverse events or other serious safety concerns related to the transplanted cells. Furthermore, there was no significant change in visual function in the study eye of any participant. In order to improve the efficacy of ES-derived RPE transplantation, I developed an improved rodent model of retinal degeneration that features focal regions of atrophic BrM. I used a diode laser to selectively ablate RPE and observed focal regions of RPE atrophy with corresponding changes in choroidal vasculature that resemble those observed in retinal degenerative disease. Moreover, transplantation of human ES- and human induced pluripotent stem cell (iPS)-derived RPE resulted in re-population and restoration of RPE morphology post ablation. Although transplanted ES-derived RPE survived well on healthy BrM, attachment and survival of RPE is compromised on BrM that exhibits AMD or senescent changes. A potential strategy to promote survival and engraftment where there is damaged BrM is to deliver ES-derived RPE on a carrier substrate. I used a bespoke electrospun scaffold consisting of poly(e-caprolactone) and seeded this with either hESC or hiPSC-derived RPE. Transplantation of ES-derived RPE resulted in a functional monolayer of RPE with correct orientation and polarity on a biodegradable, porous and biocompatible membrane. These studies support further work in large animal models using ES-derived RPE scaffolds to restore the RPE in the presence of a compromised BrM.
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Weigel, Andrea Lynn. "Gene expression profiling of the retinal pigmented epithelium oxidative stress response in vitro and in vivo /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2002. http://uclibs.org/PID/11984.

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Wood, John P. M. "Induction of cell death within the retina and retinal pigmented epithelium : the role of protein kinase C." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363764.

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Más, Gómez Néstor [Verfasser], and Olaf [Akademischer Betreuer] Strauß. "Endogenously expressed bestrophin-1 modulates calcium signaling in the retinal pigmented epithelium / Néstor Más Gómez. Betreuer: Olaf Strauß." Regensburg : Universitätsbibliothek Regensburg, 2012. http://d-nb.info/1025386140/34.

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Raisler, Brian. "Adeno-associated virus type-2 mediated expression of pigmented epithelium derived factor or kringles 1-3 of angiostatin reduced neovascular retinopathies." [Gainesville, Fla.] : University of Florida, 2003. http://purl.fcla.edu/fcla/etd/UFE0002385.

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Sun, Jianan. "Protective Effects of Human iPS-Derived Retinal Pigmented Epithelial Cells in Comparison with Human Mesenchymal Stromal Cells and Human Neural Stem Cells on the Degenerating Retina in rd1 Mice." Kyoto University, 2016. http://hdl.handle.net/2433/215387.

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Tretiach, Marina Louise. "Bovine Models of Human Retinal Disease: Effect of Perivascular Cells on Retinal Endothelial Cell Permeability." Thesis, The University of Sydney, 2005. http://hdl.handle.net/2123/1153.

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Background: Diabetic vascular complications affect both the macro- and microvasculature. Microvascular pathology in diabetes may be mediated by biochemical factors that precipitate cellular changes at both the gene and protein levels. In the diabetic retina, vascular pathology is found mainly in microvessels, including the retinal precapillary arterioles, capillaries and venules. Macular oedema secondary to breakdown of the inner blood-retinal barrier is the most common cause of vision impairment in diabetic retinopathy. Müller cells play a critical role in the trophic support of retinal neurons and blood vessels. In chronic diabetes, Müller cells are increasingly unable to maintain their supportive functions and may themselves undergo changes that exacerbate the retinal pathology. The consequences of early diabetic changes in retinal cells are primarily considered in this thesis. Aims: This thesis aims to investigate the effect of perivascular cells (Müller cells, RPE, pericytes) on retinal endothelial cell permeability using an established in vitro model. Methods: Immunohistochemistry, cell morphology and cell growth patterns were used to characterise primary bovine retinal cells (Müller cells, RPE, pericytes and endothelial cells). An in vitro model of the blood-retinal barrier was refined by coculturing retinal endothelial cells with perivascular cells (Müller cells or pericytes) on opposite sides of a permeable Transwell filter. The integrity of the barrier formed by endothelial cells was assessed by transendothelial electrical resistance (TEER) measurements. Functional characteristics of endothelial cells were compared with ultrastructural morphology to determine if different cell types have barrier-enhancing effects on endothelial cell cultures. Once the co-culture model was established, retinal endothelial cells and Müller cells were exposed to different environmental conditions (20% oxygen, normoxia; 1% oxygen, hypoxia) to examine the effect of perivascular cells on endothelial cell permeability under reduced oxygen conditions. Barrier integrity was assessed by TEER measurements and permeability was measured by passive diffusion of radiolabelled tracers from the luminal to the abluminal side of the endothelial cell barrier. A further study investigated the mechanism of laser therapy on re-establishment of retinal endothelial cell barrier integrity. Müller cells and RPE, that comprise the scar formed after laser photocoagulation, and control cells (Müller cells and pericytes, RPE cells and ECV304, an epithelial cell line) were grown in long-term culture and treated with blue-green argon laser. Lasered cells were placed underneath confluent retinal endothelial cells growing on a permeable filter, providing conditioned medium to the basal surface of endothelial cells. The effect of conditioned medium on endothelial cell permeability was determined, as above. Results: Co-cultures of retinal endothelial cells and Müller cells on opposite sides of a permeable filter showed that Müller cells can enhance the integrity of the endothelial cell barrier, most likely through soluble factors. Low basal resistances generated by endothelial cells from different retinal isolations may be the result of erratic growth characteristics (determined by ultrastructural studies) or the selection of vessel fragments without true â barrier characteristicsâ in the isolation step. When Müller cells were co-cultured in close apposition to endothelial cells under normoxic conditions, the barrier integrity was enhanced and permeability was reduced. Under hypoxic conditions, Müller cells had a detrimental effect on the integrity of the endothelial cell barrier and permeability was increased in closely apposed cells. Conditioned medium from long-term cultured Müller cells and RPE that typically comprise the scar formed after lasering, enhanced TEER and reduced permeability of cultured endothelial cells. Conclusions: These studies confirm that bovine tissues can be used as a suitable model to investigate the role of perivascular cells on the permeability of retinal endothelial cells. The dual effect of Müller cells on the retinal endothelial cell barrier under different environmental conditions, underscores the critical role of Müller cells in regulating the blood-retinal barrier in health and disease. These studies also raise the possibility that soluble factor(s) secreted by Müller cells and RPE subsequent to laser treatment reduce the permeability of retinal vascular endothelium. Future studies to identify these factor(s) may have implications for the clinical treatment of macular oedema secondary to diseases including diabetic retinopathy.
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Tretiach, Marina Louise. "Bovine Models of Human Retinal Disease: Effect of Perivascular Cells on Retinal Endothelial Cell Permeability." University of Sydney, 2005. http://hdl.handle.net/2123/1153.

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Doctor of Philosophy (Medicine)
Background: Diabetic vascular complications affect both the macro- and microvasculature. Microvascular pathology in diabetes may be mediated by biochemical factors that precipitate cellular changes at both the gene and protein levels. In the diabetic retina, vascular pathology is found mainly in microvessels, including the retinal precapillary arterioles, capillaries and venules. Macular oedema secondary to breakdown of the inner blood-retinal barrier is the most common cause of vision impairment in diabetic retinopathy. Müller cells play a critical role in the trophic support of retinal neurons and blood vessels. In chronic diabetes, Müller cells are increasingly unable to maintain their supportive functions and may themselves undergo changes that exacerbate the retinal pathology. The consequences of early diabetic changes in retinal cells are primarily considered in this thesis. Aims: This thesis aims to investigate the effect of perivascular cells (Müller cells, RPE, pericytes) on retinal endothelial cell permeability using an established in vitro model. Methods: Immunohistochemistry, cell morphology and cell growth patterns were used to characterise primary bovine retinal cells (Müller cells, RPE, pericytes and endothelial cells). An in vitro model of the blood-retinal barrier was refined by coculturing retinal endothelial cells with perivascular cells (Müller cells or pericytes) on opposite sides of a permeable Transwell filter. The integrity of the barrier formed by endothelial cells was assessed by transendothelial electrical resistance (TEER) measurements. Functional characteristics of endothelial cells were compared with ultrastructural morphology to determine if different cell types have barrier-enhancing effects on endothelial cell cultures. Once the co-culture model was established, retinal endothelial cells and Müller cells were exposed to different environmental conditions (20% oxygen, normoxia; 1% oxygen, hypoxia) to examine the effect of perivascular cells on endothelial cell permeability under reduced oxygen conditions. Barrier integrity was assessed by TEER measurements and permeability was measured by passive diffusion of radiolabelled tracers from the luminal to the abluminal side of the endothelial cell barrier. A further study investigated the mechanism of laser therapy on re-establishment of retinal endothelial cell barrier integrity. Müller cells and RPE, that comprise the scar formed after laser photocoagulation, and control cells (Müller cells and pericytes, RPE cells and ECV304, an epithelial cell line) were grown in long-term culture and treated with blue-green argon laser. Lasered cells were placed underneath confluent retinal endothelial cells growing on a permeable filter, providing conditioned medium to the basal surface of endothelial cells. The effect of conditioned medium on endothelial cell permeability was determined, as above. Results: Co-cultures of retinal endothelial cells and Müller cells on opposite sides of a permeable filter showed that Müller cells can enhance the integrity of the endothelial cell barrier, most likely through soluble factors. Low basal resistances generated by endothelial cells from different retinal isolations may be the result of erratic growth characteristics (determined by ultrastructural studies) or the selection of vessel fragments without true ‘barrier characteristics’ in the isolation step. When Müller cells were co-cultured in close apposition to endothelial cells under normoxic conditions, the barrier integrity was enhanced and permeability was reduced. Under hypoxic conditions, Müller cells had a detrimental effect on the integrity of the endothelial cell barrier and permeability was increased in closely apposed cells. Conditioned medium from long-term cultured Müller cells and RPE that typically comprise the scar formed after lasering, enhanced TEER and reduced permeability of cultured endothelial cells. Conclusions: These studies confirm that bovine tissues can be used as a suitable model to investigate the role of perivascular cells on the permeability of retinal endothelial cells. The dual effect of Müller cells on the retinal endothelial cell barrier under different environmental conditions, underscores the critical role of Müller cells in regulating the blood-retinal barrier in health and disease. These studies also raise the possibility that soluble factor(s) secreted by Müller cells and RPE subsequent to laser treatment reduce the permeability of retinal vascular endothelium. Future studies to identify these factor(s) may have implications for the clinical treatment of macular oedema secondary to diseases including diabetic retinopathy.
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Al-Hosaini, Heba. "Age-related changes in retinal pigment epithelium." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444089/.

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The retinal pigment epithelium (RPE) is a monolayer of hexagonal organized cells located between the choriocapillaris and the neurosensory retina. As the RPE is implicated in a range of eye diseases, an understanding of its structure and ability for self renewal is critical for therapeutic strategies. Analysis of human RPE cells at the extreme periphery of the retina reveals a population larger in size than those in the centre, they are highly irregular and form an annulus of 4-5 mm. Although binucleation in humans is rare, 10% of these cells are binucleated. In the central region these large binucleated cells are only found adjacent to drusen, which are age-related lipid-rich deposits. Compared with humans, rat RPE is relatively homogeneous, however, the majority of its cells are binucleated, particularly in the central region. Human and rat RPE also shows different patterns of aging. In humans, the centre of the retina shows a significant reduction in RPE cell density with age, which was not observed in aged rats. The capacity of mature RPE cells to enter the cell cycle was investigated using a proliferative marker in rats. Here a subpopulation of mature peripheral RPE cells had the capacity to enter the cell cycle, and one-third of these cells completed cellular division. As RPE proliferation occur in response to retinal detachment, this was performed on rats and the patterns of gene expression in RPE examined. An increase was observed in nestin, PCNA and Ki67 expression, which was also confirmed at a protein level by immunohistochemistry. These results suggest that RPE cells have the capacity to proliferate and may possibly differentiate if subjected to appropriate stimuli in a normal retina.
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Donahue, Vicki S. "Phospholipase c activity in retinal pigment epithelium." Virtual Press, 1997. http://liblink.bsu.edu/uhtbin/catkey/1041916.

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The role of the retinal pigment epithelial cells on the viability and renewal of photoreceptors has been well demonstrated in the Royal College of Surgeons (RCS) strain of rat. These rats are characterized by an inherited time-dependent degeneration of their photoreceptors. This degeneration is apparently due to the inability of the retinal pigment epithelial cells to adequately ingest fragments of photoreceptor membrane that are shed during the course of photoreceptor membrane renewal. The buildup of photoreceptor material in the interphotoreceptor space ultimately leads to the degeneration of photoreceptors in these animals. With regard to the pigment epithelial cells, neither the mechanism mediating the ingestion process in normal rats nor the nature of the defect of this process in RCS rats is understood.It is the goal of this proposed research to assay for the presence of phospholipase C in retinal pigment epithelial (RPE) cells and to determine possible modulators of the enzyme in an attempt to associate this with the process of phagocytosis.
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Books on the topic "Pigmented epithelium"

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Coscas, Gabriel, and Felice Cardillo Piccolino, eds. Retinal Pigment Epithelium and Macular Diseases. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5137-5.

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1946-, Garcia Charles A., ed. Retinal pigment epithelial transplantation. New York: Springer-Verlag, 1995.

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Gamulescu, Maria Andreea, Horst Helbig, and Joachim Wachtlin, eds. Retinal Pigment Epithelial Detachment. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56133-2.

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Klettner, Alexa Karina, and Stefan Dithmar, eds. Retinal Pigment Epithelium in Health and Disease. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28384-1.

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M, LaVail Matthew, Anderson Robert E, Hollyfield Joe G, and International Congress of Eye Research (8th : 1988 : San Francisco, Calif.), eds. Inherited and environmentally induced retinal degenerations: Proceedings of the International Symposium on Retinal Degenerations, held in San Francisco, California, September 2 and 3, 1988. New York: Liss, 1989.

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M, Zingirian, Cardillo Piccolino F, and International Meeting on Retinal Pigment Epithelium (1988 : Santa Margherita Ligure, Italy), eds. Retinal pigment epithelium. [Amsterdam]: Kugler & Ghedini, 1989.

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Coscas, Gabriel, and Felice Cardillo Piccolino. Retinal Pigment Epithelium and Macular Diseases. Springer, 2012.

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Coscas, Gabriel. Retinal Pigment Epithelium and Macular Diseases. Gabriel Coscas, 2012.

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Gabriel, Coscas, Cardillo Piccolino F, European Macula Group Meeting, and International Meeting on Retinal Pigment Epithelium (2nd : 1996 : Genoa, Italy), eds. Retinal pigment epithelium and macular diseases. Dordrecht: Kluwer Academic Publishers, 1998.

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Coscas, Gabriel, and Felice Cardillo Piccolino. Retinal Pigment Epithelium and Macular Diseases. Springer, 2012.

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Book chapters on the topic "Pigmented epithelium"

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Cavallotti, Carlo A. P., and Marcus Schveoller. "Aging of the Retinal Pigmented Epithelium." In Age-Related Changes of the Human Eye, 203–15. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-507-7_10.

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Klingeborn, Mikael, W. Daniel Stamer, and Catherine Bowes Rickman. "Polarized Exosome Release from the Retinal Pigmented Epithelium." In Retinal Degenerative Diseases, 539–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_65.

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Shields, Carol L., and Jerry A. Shields. "Tumors and Related Lesions of the Retinal Pigmented Epithelium." In Ocular Oncology, 101–14. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-2336-2_11.

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Croze, Roxanne H., and Dennis O. Clegg. "Differentiation of Pluripotent Stem Cells into Retinal Pigmented Epithelium." In Developments in Ophthalmology, 81–96. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000357361.

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Donaldson, K. J., W. F. Wu, H. Skelton, S. Markand, S. Ferdous, J. Sellers, M. A. Chrenek, et al. "Analysis of Damage and Wound Healing in the Retinal Pigmented Epithelium." In Retinal Degenerative Diseases, 425–30. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27378-1_70.

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Bandello, Francesco, Chiara Giuffrè, and Maurizio Battaglia Parodi. "Pigment Epithelium Detachment." In Encyclopedia of Ophthalmology, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-35951-4_1057-1.

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Krauthammer, Mark, and Laurent Kodjikian. "Retinal Pigment Epithelium." In Encyclopedia of Ophthalmology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_1129-1.

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Bandello, Francesco, Chiara Giuffrè, and Maurizio Battaglia Parodi. "Pigment Epithelium Detachment." In Encyclopedia of Ophthalmology, 1384–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_1057.

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Krauthammer, Mark, and Laurent Kodjikian. "Retinal Pigment Epithelium." In Encyclopedia of Ophthalmology, 1528–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_1129.

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Krstić, Radivoj V. "Surface Epithelia. Simple Cuboidal Epithelium. Example: Pigment Epithelium of Human and Mouse Retina." In General Histology of the Mammal, 28–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70420-8_13.

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Conference papers on the topic "Pigmented epithelium"

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Payne, Dale J., Thomas R. Jost, James J. Elliot, Brent Eilert, Laura Lott, Karen Lott, Gary D. Noojin, Richard A. Hopkins, Jr., Charles P. Lin, and Benjamin A. Rockwell. "Cavitation thresholds in the rabbit retinal pigmented epithelium." In BiOS '99 International Biomedical Optics Symposium, edited by Steven L. Jacques, Gerhard J. Mueller, Andre Roggan, and David H. Sliney. SPIE, 1999. http://dx.doi.org/10.1117/12.350019.

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Yi, Ji, and Lei Zhang. "Wavelength-dependent optical properties of melanosomes in retinal pigmented epithelium (Conference Presentation)." In Biophysics, Biology and Biophotonics II: the Crossroads, edited by Adam Wax and Vadim Backman. SPIE, 2017. http://dx.doi.org/10.1117/12.2252693.

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Groux, Kassandra, Jules Scholler, Pedro Mecê, Sacha Reichman, Valérie Fradot, Michel Pâques, Claude Boccara, and Katharine Grieve. "Stress and repair in retinal pigmented epithelium cell culture imaged with dynamic full-field OCT (Conference Presentation)." In Dynamics and Fluctuations in Biomedical Photonics XVII, edited by Valery V. Tuchin, Martin J. Leahy, and Ruikang K. Wang. SPIE, 2020. http://dx.doi.org/10.1117/12.2544653.

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White, Kerry F., Matthew Rausch, Jing Hua, Katherine H. Walsh, Christine E. Miller, Christopher C. Wells, Devapregasan Moodley, et al. "Abstract 558: MERTK-specific antibodies that have therapeutic antitumor activity in mice disrupt the integrity of the retinal pigmented epithelium in cynomolgus monkeys." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-558.

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White, Kerry F., Matthew Rausch, Jing Hua, Katherine H. Walsh, Christine E. Miller, Christopher C. Wells, Devapregasan Moodley, et al. "Abstract 558: MERTK-specific antibodies that have therapeutic antitumor activity in mice disrupt the integrity of the retinal pigmented epithelium in cynomolgus monkeys." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-558.

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Rapkin, Jeffrey S., and Julian J. Nussbaum. "Spectral Laminography of Subretinal Neovascular Membranes." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/navs.1988.wc3.

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Subretinal neovascularization occurs in association with age-related maculopathy, histoplasmosis, angioid streaks, trauma and myopia.1 Other less common associations include optic nerve head drusen, choroidal tumors, pigment epithelial hamartomas, photocoagulation, rubella retinopathy and various inflammatory disorders such as multifocal posterior pigment epitheliopathy and Harada's disease.1 The clinical appearance of subretinal neovascularization is a dirty gray or green discoloration at the level of the retinal pigment epithelium.1,2 New vessel growth may be accompanied by a serous, exudative or hemorrhagic detachment of the retinal pigment epithelium or neurosensory retina. Early treatment of neovascular membrane by laser photocoagulation has been shown to be of benefit in limiting vision loss for some patients.3,4 Prompt recognition and localization of the neovascular process is essential for successful treatment. Fluorescein angiography is the standard method used to confirm the presence and anatomical location of subretinal neovascular membranes.1,2,5,6
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Narasimhan, Arunn, and Kaushal Kumar Jha. "Bio-Heat Transfer Model of Human Eye Subjected to Retinal Laser Irradiation." In 2010 14th International Heat Transfer Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/ihtc14-22799.

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Retinopathy is a surgical process in which maladies of the human eye are treated by laser irradiation. A two-dimensional numerical model of the human eye geometry has been developed to investigate steady and transient thermal effects due to laser radiation. In particular, the influence of choroidal pigmentations and choroidal blood convection — parameterized as a function of choroidal blood perfusion are investigated in detail. The Pennes bio-heat transfer equation is invoked as the governing equation and a finite volume formulation is employed in the numerical method. The numerical model is validated with available experimental and two-dimensional numerical results. For a 500 μm diameter spot size, laser power of 0.2 W, with 100% absorption of laser radiation in the Retinal Pigmented Epithelium (RPE) region, the peak RPE temperature is observed to be 175 °C at steady state, with no blood perfusion in choroid. It reduces to 168.5 °C when the choroidal blood perfusion rate is increased to 23.3 kgm−3s−1. However, under transient simulations, the peak RPE temperature is observed to remain constant at 104 °C after 100 ms of the laser surgery period. A truncated three-dimensional model incorporating multiple laser irradiation spots is also developed to observe the spatial effect of choroidal blood perfusion. For a circular array of seven uniformly distributed spots of identical diameter and laser power of 0.2 W, steady and transient temperature evolution are presented with analysis.
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Sunness, Janet S., Mary A. Johnson, and Robert W. Massof. "Visual Function Over Drusen in Age-Related Macular Degeneration: Direct Measurements Using the Fundus Camera Stimulator." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/navs.1987.wd3.

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Age-related macular degeneration (AMD) is a spectrum of conditions affecting the eyes of the elderly, and is the leading cause of severe visual loss in people over 60 years of age.(1) Drusen, white-yellow excrescences below the retinal pigment epithelium, are associated with the development of the vision-threatening complications of age-related macular degeneration. However, drusen are seen ophthalmoscopically in over 30% of the elderly population. The vision-threatening aspects of AMD (which occur in approximately 1-3% of patients with drusen per year) include the development of a subretinal neovascular membrane and disciform scarring, retinal pigment epithelial detachment, and retinal pigment epithelial atrophy. At present, it is not possible to predict which people with drusen will go on to lose vision. Since prompt treatment of a subretinal neovascular membrane with laser photocoagulation can significantly reduce the frequency of severe visual loss,(2) there has been increased attention focused on finding ophthalmologic or visual function changes in drusen patients which may segregate a high-risk group.
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Glickman, Randolph D., Alexander E. Dontsov, Michail A. Ostrovsky, Neeru Kumar, Meena Vendal, and Mary A. Gonzales. "Photo-oxidative stress in the eye: role of retinal pigment epithelial pigments." In International Symposium on Biomedical Optics, edited by Qingming Luo, Britton Chance, Lihong V. Wang, and Steven L. Jacques. SPIE, 1999. http://dx.doi.org/10.1117/12.364425.

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Glickman, Randolph D., Alexander E. Dontsov, and Michail A. Ostrovsky. "Relative photoreactivity of pigment inclusions of the retinal pigment epithelium." In BiOS '98 International Biomedical Optics Symposium, edited by Steven L. Jacques. SPIE, 1998. http://dx.doi.org/10.1117/12.308206.

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Reports on the topic "Pigmented epithelium"

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Lin, Charles P. Mechanism of Ultrashort Pulse Laser Injury to the RPE (Retinal Pigment Epithelium). Fort Belvoir, VA: Defense Technical Information Center, February 2003. http://dx.doi.org/10.21236/ada417926.

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Mirochnik, Yelena. Design and Development of Peptides from the Anti-Angiogenic Pigment Epithelial-Derived Factor for the Therapy of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2007. http://dx.doi.org/10.21236/ada477542.

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Obringer, John W., and Martin D. Johnson. Differential Protein Expression in Explanted Human Retinal Pigment Epithelial Cells 24-Hours Post-Exposure 532 nm, 3.0 ns Pulsed Laser Light. Fort Belvoir, VA: Defense Technical Information Center, December 2004. http://dx.doi.org/10.21236/ada428875.

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Chen, Chen, Peng Chen, Xia Liu, and Hua Li. Combined 5-Fluorouracil and Low Molecular Weight Heparin for the Prevention of Postoperative Proliferative Vitreoretinopathy in Patients with Retinal Detachment. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0117.

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Review question / Objective: The aim of this meta-analysis is to evaluate the efficacy and safety of intraoperative infusion of combined 5-fluorouracil and low molecular weight heparin (LMWH) for the prevention of postoperative proliferative vitreoretinopathy in patients with retinal detachment. Condition being studied: Postoperative proliferative vitreoretinopathy (PVR) is the primary cause of failure of retinal reattachment surgery. 5-fluorouracil (5-FU) inhibits the proliferation of fibroblasts, and suppresses collagen contraction. On the other hand, heparin reduces fibrin exudation, and inhibits the adhesion and migration of retinal pigment epithelial cells. We conduct this comprehensive literature search and meta-analysis to address whether intraoperative infusion of combined 5-FU and LWMH improves the primary success rate of pars plana vitrectomy, as well as reduces postoperative PVR. Our study aims to provide clinical evidence for retinal surgeons concerning their choice of intraoperative medication.
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Jiang, yang, and shixin Qi. Diagnostic test accuracy of spectral-domain optical coherence tomography used to Differentiate PCV from nvAMD and other diseases that tend to cause serous or serosanguinous retinal pigment epithelial detachment: a systematic review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0048.

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Obringer, John W., and Martin D. Johnson. Differential Gene Expression in Explanted Human Retinal Pigment Epithelial Cells 24-Hours Post-Exposure to 532 nm, 3.0 ns Pulsed Laser Light and 1064 nm, 170 ps Pulsed Laser Light 12-Hours Post-Exposure: Results Compendium. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427356.

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