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Academic literature on the topic 'Muller cells'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Muller cells"

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Kosaka, Yudai, and Tetsuhiko Ohba. "3P174 Study on membrane microfluidity of living cells using Muller Matrix microscopy(12. Cell biology,Poster)." Seibutsu Butsuri 53, supplement1-2 (2013): S240. http://dx.doi.org/10.2142/biophys.53.s240_5.

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Newman, EA. "Membrane physiology of retinal glial (Muller) cells." Journal of Neuroscience 5, no. 8 (August 1, 1985): 2225–39. http://dx.doi.org/10.1523/jneurosci.05-08-02225.1985.

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Ripps, H., R. P. Malchow, and H. Oian. "GABA-mediated currents of skate Muller cells." Experimental Eye Research 55 (September 1992): 17. http://dx.doi.org/10.1016/0014-4835(92)90273-u.

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Bringmann, Andreas. "Role of Muller cells in retinal degenerations." Frontiers in Bioscience 6, no. 1 (2001): e77. http://dx.doi.org/10.2741/bringman.

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Linser, Paul J. "Comparative immunochemistry of elasmobranch retina muller cells and horizontal cells." Journal of Experimental Zoology 256, S5 (1990): 88–96. http://dx.doi.org/10.1002/jez.1402560513.

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Newman, Eric A. "Physiological properties and possible functions of muller cells." Neuroscience Research Supplements 4 (January 1986): S209—S220. http://dx.doi.org/10.1016/s0921-8696(86)80020-2.

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Newman, Eric A. "Physiological properties and possible functions of Muller cells." Neuroscience Research 4 (January 1986): S209—S220. http://dx.doi.org/10.1016/0168-0102(86)90084-2.

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Attwell, David, Marek Szatkowski, Muriel Bouvier, and Alessandra Amato. "Ion movements accompanying glutamate uptake into Muller cells." Experimental Eye Research 55 (September 1992): 17. http://dx.doi.org/10.1016/0014-4835(92)90271-s.

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Puro, Donald G. "Calcium-permeable ion channels in human Muller cells." Experimental Eye Research 55 (September 1992): 18. http://dx.doi.org/10.1016/0014-4835(92)90275-w.

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Puro, Donald G. "Stretch-activated channels in human retinal muller cells." Glia 4, no. 5 (1991): 456–60. http://dx.doi.org/10.1002/glia.440040505.

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Dissertations / Theses on the topic "Muller cells"

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Walker, Robert J. "Inflammatory cytokines modulated by beta adrenergic receptors on retinal Muller cells in diabetic retinopathy /." Available to subscribers only, 2007. http://proquest.umi.com/pqdweb?did=1467888651&sid=24&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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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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Eldred, Megan. "Investigating cellular and molecular mechanisms of neuronal layering in self-organising aggregates of zebrafish retinal cells." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/284080.

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The central nervous system is a complex, yet well-organised, often laminated, tissue. This robust organisation is evident in the architecture of the retina: consisting of 5 different neuronal types organised into distinct layers: Retinal Ganglion Cell (RGC), Amacrine Cell (AC), Bipolar Cell (BP), Horizontal Cell (HC) and Photoreceptor cell (PR) layers. This remarkable organisation is evolutionarily conserved in vertebrates, yet little is known about the mechanisms by which these cells form the correct layers. Live imaging has revealed overlapping periods of birth and extensive inter-digitation followed by cells sorting out into their appropriate positions, suggesting cell-cell interactions are important. To investigate possible cellular and molecular mechanisms responsible for the establishment of the tissue architecture I developed an organoid culture system for zebrafish retinal cells. To identify the cells in culture I used a Spectrum of Fates fish line which is a multiply transgenic line in which each retinal cell type can be identified based on expression of a combination of fluorescently tagged cell fate markers. The development of the protocol by which I cultured the cells and observed their cell-cell interactions involved establishing the best methods to dissociate and culture zebrafish retinal cells in a non-adhesive environment, then imaging the resulting reaggregates to examine the position of the different retinal cell types. By doing this I observed their inherent self-organising properties, in the absence of extrinsic cues or scaffolds. These cells appeared to be arranged in an inside-out layering, although all cell types are layered in the same relative order as they are in vivo. To analyse the organization in these aggregates I developed a Matlab script in collaboration with Leila Muresan which analyses the relative positioning of cells in concentric rings from the periphery to the centre of the aggregates according to the cell fate-tagged fluorescent markers. The script then fits this data as an empirical cumulative distribution function for different groups of cells to determine how spatially distinct populations of cells are. This gave me my measure of organisation. I then investigated the cell-cell interactions involved in this self-organisation by genetically or pharmacologically removing individual cell types and assaying the resulting organisation of the reaggregated, cell-type deficient, retinal organoids. I revealed that Müller Glia are important for retinal cell self-organisation. I also investigated the role of Retinal Pigment Epithelial (RPE) cells and Retinal Ganglion Cells and found they had no impact on the ability of the remaining cell types to organize. I began to investigate the role of Amacrine Cells but found that retinas void of ACs were susceptible to disaggregating in our dissection setup, preventing me from collecting the material needed for culture. I also investigated the role of candidate molecules in this system and revealed that R-Cognin is critical for retinal cells to reaggregate. Not only can I remove cells or molecules from the system, but I show how it can also be manipulated to replace molecules of interest such as laminin, by coating beads with the substance of choice and placing it amongst the cells to see if their organisational behaviour is affected. In summary, I have developed a system which provides a simple and easy platform to manipulate in various ways to help us potentially reveal some of the important players in neuronal patterning.
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Gallina, Donika. "The Role of Glucocorticoid Receptor-signaling and Wnt-signaling in Avian Retinal Regeneration." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1439204931.

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Shelton, Melissa D. "Glutaredoxin Regulation of Pro-Inflammatory Responses in a Model of Diabetic Retinopathy." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1224176018.

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Lycke, Christian. "Ko-Expression des astroglialen GFAP- und des oligodendrozytären PLP-Promotors in Müllerzellen der Retina: Aktivierung durch Läsionen." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-158668.

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Die Dissertation befasst sich mit der Untersuchung der Ko-Expression des GFAP- und des PLP-Promotors in Müllerzellen der Netzhaut transgener Mäuse. Die verwendete Mauslinie ist tripel-transgen für den GFAP- und den PLP-Promotor sowie für einen ROSA26-Reporter. Durch die Quantifizierung der EYFP-Expression in Müllerzellen konnte gezeigt werden, dass es nach akuter ischämischer Schädigung sowie einer angeborenen retinalen Degeneration in Müllerzellen zu einer Aktivierung des oligodendrozytären PLP-Promotors kommt. Weiterhin wurde festgestellt, dass die Aktivierung des Transkriptionsfaktors Sox-9, der sowohl für die Entwicklung der Müllerzellen als auch für die Oligodendrogenese von entscheidender Rolle ist, mit dieser Promotoraktivierung korreliert. Diese Ergebnisse implizieren, dass Müllerzellen im Rahmen ihrer Stammzelleigenschaften in der Lage sind, auf embryonale Entwicklungsprozesse, die auch die oligodendrozytäre Zellreihe beinhalten, zurückgreifen zu können.
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Pringle, R. S. "The role of advanced glycation in the pathogenesis of retinal muller cell dysfunction during diabetes." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517057.

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Charlton-Perkins, Mark. "Control of Drosophila Eye Specification, Patterning and Function by the Transcription Factors prospero and Pax2." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406819630.

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Allan, Kristin. "Exploring the Roles of Muller Glia and Activated Leukocyte Cell Adhesion Molecule A in Zebrafish Retinal Regeneration." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1607705752486913.

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Books on the topic "Muller cells"

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Patricia, Rather, and Frerichs John B, eds. Johannes Müller and the nineteenth-century origins of tumor cell theory. Canton, MA: Science History Publications U.S.A., 1986.

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Rather, L. J., Patricia Rather, and J. B. Freriches. Johannes Muller and the 19th Century Origins of Tumor Cell Theory (Resources in Medical History). Watson Pub Intl, 1987.

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The Retinal Muller Cell: Structure & Function (Perspectives in Vision Research). Springer, 2001.

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Hope, James, and Mark P. Dagleish. Prion-protein-related diseases of animals and man. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0041.

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Scrapie, bovine spongiform encephalopathy (BSE), Creutzfeldt–Jakob disease (CJD), and related diseases of mink (transmissible mink encephalopathy), mule deer and elk (chronic wasting disease) are the founder members of a group of diseases called the transmissible degenerative (or spongiform) encephalopathies (TSE). These diseases can be transmitted by prions from affected to healthy animals by inoculation or by feeding diseased tissues. Prions are cellular proteins that can transfer metabolic and pathological phenotypes vertically from parent to progeny or horizontally between cells and animals. TSEs are characterised by the accumulation of the prion form of the mammalian prion protein (PrPC) in the central nervous system or peripheral tissues of animals and humans. Mutations of the human PrP gene are linked to rare, familial forms of disease and prion-protein gene polymorphisms in humans and other species are linked to survival time and disease characteristics in affected individuals. Iatrogenic transmission of CJD in man has occurred, and a variant form of CJD (vCJD) is due to cross-species transmission of BSE from cattle to humans. Atypical forms of scrapie and BSE have been identified during large-scale monitoring for TSEs worldwide. This chapter outlines our current understanding of scrapie, BSE, CJD and other TSEs and highlights recent progress in defining the role in disease of the prion protein, PrP.
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Book chapters on the topic "Muller cells"

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Budd, G. Colin, and Ben Pansky. "Synthesis of Insulin or a Similar Peptide in the Pituitary Gland and in Retinal Muller Cells." In Insulin, Insulin-like Growth Factors, and Their Receptors in the Central Nervous System, 139–49. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5380-5_11.

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L., Teri, Ellen C., Jonathan M., and Subramanian Dharmaraj. "Reactive Muller Glia as Potential Retinal Progenitors." In Neural Stem Cells - New Perspectives. InTech, 2013. http://dx.doi.org/10.5772/55150.

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de Sá Quirino Makarczyk, Luciana. "Internal Limiting Membrane Peeling in Idiopathic Epiretinal Membrane." In Medical and Surgical Retina - Recent Innovation, New Perspective, and Applications [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.108772.

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The primary management for epiretinal membrane (ERM) is membrane peel after pars plana vitrectomy. However, the rates of postoperative recurrence of epiretinal membrane reported range from 10 to 21%. Internal limiting membrane (ILM) peeling combined with ERM removal has been introduced in an attempt to diminish this recurrence. Some studies showed that this method largely prevented the recurrence compared with those without ILM peeling. Conversely, other studies demonstrated that combined ERM and ILM peeling did not provide a lower recurrence rate. Since the ILM is formed by the basal lamina of Muller cells, removal of this structure must be pondered due to possible mechanical and functional damage to those important cells. In this chapter, current data on this topic are covered.
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Khan, Rujman, Xin Yee Ooi, Matthew Parvus, Laura Valdez, and Andrew Tsin. "Advanced Glycation End Products: Formation, Role in Diabetic Complications, and Potential in Clinical Applications." In The Eye and Foot in Diabetes. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89408.

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Hyperglycemic conditions and disruptions to glucose-regulating pathways lead to increased formation of highly reactive aldehydes, methylglyoxal and glyoxal, which react with certain arginine and lysine residues in proteins to form advanced glycation end products (AGEs). These AGEs damage the integrity of the retinal vasculature predominantly through two mechanisms: non-receptor-mediated damage, which pertains to the interaction with extracellular matrix and its functional properties, and receptor-mediated damage through AGE interactions with their receptors (RAGE) on pericytes and Muller cells. Damage occurring between AGE and RAGE potentially generates reactive oxygen species, inflammatory cytokines, and growth factors. Both mechanisms result in increased permeability of endothelial tight junctions, and this increased permeability can lead to leaking and eventually ischemia. Once this ischemia becomes significant, neovascularization can occur, the hallmark of proliferative diabetic retinopathy. Current pharmaceutical studies have shown the potential of AGE inhibitors, such as aminoguanidine, in decreasing AGE production, thus minimizing its effects in hyperglycemic conditions. Other pharmaceutical interventions, such as Tanshinone IIA, aim to protect cells from the impacts of AGEs. Future research will not only continue to understand the properties of AGEs and their effects on diabetes and diabetic complications like diabetic retinopathy but will also explore how they impact other diseases.
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Félix, Synara Suellen Lebre, Natany de Sousa França, Angela dos Santos Avakian, Maria de Fátima Lopes de Oliveira, Witallo Johnatan Santos de Souza, Fabrício da Silva Sperandio, and Jhonny Blendo Fernandes. "ANEMIA FALCIFORME NA INFÂNCIA E ADOLESCÊNCIA SICKLE CELL ANEMIA IN CHILDHOOD AND ADOLESCENCE." In Saúde da Mulher, Criança e Adolescente, 184–94. Stricto Sensu Editora, 2020. http://dx.doi.org/10.35170/ss.ed.9786586283150.14.

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Brown, Ronald T. "Why a Comprehensive Handbook on Pediatric Psychosocial Oncology/Hematology." In Comprehensive Handbook of Childhood Cancer and Sickle Cell Disease. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195169850.003.0005.

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Over the past 25 to 30 years, monumental strides in national policy have been made in the management, treatment, and prevention of cancer. Rowland (2005) summarized these accomplishments, including legislation that provides for revenues and resources for research in cancer prevention and control. In addition, other pertinent policy issues have emerged from the Institute of Medicine, the National Cancer Institute, the Centers for Disease Control and Prevention, and the Lance Armstrong Foundation, all of which have served to increase the awareness of cancer, prevent the occurrence of cancer, and address cancer survivorship. Cancer policy issues have been models for increased resources and revenues for patient care, research, and quality-of-life enhancement. Nowhere is the success that we have had with policy more evident than in pediatric psychosocial oncology. The enormous advances in the prevention, medical treatment, medical management of late effects, and quality-of-life issues in children and adolescents surviving cancer have spawned a host of research in pediatric psychosocial oncology. These investigations likely surpass most research efforts for other chronic diseases. In fact, Bearison and Mulhern (1994) observed that there are more studies related to psychosocial oncology than perhaps there have been children with the disease. In my role as editor of the Journal of Pediatric Psychology, I conducted an informal survey of manuscripts; it indicated we process more submissions related to cancer than any other disease or chronic illness. Bearison and Mulhern also noted that psychological studies in the area of pediatric oncology have permeated most psychology and pediatric journals. Even the most dedicated scholar in psychosocial oncology and hematology has a difficult time keeping up with the everburgeoning literature body. Bearison and Mulhern published the last handbook on psychosocial issues in pediatric hematology/oncology in 1994. Since then, a proliferation of literature in the field has been concomitant with major developments in pediatric oncology, including increased use of chemotherapy, the evolution of bone marrow transplantation as a means of treating children and adolescents who have been refractory to chemotherapy and radiation therapy, and intensive investigation of survivorship and the late effects that many of these children endure.
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"DMA Amplification." In DNA Fingerprinting, edited by Lorne t. Kirby. Oxford University Press, 1993. http://dx.doi.org/10.1093/oso/9780716770015.003.0008.

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Amplification of DNA may be necessary to increase the quantity of sample available for profiling, to reduce the analysis time, or to produce probes for the hybridization process (Higuchi 1989, Li 1988, Marx 1988, Mullis 1990, Paabo 1989, Saiki 1986). Stretches of nucleotides up to at least 3,000 bp from any DNA-containing samples may be efficiently amplified by the polymerase chain reaction (PCR). Alternatively, living tissue can be placed in culture, and fibroblasts, epithelial type cells, or lymphoblasts grown. The culture process differs considerably from the PCR approach in that the total genome is reproduced. Also, tissue culture is usually at least a two-week procedure, whereas the polymerase chain reaction requires only a few hours. Cultured cells can be used for enzyme and other biochemical tests, and storage in liquid nitrogen is a standard practice for regrowth at a later time. Probe material, that is, DNA capable of hybridizing with its complementary region in the genome, must be amplified, aliquoted, and stored to provide an ongoing source for use with each profile analysis. Probe amplification has been mainly carried out in bacterial culture; however, probes can be chemically synthesized as discussed in Chapter 2 or amplified by the PCR system. At least 10 to 50 ng of high molecular weight genomic DNA are required for VNTR analysis using single-locus probes, and at least 0.5 to 1.0 μg required if multilocus probes are used. If only a small quantity of DNA is available, amplification using the PCR may be the only feasible option for obtaining sufficient material for analysis. PCR has revolutionized the approach to the recovery of DNA from a variety of sources. Microgram quantities of DNA can be produced in vitro by the amplification of picogram starting amounts. Single-copy genomic sequences greater than 2 kb in length have been amplified more than 10 millionfold in a few hours. Amplified material can also be directly sequenced without the necessity of incorporating DNA fragments into vectors such as M13 (Gyllensten 1989,1989a). Availability of oligonucleotide primers is the key to the amplification process.
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Souza, Ilany Francisca Sandoval de, and Mirelia Rodrigues de Araújo. "Oncologia em saúde da mulher: carcinomas de células escamosas do colo do útero cervical Squamous Cell Carcinomas." In Tópicos Especiais em Ciências da Saúde: teoria, métodos e práticas 9, 209–18. Aya Editora, 2022. http://dx.doi.org/10.47573/aya.5379.2.137.19.

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Katz, Ernest R., and Avi Madan-Swain. "Maximizing School, Academic, and Social Outcomes in Children and Adolescents With Cancer." In Comprehensive Handbook of Childhood Cancer and Sickle Cell Disease. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195169850.003.0023.

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Medical advances incorporating intensive and difficult multimodal therapies have resulted in improved rates of survival in childhood cancer (Institute of Medicine, 2003). With improvements in disease management and survival, maintaining and enhancing maximal quality of life in young people living with cancer is the accepted psychosocial goal of comprehensive care (Armstrong & Briery, 2004; Institute of Medicine, 2003; Madan-Swain, Katz, & LaGory, 2004). As the primary venue for academic, cognitive, social, and emotional development during childhood and adolescence, ongoing participation and success in school are essential for positive health outcomes in young people (Brown, 2004; Madan- Swain et al., 2004). Actively engaging in school activities is an opportunity for the young person living with cancer and its often-difficult treatment to normalize an otherwise-disrupted life experience. School participation enhances quality of life and provides youths with hope for the future (Katz, 1980; Katz, Dolgin, & Varni, 1990; Katz, Kellerman, Rigler, Williams, & Siegel, 1977; Madan-Swain, Fredrick, & Wallender, 1999). Cancer and its treatment have been associated with multiple school-related difficulties, including attendance problems, fatigue, pain, teasing and social isolation from peers, neurocognitive impairments, and academic deficiencies (Armstrong, 2003; R. Butler & Copeland, 2002; Katz, 1980; Katz et al., 1977; Katz, Rubinstein, Hubert, & Blew, 1988; Keene, 2003; Madan-Swain et al., 1999; Mitby et al., 2003; Spinetta & Deasy-Spinetta, 1986). Psychosocial factors such as singleparent families, high levels of maternal distress, and non-English-speaking immigrant families each may further negatively impact a family’s ability to manage school and social difficulties experienced by their children (Madan-Swain et al., 2004; Madan-Swain, Katz, LaGory, 2004; Kazak et al., 1998; Mulhern, Wasserman, Friedman, & Fairclough, 1989; Sahler et al., 2005; Varni, Burwinkle, Katz, Meeske, & Dickinson, 2002). School and social difficulties in children and adolescents with cancer can best be understood within the disability, stress, and coping theoretical model of pediatric chronic physical disorders proposed by Varni and Wallender (Varni & Wallender, 1988; Wallender & Varni, 1989). Cancer produces chronic strains for both children and parents. Strains are defined as persistent objective conditions that require continual readjustment, repeatedly interfering with the adequate performance of ordinary role-related activities such as school and social relationships.
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Conference papers on the topic "Muller cells"

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Sieving, Paul A., Koichiro Murayama, and Franklin Naarendorp. "Push-Pull Mechanism of the Primate Photopic Electroretinogram B-Wave." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1993. http://dx.doi.org/10.1364/navs.1993.nmd.3.

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The PI, PII, and PIII fundamental "Processes" described by Granit (1933) form the major component waves of the electroretinogram (ERG), particularily under dark-adapted (scotopic) conditions. The leading edge of scotopic PIII (i.e. "fast PIII") shapes the negative a-wave which originates directly from light evoked hyperpolarization of rod photoreceptors (Penn and Hagins, 1969). Scotopic PII is seen primarily as the phasic positive b-wave which results from local depolarization of Muller glial cells by a light-evoked K+ efflux from bipolar cells in distal retina (Faber, 1969; Miller and Dowling, 1970)
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Sutter, E. E., S. Wu, and Adam Reeves. "ERG Components from Achromatic and L-M Opponent Mechanisms." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1993. http://dx.doi.org/10.1364/navs.1993.nmd.2.

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It is generally accepted that most of the photopic ERG response to luminance stimulation originates from sources in the distal retina. At best a very small contribution is attributed to amacrine and ganglion cells. This assertion finds support in our recent topographic study. Using the same systems analysis technique applied in the present study, we have shown that the topography of the response density to achromatic local flicker stimulation mirrors that of cone densities (Sutter and Tran, 1992). Thus, the largest signal contribution attributed to Muller cells (b-wave) can be directly related to receptor response. Based on these findings, it seemed reasonable to ask how much of this response is mediated by L- and M-cones. (S-cones add little to the response and the contribution of rods is negligible with fast photopic stimulation.) If there are ERG components originating from the two receptors populations and if they are devoid of any lateral mechanisms, they must reflect the densities of L- and M-cones (assuming equal response properties of the two cone types). These components might be found in the early a-wave obtained under stimulation conditions of M-silent and L-silent substitution.
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Coquil, Thomas, and Laurent Pilon. "Thermal Conductivity of Sol-Gel Amorphous Mesoporous Silica Thin Films: Molecular Dynamics Simulations Versus Experiments." In ASME/JSME 2011 8th Thermal Engineering Joint Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/ajtec2011-44046.

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This study reports non-equilibrium molecular dynamics (MD) simulations predicting the thermal conductivity of amorphous mesoporous silica. The heat flux was imposed using the Muller-Plathe method and interatomic interactions were modeled using the van Beest, Kramer and van Santen (BKS) potential. First, simulations were validated against results reported in the literature for dense quartz and amorphous silica. The BKS potential was found to significantly overestimate the thermal conductivity of dense amorphous silica and results depended on the length of the simulation cell. Then, highly ordered pores were introduced in an amorphous silica matrix by removing atoms within selected areas of the simulation cell. Effects of the simulation cell length, pore size, and porosity on the thermal conductivity were investigated at room temperature. Results were compared with predictions from commonly used effective medium approximations as well as with previously reported experimental data for films with porosity and pore diameter ranging from 20% to 48% and 30 to 180 Å, respectively. Predictions of MD simulations overestimated the experimental data and agreed with predictions from the coherent potential model. However, MD simulations confirmed that thermal conductivity in sol-gel amorphous mesoporous materials was independent of pore size and depended only on porosity.
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4

Park, Seong Hye, Dae-Hee Lee, Jung Lim Kim, Sun Il Lee, Bo Ram Kim, Yoo Jin Na, Suk Young Lee, et al. "Abstract 3497: Metformin enhances TRAIL-induced apoptosis by Mcl-1 degradation via Mule in colorectal cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3497.

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5

Mason, J. A., W. Hage, R. Price, A. C. Tolchard, and A. C. N. Towner. "An Automated Non-Destructive Assay System for the Measurement and Characterization of Radioactive Waste." In ASME 2003 9th International Conference on Radioactive Waste Management and Environmental Remediation. ASMEDC, 2003. http://dx.doi.org/10.1115/icem2003-4654.

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The paper describes an automated non-destructive assay (NDA) system for the measurement and characterization of radioactive waste. The Waste Characterisation System (WCS) can be adapted to measure a variety of drum sizes: 60, 220 (55 gallon) and 440 liter, the latter with a maximum weight of 1500 kg (1.5 tonnes). The NDA system includes a Tomographic Segmented Gamma Scanner (TSGS) and an active/passive neutron Differential Die-away (DDA or DDT). The system can assay a wide variety of waste types in a range of waste matrices. The assay stations are linked by a heavy duty roller conveyor which incorporates a 20 drum buffer store, a load cell (built into the conveyor), bar code readers and a dose rate measurement station. The Tomographic Segmented Gamma Scanner (TSGS) combines conventional high resolution gamma spectrometry and a tranission source to interrogate a waste drum in vertical slices (segments) as for Segmented Gamma Scanner (SGS) measurements. However, in the case of the TSGS, while the drum is rotated, it is also moved in the horizontal direction leading to an enhanced ability to correct the gamma ray energies, from the nuclides of interest, for the attenuation of the matrix. The TSGS can also be operated as a conventional SGS for the measurement of homogeneous waste drums. The DDA is a very sensitive active neutron interrogation method that uses thermalised neutrons from a pulsed source within the chamber to irradiate a waste drum. Prompt neutrons from fissile material present in the waste (e. g. 239Pu, 235U) are detected and provide a measure of the fissile content in the drum. In passive mode, the DDA determines the even Pu nuclides exhibiting significant spontaneous fission (e.g. 240Pu). Measurement accuracy depends on correction algorithms to compensate for self-shielding and matrix effects in waste drums containing hydrogenous materials. In addition, the DDA will be provided with the Fission-Fission Neutron Correlation Analysis System (FFnC) which is an absolute technique eliminating the need for matrix dependent mass calibrations, and allowing separate U and Pu determination using delayed neutron counting. The FFnC technique will be tested for the first time on the WCS. The NDA system incorporates integrated stations to determine the weight and dose rate of each drum, the former built into the conveyor the latter as part of the TSGS. Six Geiger Muller tubes measure the surface dose at three positions on the drum side, one at 1 metre from the drum and one each measuring the surface dose of the top and bottom of the drum. The assay instruments are linked to a heavy duty conveyor system onto which up to 20 waste drums can be loaded for delivery to the various measurement stations, thus permitting unattended, automated operation. Once measured, the drums remain on the conveyer in a holding system waiting to be unloaded. Automation is provided using a programmable logic controller (PLC) and associated computers. A central computer and associated software is used for data acquisition and management.
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da Silva, Priscilla Veiga Pereira, Vera Lúcia Mota da Fonseca, Roberto de Azevedo Antunes, and Afranio Coelho-Oliveira. "Tumor ovariano das células da granulosa tipo adulto: relato de caso." In 44° Congresso da SGORJ - XXIII Trocando Ideias. Zeppelini Editorial e Comunicação, 2020. http://dx.doi.org/10.5327/jbg-0368-1416-2020130209.

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Introdução: Os tumores de células da granulosa (TCG) são neoplasias ovarianas malignas raras, porém são as mais frequentes entre as neoplasias estromais do cordão sexual. São responsáveis por 3 a 5% de todas as neoplasias ovarianas. O TCG tipo adulto (TCGA) apresenta maior prevalência no climatério (média de 50 anos). Em razão do hiperestrogenismo causado pelo tumor, os sintomas variam de acordo com a faixa etária. O tratamento e o estadiamento são cirúrgicos. A imuno-histoquímica auxilia na elucidação diagnóstica. Em razão da grande probabilidade de recidiva, é necessário um seguimento a longo prazo. Objetivo: Relatar o caso de uma paciente com TCG acompanhada em hospital público do Rio de Janeiro. Materiais e Métodos: Análise de prontuário e revisão bibliográfica por meio do PubMed. Resultado: Mulher, 59 anos, portadora de HAS, DM tipo 2 e obesidade. Menopausa aos 48 anos, sem terapia de reposição hormonal, GX PIX. Sem histórico familiar de neoplasia. Deu entrada no ambulatório de Ginecologia apresentando sangramento pós-menopausa com duração de até 20 dias, iniciado há 3 anos, em uso de Depoprovera. Exame físico: abdômen globoso, com tumoração irregular, algo móvel, em hipogástrio. Exame especular: discreto sangramento oriundo do orifício externo do colo do útero. Ao toque: útero aumentado, de difícil delimitação e tumor de consistência endurecida ocupando todo o hipogástrio até 4 cm acima da cicatriz umbilical. Realizada curetagem uterina com histopatológico de restos deciduais com necrose. Vídeo-histeroscopia: endométrio hipertrófico de aspecto polipoide não compatível com medicações em uso. Biópsia endometrial: compatível com ciclo anovulatório. Ressonância magnética: volumosa lesão expansiva de contorno lobulado, sólido-cística em topografia anexial bilateral. CA 125: 915. Realizada histerectomia total abdominal, anexectomia bilateral e omentectomia. Visualizada grande quantidade de líquido ascítico e tumor volumoso, irregular, de aspecto maligno em região anexial esquerda. Congelação peroperatória: TCG x Small Cell carcinoma. Histopatológico definitivo: TCGA, com lesão tumoral de 28 cm no maior eixo. Imuno-histoquímica: Ki-67 positivo de 20‒30%, calretinina e inibina positivos. Conclusão: TCGA ovariano. CA 125: 20 no pós-operatório. Após avaliação no serviço de Oncologia, foi orientada a manter seguimento pela Ginecologia. Conclusão: O TCG é um tumor raro. A referida paciente apresentou quadro clássico, com hiperplasia endometrial e sangramento uterino anormal. A imuno-histoquímica foi indispensável para o diagnóstico. Em um hospital público no Rio de Janeiro, no período de 1º de janeiro de 2000 a 28 de novembro de 2018, foram encontrados 2 casos de TCG entre 337 pacientes submetidas à ooforectomia (0,6%). Após uma revisão bibliográfica que mostra a falta de consenso para o seguimento e tratamento de recidivas, é observada a importância de conduta individualizada. Ainda são necessários estudos clínicos randomizados para elaboração de protocolos, o que é dificultado pelo pequeno número de pacientes portadoras dessa enfermidade.
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