Academic literature on the topic 'Blood retinal barrier'
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Journal articles on the topic "Blood retinal barrier"
Yemanyi, Felix, Kiran Bora, Alexandra K. Blomfield, Zhongxiao Wang, and Jing Chen. "Wnt Signaling in Inner Blood–Retinal Barrier Maintenance." International Journal of Molecular Sciences 22, no. 21 (November 2, 2021): 11877. http://dx.doi.org/10.3390/ijms222111877.
Full textCunha-Vaz, José. "The Blood–Retinal Barrier in Retinal Disease." European Ophthalmic Review 03, no. 02 (2009): 105. http://dx.doi.org/10.17925/eor.2009.03.02.105.
Full textCunha-Vaz, José, Rui Bernardes, and Conceição Lobo. "Blood-Retinal Barrier." European Journal of Ophthalmology 21, no. 6_suppl (November 2011): 3–9. http://dx.doi.org/10.5301/ejo.2010.6049.
Full textVinores, S. A., R. McGehee, A. Lee, C. Gadegbeku, and P. A. Campochiaro. "Ultrastructural localization of blood-retinal barrier breakdown in diabetic and galactosemic rats." Journal of Histochemistry & Cytochemistry 38, no. 9 (September 1990): 1341–52. http://dx.doi.org/10.1177/38.9.2117624.
Full textNaylor, Aisling, Alan Hopkins, Natalie Hudson, and Matthew Campbell. "Tight Junctions of the Outer Blood Retina Barrier." International Journal of Molecular Sciences 21, no. 1 (December 27, 2019): 211. http://dx.doi.org/10.3390/ijms21010211.
Full textMENDES-JORGE, L., D. RAMOS, M. LUPPO, A. VALENçA, J. CATITA, CM DUARTE, M. SIMõES, et al. "Blood-retinal barrier serum ferritin transport in mouse retina." Acta Ophthalmologica 90 (August 6, 2012): 0. http://dx.doi.org/10.1111/j.1755-3768.2012.t029.x.
Full textSilva, Rufino M., J. R. Faria de Abreu, and J. G. Cunha-Vaz. "Blood-retina barrier in acute retinal branch vein occlusion." Graefe's Archive for Clinical and Experimental Ophthalmology 233, no. 11 (November 1995): 721–26. http://dx.doi.org/10.1007/bf00164677.
Full textYanagi, Yasuo. "Role of Peoxisome Proliferator Activator Receptor on Blood Retinal Barrier Breakdown." PPAR Research 2008 (2008): 1–4. http://dx.doi.org/10.1155/2008/679237.
Full textKubo, Yoshiyuki, Shinichi Akanuma, and Ken-ichi Hosoya. "The blood-retinal barrier transporters in retinal drug delivery." Drug Delivery System 27, no. 5 (2012): 361–69. http://dx.doi.org/10.2745/dds.27.361.
Full textD, Shah. "Resolution of Bilateral Exudative Retinal Detachment Secondary to Renal Hypertension with Systemic Management." Open Access Journal of Ophthalmology 7, no. 2 (July 1, 2022): 1–2. http://dx.doi.org/10.23880/oajo-16000252.
Full textDissertations / Theses on the topic "Blood retinal barrier"
Bamforth, Simon David. "The effects of inflammatory agents on the blood-retinal barrier." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244263.
Full textTretiach, 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.
Full textTretiach, 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.
Full textBackground: 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 âbarrier 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.
Ojima, Tomonari. "EphrinA1 inhibits vascular endothelial growth factor-induced intracellular signaling and suppresses retinal neovascularization and blood-retinal barrier breakdown." Kyoto University, 2006. http://hdl.handle.net/2433/143818.
Full textMoyer, Andrea Leigh. "Mechanisms of blood retina barrier permeability during Bacillus cereus endophthalmitis." Oklahoma City : [s.n.], 2008.
Find full textMelhorn, Mark Ivan [Verfasser]. "A model to examine the outer blood-retinal barrier in rodents / Mark Ivan Melhorn." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2012. http://d-nb.info/102282631X/34.
Full textLipski, Deborah. "Study of the mechanisms of local auto-antigen presentation and inner blood-retinal barrier breakdown during non-infectious uveitis." Doctoral thesis, Universite Libre de Bruxelles, 2018. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/262873.
Full textDoctorat en Sciences médicales (Médecine)
info:eu-repo/semantics/nonPublished
Rosales, Mariana Aparecida Brunini 1983. "O estresse nitrosativo na patogênese da retinopatia diabética = implicações na barreira hemato-retiniana externa e possíveis alvos terapêuticos = Nitrosative stress in the pathogenesis of diabetic retinopathy: implications in the outer blood retinal barrier and possible therapeutics targets." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309781.
Full textTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A patogênese da retinopatia diabética (RD) está associada ao estresse nitrosativo. Alterações na barreira hemato-retiniana (BHR) externa, formada pelas células do epitélio pigmentar da retina (EPR), estão associadas às fases precoces da RD e podem acarretar no desequilíbrio da manutenção dos fotorreceptores e consequentemente promoverem mudanças nas células neuronais da retina. O estresse nitrosativo como conseqüência do aumento da produção de óxido nítrico (NO¿) produzido pela super expressão da óxido nítrico sintetase induzida (iNOS) esteve presente em todas as camadas da retina, inclusive no EPR em condições de RD experimental in vivo precoce ou na linhagem celular humana do EPR (ARPE-19) expostas à alta concentração de glicose. O tratamento com agentes químicos como a S-nitrosoglutationa (GSNO), ou naturais (cacau enriquecido com polifenol) atuaram em diferentes vias de inibição da iNOS, prevenindo o estresse nitrosativo. Para o estudo in vivo com o colírio de GSNO (artigo I) foram utilizados animais espontaneamente hipertensos (SHR) com 4 semanas de idade. O diabetes (DM) foi induzido por STZ. Após a confirmação do DM (48 horas), os animais foram divididos em 6 grupos: controles (CTs) veículo; GSNO 900nm e GSNO 10?m ou DMs veículo; GSNO 900nm e GSNO 10?m. O efeito do tratamento com colírio de GSNO foi dependente da presença ou ausência da condição do DM. Nos animais CT, o GSNO atuou como um agente nitrosativo e nos animais DM preveniu o aumento da expressão da iNOS, preservando a retina funcional. Os estudos in vitro, demonstraram que o efeito do GSNO foi deletério ou protetor dependente da concentração de glicose. Nas células ARPE-19 expostas a condições normais de glicose, o tratamento promoveu um aumento na produção de NO¿ sem aumentar a expressão de iNOS e nas células sob alta glicose induziu uma modificação pós-translacional de proteína, a S-glutationilação da iNOS prevenindo o estresse nitrosativo. No estudo do cacau (artigo II), foi avaliado in vitro (ARPE-19 exposta a alta concentração de glicose) o seu efeito protetor dependente da concentração de polifenóis. Para isso foram testadas duas formulações de cacau que diferiram somente na concentração de polifenol: 0,5% para o cacau com baixo teor de polifenol e 60,5% para o cacau com alto teor de polifenol. A epicatequina (EC), encontrada na concentração de 12% no cacau com alto teor de polifenol foi tão eficaz quanto o próprio e esteve envolvida no controle da expressão da iNOS através da estimulação do receptor ?-opióide (DOR) diminuindo os níveis de TNF-?. A modulação da iNOS, preveniu a S-nitrosilação da caveolina-1 (CAV-1) e diminuição da expressão das junções intercelulares claudina-1 e ocludina através da prevenção da interação CAV-1?junções. Em ambos os estudos, o alvo terapêutico foi a iNOS em duas diferentes modalidades: modificação pós-translacional de proteína e modulação do TNF-? via DOR no EPR em modelos experimentais de RD. Os tratamentos apresentados neste trabalho demonstraram a iNOS como alvo terapêutico e mostraram-se eficaz em conter danos funcionais e morfológicos promovidas pela situação de mimetismo do DM no EPR demonstrando o importante papel da iNOS no desenvolvimento da RD
Abstract: The pathogenesis of diabetic retinopathy (DR) is associated with nitrosative stress. Changes in outer blood-retinal barrier (BRB), formed by retinal pigment epithelium cells (RPE) are associated in the early stages of DR and can cause imbalance in the maintenance of photoreceptors and thereby cause changes on retinal neuronal cells. The nitrosative stress as a result of increased production of nitric oxide (NO) produced by overexpression of nitric oxide synthase (iNOS) was present in all layers of the retina and mainly in RPE cells in early in vivo experimental DR or in human RPE cell line (ARPE-19) exposed to high glucose condition. Therapy with chemical agents such as S-Nitrosoglutathione (GSNO) or natural compounds (enriched cocoa polyphenol) acted in different pathways of iNOS inhibition, preventing nitrosative stress. For the in vivo study with GSNO eye drops (article I), it were used spontaneously hypertensive rats (SHR) rats with 4 week old. Diabetes (DM) was induced by streptozotocin (STZ). After DM confirmation (48 hours), the animals were divided into 6 groups: controls (CTs) vehicle; GSNO 900nm and GSNO 10?m or DMs vehicle; GSNO 900nm e GSNO 10?m. The effects of treatments were dependent on glucose concentration. In CT animals, GSNO acted as a nitrosative agent and in DM rats prevented iNOS overexpression, preserving the retina function. In vitro study showed that GSNO protective or deleterious effects were dependent on the glucose concentration. In ARPE-19 cells exposed to normal glucose, the treatment promoted an increase of NO¿ production without increase iNOS expression and in cells under high glucose (HG) condition induced post-translational protein modification, S-glutationylation of iNOS, preventing nitrosative stress. In the study with cocoa (article II), it was evaluated its protective effect dependent on concentration of polyphenols in ARPE-19 cells under HG condition. For this study, the composition of cocoa was the same in both preparations with the only difference in the amounts of polyphenol, 0.5% for low polyphenol cocoa (LPC) and 60.5% for high polyphenol cocoa (HPC). Epicatechin (EC), found in 12% of HPC was similarly protective compare to HPC and it was involved in controlling iNOS expression by stimulation of the delta opioid receptor decreasing TNF- ? levels. The modulation of iNOS prevented S-nitrosylation of caveolin-1 (CAV-1) and decreased expression of claudin-1 and occluding tight junctions by preventing CAV-1/junctions interactions. The treatments presented here showed iNOS as a therapeutic target containing functional and morphological changes promoted by DM milieu in RPE showing the important role of iNOS in the development of DR
Doutorado
Clinica Medica
Doutora em Clínica Médica
Valença, Andreia Barbosa. "Analysis of TIM2 deficiency in the mouse retina." Doctoral thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2019. http://hdl.handle.net/10400.5/18022.
Full textCareful control of iron availability in the retina is central to maintenance of iron homeostasis, as its imbalance is associated with oxidative stress and progress of several retinopathies, such as diabetic retinopathy. Ferritin, known for its role in iron storage and detoxification, has also been proposed as an iron-transporter and can be regarded as a potential deliverer of a considerable large amount of iron to the retina compared to transferrin, the classical ironcarrier protein. Ferritin can bind to scavenger receptor class A member 5 (Scara5) and T-cell immunoglobulin and mucin-domain 2 (TIM2) receptors and is likely endocytosed. In this study, the presence of TIM2, which remained unknown in the retina, was investigated. Although no human ortholog for mouse TIM2 has been identified, human TIM1 and mouse TIM2 have similar functions. Our results revealed for the first time the presence of TIM2 receptors in the mouse retina, mainly expressed in Müller cells, unveiling new aspects of retinal iron metabolism regarding the putative role of TIM2 in this tissue. A knockout mouse for this membrane receptor was generated in order to better understand TIM2 functions in the retina. TIM2 deficiency affected retinal iron metabolism. Iron-loaded ferritin accumulation, probably due to increased ferritin uptake mediated by Scara5, and increased iron uptake by transferrin receptor 1 (TfR1)- transferrin binding led to retinal iron overload. Consequently, increased vascular permeability and blood-retinal barrier (BRB) breakdown were observed, inducing edema of the central retina. Paracellular and transcellular transports were impaired with tight junction integrity loss and increased caveolae number. Two mechanisms seem to be involved in this process: association of iron and ferritin overload with vascular endothelial growth factor (VEGF) overexpression and oxidative stress triggered by reactive oxygen species (ROS) overproduction generated by retinal iron overload. Altogether, these results point to TIM2 as a new key player in iron homeostasis in the mouse retina, possibly modulating cellular iron levels, and a potential target for the treatment of diabetic macular edema.
RESUMO - Análise da deficiência de TIM2 na retina de murganho - A retina necessita especificamente de ferro, devido a este ser um co-factor essencial da enzima guanilato ciclase que assegura a síntese de monofosfato de guanosina cíclico, segundo mensageiro na cascata de fototransdução. Para além disso, a retina é particularmente dependente de ferro devido à contínua necessidade de síntese de membranas, para suprir a constante renovação dos segmentos externos dos fotorrecetores, que requer como co-factor este elemento. Porém, o desequilíbrio da homeostasia do ferro está associado ao dano oxidativo e ao desenvolvimento de várias situações de retinopatia, como por exemplo a retinopatia diabética. A retina é particularmente propensa a stress oxidativo e o excesso de ferro exacerba potencialmente esta situação, devido à participação do ferro na reação de Fenton, que gera a superprodução de espécies reativas de oxigénio que, por sua vez, desencadeiam stress oxidativo. Por conseguinte, a manutenção da homeostasia do ferro é crucial neste tecido. Contudo, mecanismos de regulação do ferro na retina ainda não são completamente conhecidos. A retina obtém ferro a partir da circulação sanguínea. No entanto, a barreira hemato-retiana isola a retina da circulação sanguínea, protegendo-a de potenciais estímulos nocivos. Assim, são necessários mecanismos específicos e rigorosamente regulados de absorção de ferro para atravessar esta barreira e importar a quantidade de ferro estritamente essencial para o normal funcionamento da retina. Classicamente, a transferrina foi estabelecida como a proteína transportadora de ferro na retina, sendo aceite que a transferrina sérica se liga ao seu recetor de membrana, recetor da transferrina 1, na superfície das células endoteliais e do epitélio pigmentar da retina. Após a endocitose deste complexo, o ferro é libertado no parênquima retiniano. Mais recentemente, a ferritina, considerada classicamente como uma proteína de armazenamento de ferro e destoxificação, foi também proposta como uma proteína transportadora deste elemento. A vantagem da ferritina sérica em relação à transferrina no transporte de ferro prende-se na capacidade da ferritina de incorporar ~ 4,500 átomos de ferro, ao passo que a transferrina apenas transporta 2 átomos de ferro, constituindo, assim, a ferritina uma fonte muito eficiente de ferro para os tecidos. A molécula da ferritina é composta por 24 subunidades de dois tipos: cadeia leve (L) e cadeia pesada (H) que se unem aos recetores Scara5 (scavenger receptor class A member 5) e TIM2 (T-cell immunoglobulin and mucin-domain 2), respetivamente. O nosso grupo identificou pela primeira vez a presença de recetores Scara5 na retina humana e do murganho. No entanto, até à data, a presença de recetores TIM2 na retina não foi reportada na bibliografia. O TIM2, uma proteína transmembranar do tipo 1, é um membro da família de genes portadores dos domínios mucina e imunoglobulina de células T e, para além de ser um recetor para a ferritina-H, está envolvido na regulação da resposta imunitária...
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Chapy, Hélène. "Identification fonctionnelle et moléculaire d'un transporteur de psychotropes et substances d'abus." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05P603.
Full textThe central nervous system is a privilege organ protected by histological barriers between the blood and the nervous tissue. The blood-brain barrier (BBB) and the blood-retinal barrier (BRB) separate cerebral parenchyma and retina from the circulating blood and both express tight junctions and membrane transporters, allowing a precise regulation of the exchanges between the blood and nervous tissues. We studied a new cationic transporter functionally evidenced at the mouse BBB. This molecularly unknown transporter belong to the solute carrier super family (SLC) and is a proton antiporter. It could constitute a new actor in the cerebral permeability and may be a new brain access pathway. First, we worked on the functional identification studying new substrates and new localization. Psychotropic brain transport was studied in vivo by brain in situ perfusion on mouse and in vitro with human immortalized endothelial cells (hCMEC/D3). We showed that cocaine brain entry depends on passive diffusion but also mainly on a proton antiporter. Brain entry rate of drugs of abuse is associated with modulation of addiction liability, making this transporter a new component of brain entry of cocaine, and also nicotine and some amphetamines such as ecstasy and MDPV. This proton antiporter appears to be a new potential target in addiction. Various chemical entities interact with this transporter; however concentrations used to inhibit the transporter are much higher than the one possibly found in the blood. In order to help find or design new selective and potent inhibitors, we developed a pharmacophore model of the proton antiporter inhibitors using in vitro data and the FLAPpharm approach. The model predicts well new possible inhibitors of this transporter. We also studied the impact of the ABC transporters and the proton antiporter at the BBB and the BRB using specific or multi-specific substrates such as verapamil. The proton antiporter is functionally expressed at the BRB and transports clonidine, DPH and verapamil. However, for the multi-specific (P-gp and SLC) compound verapamil, influx transport by the proton antiporter is visible at the BBB only when P-gp efflux is neutralized. On the contrary, at the BRB, the proton antiporter influx is always visible. This is certainly due to the lower impact (by 6.3 fold) of P-gp at the BRB compared to the BBB. These results show the difficulty to predict the functional impact of a transporter for multi-specific compounds and a probable transport prioritization. Finally we worked on the molecular identification of the proton antiporter using a photolabeling method. This work evidenced the importance of the proton antiporter in the brain distribution of psychotropic and drugs of abuse and opened toward new perspectives in addiction and transport comprehension
Books on the topic "Blood retinal barrier"
The blood-brain and other neural barriers: Reviews and protocols. New York, N.Y: Humana Press, 2011.
Find full textBiology and regulation of blood-tissue barriers. New York, N.Y: Springer Science+Business Media, 2012.
Find full textCheng, C. Yan. Biology and regulation of blood-tissue barriers. New York, N.Y: Springer Science+Business Media, 2012.
Find full textOcular drug delivery systems: Barriers and application of nanoparticulate systems. Boca Raton: CRC Press/Taylor & Francis, 2013.
Find full textNag, Sukriti. Blood-Brain and Other Neural Barriers: Reviews and Protocols. Humana Press, 2016.
Find full textCunha-Vaz, José. Blood-Retinal Barriers. Springer London, Limited, 2013.
Find full textCunha-Vaz, Jose G. The Blood-Retinal Barriers. Springer, 2013.
Find full textCunha-Vaz, José. The Blood-Retinal Barriers. Springer, 2014.
Find full textThassu, Deepak, and Gerald J. Chader. Ocular Drug Delivery Systems: Barriers and Application of Nanoparticulate Systems. Taylor & Francis Group, 2012.
Find full textThassu, Deepak, and Gerald J. Chader. Ocular Drug Delivery Systems: Barriers and Application of Nanoparticulate Systems. Taylor & Francis Group, 2012.
Find full textBook chapters on the topic "Blood retinal barrier"
Hayreh, Sohan Singh. "The Blood-Retinal Barrier." In Ocular Vascular Occlusive Disorders, 165–71. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12781-1_9.
Full textKubo, Yoshiyuki, Shin-ichi Akanuma, and Ken-ichi Hosoya. "In Vivo Analysis to Study Transport Across the Blood-Retinal Barrier." In Blood-Brain Barrier, 249–65. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8946-1_15.
Full textHosoya, Ken-ichi, and Masanori Tachikawa. "The Inner Blood-Retinal Barrier." In Advances in Experimental Medicine and Biology, 85–104. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-4711-5_4.
Full textHudson, Natalie, and Matthew Campbell. "Inner Blood-Retinal Barrier Regulation in Retinopathies." In Retinal Degenerative Diseases, 329–33. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27378-1_54.
Full textIshiko, Satoshi, Akitoshi Yoshida, and Norihiko Kitaya. "Blood-Retinal Barrier in Experimental Myopia." In Myopia Updates, 270–77. Tokyo: Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-66959-3_49.
Full textGreenwood, John, Simon Bamforth, Yufei Wang, and Lesley Devine. "The Blood-Retinal Barrier in Immune-Mediated Diseases of the Retina." In New Concepts of a Blood—Brain Barrier, 315–26. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-1054-7_31.
Full textGreenwood, J. "Experimental Manipulation of the Blood-Brain ”and Blood-Retinal Barriers." In Physiology and Pharmacology of the Blood-Brain Barrier, 459–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76894-1_19.
Full textRunkle, E. Aaron, and David A. Antonetti. "The Blood-Retinal Barrier: Structure and Functional Significance." In Methods in Molecular Biology, 133–48. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-938-3_5.
Full textLiu, Li, and Xiaodong Liu. "Roles of Drug Transporters in Blood-Retinal Barrier." In Advances in Experimental Medicine and Biology, 467–504. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7647-4_10.
Full textCunha-Vaz, J. G. "Blood—retinal barrier and new perspectives of management of retinal disease." In Documenta Ophthalmologica Proceedings Series, 5–11. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5137-5_2.
Full textConference papers on the topic "Blood retinal barrier"
Schuschereba, Steven T., Jeremiah Brown, Bruce E. Stuck, and John Marshall. "Untoward effects of high-dose methylprednisolone therapy on blood-retinal barrier closure, retinal hole repair, and long-term scarring." In BiOS 2001 The International Symposium on Biomedical Optics, edited by Bruce E. Stuck and Michael Belkin. SPIE, 2001. http://dx.doi.org/10.1117/12.426715.
Full textDaley, Michael L., George A. Burghen, David Meyer, and Paul Maisky. "Racial Difference of Blue-Sensitive Mechanism." In Advances in Color Vision. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/acv.1992.fb9.
Full textCurcio, Christine A. "Aging and topography of human photoreceptors." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1986. http://dx.doi.org/10.1364/oam.1986.wc1.
Full textKoester, Charles J., R. Theodore Smith, and Charles J. Campbell. "Deconvolution of ocular fluorophotometer data." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1985. http://dx.doi.org/10.1364/oam.1985.thp1.
Full textBungay, P. M., M. S. Roy, and R. F. Bonner. "New Scheme for Analyzing Vitreous Fluorophotometry (VFP) Scans." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/navs.1987.wc3.
Full text