Relevant bibliographies by topics / Retina Diseases

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Retina Diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Retina Diseases"

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Holan, Vladimir, Katerina Palacka, and Barbora Hermankova. "Mesenchymal Stem Cell-Based Therapy for Retinal Degenerative Diseases: Experimental Models and Clinical Trials." Cells 10, no. 3 (March 7, 2021): 588. http://dx.doi.org/10.3390/cells10030588.

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Retinal degenerative diseases, such as age-related macular degeneration, retinitis pigmentosa, diabetic retinopathy or glaucoma, represent the main causes of a decreased quality of vision or even blindness worldwide. However, despite considerable efforts, the treatment possibilities for these disorders remain very limited. A perspective is offered by cell therapy using mesenchymal stem cells (MSCs). These cells can be obtained from the bone marrow or adipose tissue of a particular patient, expanded in vitro and used as the autologous cells. MSCs possess potent immunoregulatory properties and can inhibit a harmful inflammatory reaction in the diseased retina. By the production of numerous growth and neurotrophic factors, they support the survival and growth of retinal cells. In addition, MSCs can protect retinal cells by antiapoptotic properties and could contribute to the regeneration of the diseased retina by their ability to differentiate into various cell types, including the cells of the retina. All of these properties indicate the potential of MSCs for the therapy of diseased retinas. This view is supported by the recent results of numerous experimental studies in different preclinical models. Here we provide an overview of the therapeutic properties of MSCs, and their use in experimental models of retinal diseases and in clinical trials.
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Balicka, A., M. Lapsanska, and A. Trbolova. "Retinal Diseases of Senior Dogs." Folia Veterinaria 64, no. 4 (December 1, 2020): 71–77. http://dx.doi.org/10.2478/fv-2020-0040.

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AbstractAging consists of a physiological decline of an organism’s functional activity. During the aging process, the structural and functional changes of the retina can be observed. In most cases, progressive vision loss occurs due to the age related changes of the anterior segment. Retinal diseases, characteristic for senior dogs are: retinal detachment, hypertensive chorioretinopathy, sudden acquired retinal degeneration syndrome (SARDS), progressive retinal atrophy (PRA), glaucoma, retinopathy, cystoid degeneration and neoplasms. The examination of the retina in senior dogs is based on: ophthalmoscopic examination, electroretinography, spectral-domain optical coherence tomography (AD-OCT) and if necessary, histopathological examinations. Comprehensive knowledge regarding the senior dog’s health, significantly increases their quality of life.
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Nagamani, Gilakara Muni, and Theertagiri Sudhakar. "An improved dynamic-layered classification of retinal diseases." IAES International Journal of Artificial Intelligence (IJ-AI) 13, no. 1 (March 1, 2024): 417. http://dx.doi.org/10.11591/ijai.v13.i1.pp417-429.

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<span>Retina is main part of the human eye and every disease shows the effect on retina. Eye diseases such as choroidal neovascularization (CNV), DRUSEN, diabetic macular edema (DME) are the main retinal diseases that damage the retina and if these damages are identified in the later stages, it is very difficult to reverse the vision for these retinal diseases. Optical coherence tomography (OCT) is a non-nosy image testing for finding the retinal diseases. OCT mainly collects the cross-section images of retina. Deep learning (DL) is used to analyze the patterns in several complex research applications especially in the disease prediction. In DL, multiple layers give the accurate detection of abnormalities in the retinal images. In this paper, an improved dynamic-layered classification (IDLC) is introduced to classify retinal diseases based on their abnormality. Image filters are used to filter the noise present in the input images. ResNet is the pre-trained model which is used to train the features of retinal diseases. Convolutional neural networks (CNN) are the DL model used to analyze the OCT image. The dataset consists of three types of OCT disease datasets from Kaggle. Evaluation results show the performance of IDLC compared with state-of-art algorithms. A better performance is obtained by using the IDLC and achieved the better accuracy. </span>
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Greco, Jordan A., Nicole L. Wagner, Ralph J. Jensen, Daniel B. Lawrence, Matthew J. Ranaghan, Megan N. Sandberg, Daniel J. Sandberg, and Robert R. Birge. "Activation of retinal ganglion cells using a biomimetic artificial retina." Journal of Neural Engineering 18, no. 6 (December 1, 2021): 066027. http://dx.doi.org/10.1088/1741-2552/ac395c.

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Abstract Objective. Biomimetic protein-based artificial retinas offer a new paradigm for restoring vision for patients blinded by retinal degeneration. Artificial retinas, comprised of an ion-permeable membrane and alternating layers of bacteriorhodopsin (BR) and a polycation binder, are assembled using layer-by-layer electrostatic adsorption. Upon light absorption, the oriented BR layers generate a unidirectional proton gradient. The main objective of this investigation is to demonstrate the ability of the ion-mediated subretinal artificial retina to activate retinal ganglion cells (RGCs) of degenerated retinal tissue. Approach. Ex vivo extracellular recording experiments with P23H line 1 rats are used to measure the response of RGCs following selective stimulation of our artificial retina using a pulsed light source. Single-unit recording is used to evaluate the efficiency and latency of activation, while a multielectrode array (MEA) is used to assess the spatial sensitivity of the artificial retina films. Main results. The activation efficiency of the artificial retina increases with increased incident light intensity and demonstrates an activation latency of ∼150 ms. The results suggest that the implant is most efficient with 200 BR layers and can stimulate the retina using light intensities comparable to indoor ambient light. Results from using an MEA show that activation is limited to the targeted receptive field. Significance. The results of this study establish potential effectiveness of using an ion-mediated artificial retina to restore vision for those with degenerative retinal diseases, including retinitis pigmentosa.
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Shelke, D. A., and S. Shirolkar. "DRUG DELIVERY TO RETINA: A REVIEW." INDIAN DRUGS 56, no. 09 (September 28, 2019): 7–21. http://dx.doi.org/10.53879/id.56.09.11991.

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The drug delivery to posterior segment especially to retina of eye is difficult due to various barriers. The diseases affecting the retina of eye are increasing and hence there is need to develop approaches for drug delivery to retina. This review describes the anatomy of retina, barriers associated with it, and diseases of retina. The drug delivery to retina by systemic, topical, intravitreal injection, intravitreal implant along with advance nanotechnology based and transporter mediated drug delivery is discussed here. The recent technologies in retinal drug delivery are also discussed to give comprehensive recent information about retinal drug delivery
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Makabe, Kenichi, Sunao Sugita, Yoko Futatsugi, and Masayo Takahashi. "Dynamics of Cyclooxygenase-1 Positive Microglia/Macrophage in the Retina of Pathological Model Mice as a Biomarker of the Retinal Inflammatory Diseases." International Journal of Molecular Sciences 22, no. 7 (March 25, 2021): 3396. http://dx.doi.org/10.3390/ijms22073396.

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In an intraocular inflammatory state, microglia residing in the retina become active and migrate inside the retina. In this study, we investigated whether cyclooxygenase-1 (COX-1) expressed by retinal microglia/macrophage can be a biomarker for the diagnosis of retinal diseases. COX-1 was immunopositive in microglia/macrophage and neutrophils, while COX-2 was immunopositive in astrocytes and neurons in the inner layer of normal retina. The number of COX-1 positive cells per section of the retinal tissue was 14 ± 2.8 (mean ± standard deviation) in normal mice, which showed significant increase in the lipopolysaccharide (LPS)-administrated model (62 ± 5.0, p = 8.7 × 10−9). In addition to microglia, we found neutrophils that were positive for COX-1. In the early stage of inflammation in the experimental autoimmune uveoretinitis (EAU), COX-1 positive cells, infiltrating from the ciliary body into the retinal outer nuclear layer, were observed. The number of infiltrating COX-1 positive cells correlated with the severity of EAU. Taken together, the increased number of COX-1 positive microglia/macrophage with morphological changes were observed in the retinas of retinal inflammatory disease models. This suggests that COX-1 can be a marker of disease-related activities of microglia/macrophage, which should be useful for the diagnosis of retinal diseases.
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Sun, Ye, and Lois E. H. Smith. "Retinal Vasculature in Development and Diseases." Annual Review of Vision Science 4, no. 1 (September 15, 2018): 101–22. http://dx.doi.org/10.1146/annurev-vision-091517-034018.

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The retina is one of the most metabolically active tissues in the body, consuming high levels of oxygen and nutrients. A well-organized ocular vascular system adapts to meet the metabolic requirements of the retina to ensure visual function. Pathological conditions affect growth of the blood vessels in the eye. Understanding the neuronal biological processes that govern retinal vascular development is of interest for translational researchers and clinicians to develop preventive and interventional therapeutics for vascular eye diseases that address early drivers of abnormal vascular growth. This review summarizes the current knowledge of the cellular and molecular processes governing both physiological and pathological retinal vascular development, which is dependent on the interaction among retinal cell populations, including neurons, glia, immune cells, and vascular endothelial cells. We also review animal models currently used for studying retinal vascular development.
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Li, Yan, Ting Luo, and Hong-Bin Lyu. "Therapeutic potential of iron chelators in retinal vascular diseases." International Journal of Ophthalmology 16, no. 11 (November 18, 2023): 1899–910. http://dx.doi.org/10.18240/ijo.2023.11.24.

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Iron is one of the necessary metal elements in the human body. There are numerous factors that control the balance of iron metabolism, and its storage and transportation mechanisms are intricate. As one of the most energy-intensive tissues in the body, the retina is susceptible to iron imbalance. The occurrence of iron overload in the retina leads to the generation of a significant quantity of reactive oxygen species. This will aggravate local oxidative stress and inflammatory reactions and even lead to ferroptosis, eventually resulting in retinal dysfunction. The blood-retina-retinal barrier is eventually harmed by oxidative stress and elevated inflammation, which are characteristics of retinal vascular disorders. The pathophysiology of retinal vascular disorders may be significantly influenced by iron. Recently, iron-chelating agents have been found to have antioxidative and anti-inflammatory actions in addition to iron chelating. Therefore, iron neutralization is considered to be a new and potentially useful therapeutic strategy. This article reviews the iron overload in retinal vascular diseases and discusses the therapeutic potential of iron-chelating agents.
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Schilardi, Giulia, Jakub Kralik, and Sonja Kleinlogel. "Selective Block of Upregulated Kv1.3 Potassium Channels in ON-Bipolar Cells of the Blind Retina Enhances Optogenetically Restored Signaling." International Journal of Molecular Sciences 24, no. 18 (September 18, 2023): 14207. http://dx.doi.org/10.3390/ijms241814207.

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Loss of photoreceptors in retinal degenerative diseases also impacts the inner retina: bipolar cell dendrites retract, neurons rewire, and protein expression changes. ON-bipolar cells (OBCs) represent an attractive target for optogenetic vision restoration. However, the above-described maladaptations may negatively impact the quality of restored vision. To investigate this question, we employed human post-mortem retinas and transgenic rd1_Opto-mGluR6 mice expressing the optogenetic construct Opto-mGluR6 in OBCs and carrying the retinal degeneration rd1 mutation. We found significant changes in delayed rectifier potassium channel expression in OBCs of degenerative retinas. In particular, we found an increase in Kv1.3 expression already in early stages of degeneration. Immunohistochemistry localized Kv1.3 channels specifically to OBC axons. In whole-cell patch-clamp experiments, OBCs in the degenerated murine retina were less responsive, which could be reversed by application of the specific Kv1.3 antagonist Psora-4. Notably, Kv1.3 block significantly increased the amplitude and kinetics of Opto-mGluR6-mediated light responses in OBCs of the blind retina and increased the signal-to-noise ratio of light-triggered responses in retinal ganglion cells. We propose that reduction in Kv1.3 activity in the degenerated retina, either by pharmacological block or by KCNA3 gene silencing, could improve the quality of restored vision.
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Dolar-Szczasny, Joanna, Anna Święch-Zubilewicz, and Jerzy Mackiewicz. "Innovation in retinal diseases – ultra-widefield imaging." Polish Journal of Public Health 125, no. 1 (March 1, 2015): 14–16. http://dx.doi.org/10.1515/pjph-2015-0014.

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Abstract The understanding of retinal disease has evolved rapidly with a growing number of clinical evidence supplied by ultrawidefield retinal imaging. Optos 200Tx ultra-widefield retinal imaging system uses a scanning laser ophthalmoscope, as well as an ellipsoid mirror. This creates a possibility of making a virtual focal point inside the eye and, in turn, enables the system to simultaneously make a single capture of the central retina and periphery. This system offers multimodal ultra-widefield imaging, including color photographs, fundus autofluorescence images, red-free images and fluorescein angiography (FA), allowing visualization of the retinal circulation. For color photographs, green and red lasers are used simultaneously to allow visualization of retinal substructures from the sensory retina and retinal pigment epithelium to the choroid. In our clinic ultra-widefield fluorescein angiography has became an elegant diagnostic imaging modality that has improved our ability to diagnose and plan treatment strategies. In the future widefield imaging will probably be coupled with OCT (optical coherence tomography) option to better evaluate retinal pathologies in the periphery.
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Dissertations / Theses on the topic "Retina Diseases"

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Wu, Kathy H. "Histopathological studies of the aging human retina." Thesis, The University of Sydney, 2002. https://hdl.handle.net/2123/27837.

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Age-related macular degeneration (AMD) is the leading cause of untreatable blindness. Its global prevalence continues to increase in relation to aging of the population. Despite the increasing impact of AMD, its pathogenesis remains to be fully defined. Improved therapeutic measures such as photodynamic therapy and pharmacological interventions are being developed for some cases of Wet AMD; however, treatment remains unavailable for the Dry form which accounts for a significant proportion of AMD cases. Neither has any intervention been developed to reduce the incidence of the disease.
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梁欣珮 and Yan-pui Irene Leung. "Potential impact of alzheimer's disease on retina." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42905059.

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Chang, Hui. "Oxidative stress in the retina an experimental study in the rat /." Lund : Dept. of Ophthalmology, University Hospital, Lund University, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39725792.html.

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Källmark, Fredrik. "Investigations of perimetry and gaze-stability in the healthy and deceased retina /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-561-5/.

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Bhagavatheeshwaran, Govind. "Magnetic Resonance Imaging of the Rat Retina." Worcester, Mass. : Worcester Polytechnic Institute, 2008. http://www.wpi.edu/Pubs/ETD/Available/etd-041608-144837/.

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Thesis (Ph.D.)--Worcester Polytechnic Institute.
Keywords: Mn54-autoradiography, rat retina, manganese enchanced mri, rcs rat, magnetic resonance imaging, retinal degeneration, high-resolution mri, blood volume imaging Includes bibliographical references (leaves 211-226).
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Mellough, Carla Bernadette. "An assessment of the cell replacement capability of immortalised, clonal and primary neural tissues following their intravitreal transplantation into rodent models of selective retinal ganglion cell depletion." University of Western Australia. School of Anatomy and Human Biology, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0101.

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[Truncated abstract] Microenvironmental changes associated with apoptotic neural degeneration may instruct a proportion of newly transplanted donor cells to differentiate towards the fate of the deteriorating host cellular phenotype. In the work described in this thesis, this hypothesis was tested by inducing apoptotic retinal ganglion cell (RGC) death in neonatal and adult rats and mice, and then examining whether intravitreally grafted cells from a range of sources of donor neural tissue became incorporated into these selectively depleted retinae. Donor tissues were: a postnatal murine cerebellar-derived immortalised neural precursor cell line (C17.2); an adult rat hippocampal-derived clonal stem-like line (HCN/GFP); mouse embryonic day 14 (E14) primary dissociated retinal cells (Gt[ROSA]26); and adult mouse ciliary pigmented margin-derived primary neurospheres (Gt[ROSA]26). In neonates, rapid RGC death was induced by removal of the contralateral superior colliculus (SC), and in adults, delayed RGC death was induced by unilateral optic nerve (ON) transection. Some adult hosts received ON transection coupled with an autologous peripheral nerve (PN) graft. Donor cells were injected intravitreally 6-48 h after SC ablation (neonates) or 0, 5, 7 or 14 days after ON injury (adults). Cells were also injected into non-RGC depleted neonatal and adult retinae. At 4 or 8 weeks, transplanted cells were identified, quantified and their differentiation fate within host retinae was assessed. Transplanted male C17.2 cells were identified in host retinae using a Y-chromosome marker and in situ hybridisation, or by their expression of the lacZ reporter gene product Escherichia coli beta-galactosidase (beta-gal) using Xgal histochemistry or a beta-gal antibody. No C17.2 cells were identified in axotomised adult-injected eyes undergoing delayed RGC apoptosis (n = 16). Donor cells were, however, stably integrated within the retina in 29% (15/55) of mice that received C17.2 cell injections 24 h after neonatal SC ablation; 6-31% of surviving cells were found in the RGC layer (GCL). These NSC-like cells were also present in intact retinae, but on average there were fewer cells in GCL. In SC-ablated mice, most grafted cells did not express retinal-specific markers, although occasional donor cells in the GCL were immunopositive for beta-III tubulin (TUJ1), a protein highly iii expressed by, but not specific to, developing RGCs. Targeted rapid RGC depletion thus increased C17.2 cell incorporation into the GCL, but grafted C17.2 cells did not appear to differentiate into an RGC phenotype.
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Zanoni, Diogo Sousa [UNESP]. "Experimental glaucoma model (ischemia and reperfusion): histology, morphometry, protein and gene espression of apoptosis pathway." Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/132013.

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Made available in DSpace on 2015-12-10T14:23:03Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-05-28. Added 1 bitstream(s) on 2015-12-10T14:29:18Z : No. of bitstreams: 1 000852681.pdf: 1224340 bytes, checksum: 7e3993edae8f0d4badfed835114ffa9b (MD5)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Purpose: The aims of this study were to better understand the mechanism of cell death by apoptosis in a glaucoma model (ischemia / reperfusion) and evaluate the role of apoptosis in this model and if treatment with Sildenafil helps prevent apoptosis. Methods: 36 rats, from 4 to 6 months, males, Lewis and weighing ± 350g were divided in 5 groups: control group (6 animals) and for groups with ischemia / reperfusion (7 and 21 days), two groups consisting of ten animals treated with sildenafil and two groups of Five animals treated with placebo. Paracentesis of the anterior chamber with needle 30G coupled to saline (0.9%) was made and maintained for 60 minutes. Intraocular pressure was measured by rebound tonometer (Tonovet®). There was histological, morphometric by hematoxylin and eosin and, immunohistochemical staining and qRT-PCR analysis by Caspase-7, Caspase-6, Caspase-9, Tnf-r2, Fas-l, Bcl-2 and Bax. For statistic analysis we used ANOVA and t-test for morphometric analysis and, for immunohistochemistry and qRT-PCR, Fisher exact test was employed with a statistical significance level of p <0.05 Results: Histology and morphometric analysis, proved more changes in the untreated group compared to the treatment and control group. Analysis of immunohistochemistry and qRT-PCR observed the more significant expression in untreated eyes. Conclusion: Sildenafil apperead to be protective to ganglion cell apoptosis. Cell survival was evident in histology and morphometry. For immunohistochemistry and RT-PCR was observed protective effect in the apoptosis pathways with similar or below expression compared to the control
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Zanoni, Diogo Sousa. "Experimental glaucoma model (ischemia and reperfusion) : histology, morphometry, protein and gene espression of apoptosis pathway /." Botucatu, 2015. http://hdl.handle.net/11449/132013.

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Orientador: Renée Laufer Amorim
Coorientador: José Luiz Laus
Banca: Juliany Quitzan Gomes
Banca: Alvio Isao Shiguematsu
Resumo: Não disponível
Abstract: Purpose: The aims of this study were to better understand the mechanism of cell death by apoptosis in a glaucoma model (ischemia / reperfusion) and evaluate the role of apoptosis in this model and if treatment with Sildenafil helps prevent apoptosis. Methods: 36 rats, from 4 to 6 months, males, Lewis and weighing ± 350g were divided in 5 groups: control group (6 animals) and for groups with ischemia / reperfusion (7 and 21 days), two groups consisting of ten animals treated with sildenafil and two groups of Five animals treated with placebo. Paracentesis of the anterior chamber with needle 30G coupled to saline (0.9%) was made and maintained for 60 minutes. Intraocular pressure was measured by rebound tonometer (Tonovet®). There was histological, morphometric by hematoxylin and eosin and, immunohistochemical staining and qRT-PCR analysis by Caspase-7, Caspase-6, Caspase-9, Tnf-r2, Fas-l, Bcl-2 and Bax. For statistic analysis we used ANOVA and t-test for morphometric analysis and, for immunohistochemistry and qRT-PCR, Fisher exact test was employed with a statistical significance level of p <0.05 Results: Histology and morphometric analysis, proved more changes in the untreated group compared to the treatment and control group. Analysis of immunohistochemistry and qRT-PCR observed the more significant expression in untreated eyes. Conclusion: Sildenafil apperead to be protective to ganglion cell apoptosis. Cell survival was evident in histology and morphometry. For immunohistochemistry and RT-PCR was observed protective effect in the apoptosis pathways with similar or below expression compared to the control
Mestre
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Frida, Jonsson. "Underlying genetic mechanisms of hereditary dystrophies in retina and cornea." Doctoral thesis, Umeå universitet, Institutionen för medicinsk biovetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-130538.

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Inherited retinal and corneal dystrophies represent a group of disorders with great genetic heterogeneity. Over 250 genes are associated with retinal diseases and 16 genes are causative of corneal dystrophies. This thesis is focused on finding the genetic causes of corneal dystrophy, Leber congenital amaurosis (LCA), Stargardt disease and retinitis pigmentosa in families from northern Sweden.  By whole exome sequencing a novel mutation, c.2816C>T, p.Thr939Ile, in Collagen Type XVII, Alpha 1 chain, COL17A1, gene was identified in several families with epithelial recurrent erosion dystrophy (ERED). We showed that the COL17A1 protein is expressed in the basement membrane of the cornea, explaining the mutation involvement in the corneal symptoms. We could link all the families in this study to a couple born in the late 1700s confirming a founder mutation in northern Sweden. Our finding highlights role of COL17A1 in ERED and suggests screening of this gene in patients with similar phenotype worldwide. Furthermore the genetic causes in several retinal degenerations were identified. In one family with two recessive disorders, LCA and Stargardt disease, a novel stop mutation, c.2557C>T, p.Gln853Stop, was detected in all LCA patients. In the Stargardt patients two intronic variants, the novel c.4773+3A>G and c.5461-10T>C, were detected in the ABCA4 gene. One individual was homozygous for the known variant c.5461-10T>C and the other one was compound heterozygote with both variants present. Both variants, c.4773+3A>G and c.5461-10T>C caused exon skipping in HEK293T cells demonstrated by in vitro splice assay, proving their pathogenicity in Stargardt disease. Finally, in recessive retinitis pigmentosa, Bothnia Dystrophy (BD), we identified a second mutation in the RLBP1 gene, c.677T>A, p.Met226Lys. Thus, BD is caused not only by common c.700C>T variant but also by homozygosity of c.677T>A or compound heterozygosity. Notably, known variant, c.40C>T, p.R14W in the CAIV gene associated with a dominant retinal dystrophy RP17 was detected in one of the compound BD heterozygote and his unaffected mother. This variant appears to be a benign variant in the population of northern Sweden. In conclusion, novel genetic causes of retinal dystrophies in northern Sweden were found demonstrating the heterogeneity and complexity of retinal diseases. Identification of the genetic defect in COL17A1 in the corneal dystrophy contributes to understanding ERED pathogenesis and encourages refinement of IC3D classification. Our results provide valuable information for future molecular testing and genetic counselling of the families.
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López, Begines Santiago. "Unveiling novel components of the protein complex responsible for cGMP synthesis in retinal photoreceptors: role in cell physiology and disease." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/461890.

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In photoreceptor cells of the retina, light triggers a protein G-mediated enzymatic cascade that leads to hydrolysis of cGMP. The drop in cGMP levels causes the closure of cGMP-channel at the plasma membrane, decreasing the influx of cations, mainly Na+ and Ca2+, hyperpolarizing the cell. This hyperpolarization decreases the rate of neurotransmitter release at the synaptic terminal. Photoreceptor cells must recover the darkness equilibrium and adapt their light sensitivity to the wide range of light intensities present in the natural world. Genetic defects at both activation and termination cascades leads to inherited retinal dystrophies. The cGMP levels are restored to darkness equilibrium by new synthesis by the complex formed by a membrane form of guanylate cyclase (RetGC) which is bound to a couple of proteins that confers it calcium sensitivity, Guanylate Cyclase Activating Proteins (GCAP1 and GCAP2). RetGC activity is stimulated by the drop of Ca2+ concentration because of close of cGMP-channels. There is a feedback loop between cGMP and Ca2+ that has a fundamental role in the processes of termination of light response and light adaptation. RetGC1 is responsible for cGMP synthesis in rods and cones. Mutations of genes involved in the cGMP synthesis complex have been linked to autosomal dominant inherited retinal dystrophies, both retinitis pigmentosa (adRP) as Leber’s congenital amaurosis (LCA) The regulation of RetGC by GCAPs proteins has been extensively studied in vitro, at biochemical and structural levels. However, many relevant aspects of regulation and trafficking of this complex in vivo remains unknown. By subretinal electroporation, we have analyzed the molecular determinants of subcellular distribution of GCAPs. We have determined that the complex between RetGC1 and GCAP1 is assembled in the inner segment and then transported to the outer segment, playing a determinant role the myristoylation of GCAP1 and the binding of GCAP1 to the cyclase. On the other hand, phosphorylation plays an essential role in subcellular distribution of GCAP2, and failures in subcellular localization of GCAP2 could contribute to explain the pathophysiology of the human G157R mutation linked to adRP. We here report a proteomic approach to identify novel interactors of Guanylate Cyclase Activating Protein 1 (GCAP1) that led to the unexpected discovery of inosine monophosphate dehydrogenase 1 (IMPDH1) interaction with retinal guanylate cyclase 1 (RetGC1). IMPDH1 is the rate-limiting step in de novo GTP synthesis, and mutations in impdh1 gene have been associated to adRP and LCA. We reveal an unanticipated direct interaction between IMPDH1 and RetGC1 at photoreceptor outer segments where phototransduction takes place. The interaction involves the dimerization and catalytic domains of RetGC1, and is significantly affected by IMPDH1 mutations associated to blindness. This finding links de novo GTP synthesis to GTP conversion to cGMP, bridging blindness-causative genes so far considered unrelated and creating a new scenario for the development of therapeutic strategies. By bridging distinct blindness-causative genes in a common biochemical pathway, we here contribute to reduce the apparent complexity of inherited retinal dystrophies grouping them on base common metabolic pathways. The main aim of this strategy of grouping genes on base of their function is to identify “hubs” of cell damage. We also have characterized the interaction between RetGC1 and Creatine kinase B, which could be supplying locally the ATP needed to maintain the catalytic activity in cones. This work aid to understanding about regulation and trafficking of RetGC/GCAPs complex, as well as the interplaying between the cGMP synthesis complex and de novo GTP synthesis, opening a new conceptual framework for pharmacological treatment of diseases that trigger changes in intracellular levels of cGMP, which in a prolonged way affect to cell survival, leading to inherited blindness.
En fotorreceptores de retina, la respuesta a luz desencadena la hidrólisis del cGMP. La síntesis de cGMP recae en el complejo formado por una forma de membrana de la guanilato ciclasa (RetGC1 y RetGC2) y unas proteínas que le confieren sensibilidad a calcio (Guanylate Cyclase Activating Proteins GCAP1 y GCAP2). Mutaciones en los genes que codifican para las proteínas integrantes de este complejo han sido ligadas distrofias hereditarias de retina autosómicas dominantes. La regulación de este complejo ha sido extensamente estudiada in vitro, sin embargo, muchos aspectos relacionados con este complejo en el entorno de la célula viva se desconocen. Determinamos mediante electroporación subretinal que el ensamblaje del complejo formado por RetGC1 y GCAP1 precede a su transporte hacia el segmento externo y tanto la miristoilación como la unión a la ciclasa por parte de GCAP1 son necesarias para su transporte. Por otro lado, la fosforilación juega un papel clave en la distribución celular de GCAP2, y fallos en la localización de GCAP2 podrían contribuir a explicar la patofisiología de la mutación hG157R ligada a retinosis pigmentaria autosómica dominante. Mediante una aproximación proteómica para identificar nuevos interactores de GCAP1, hemos caracterizado la interacción directa entre la guanilato ciclasa y la inosina monofosfato deshidrogenasa (IMPDH1), la enzima responsable del paso limitante en la síntesis de novo de GTP. Mutaciones en el gen impdh1 se han asociado a distrofias hereditarias de retina autosómicas dominantes. Ambas proteínas se localizan en el compartimento sensorial, interaccionan en el orden micromolar, involucrando a los dominios de dimerización y catalítico de RetGC1 y la interacción se afecta significativamente por los mutantes asociados a ceguera en IMPDH1. Además también se ha caracterizado la interacción de RetGC con la Creatina quinasa B (CKB), la cual podría está proporcionando el ATP local necesario para mantener la actividad catalítica específicamente en conos. Este trabajo arroja luz sobre la regulación y transporte del complejo RetGC/GCAPs, así como la interconexión entre los complejos de síntesis de cGMP y síntesis de novo de GTP, integrando genes asociados a enfermedad en base a su implicación en procesos metabólicos comunes, abriendo un nuevo escenario para el tratamiento farmacológico de enfermedades que provoquen cambios en los niveles de cGMP intracelulares.
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Books on the topic "Retina Diseases"

1

Wu, Gloria. Retina: The fundamentals. Philadelphia: W.B. Saunders, 1995.

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Wahler, Connie, and Lauren Wilkinson. Retinopathy: New research. Hauppauge, N.Y: Nova Science Publishers, 2011.

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Richard, Spaide, and SpringerLink (Online service), eds. Medical Retina: Focus on Retinal Imaging. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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European School for Advanced Studies in Ophthalmology, ed. Surgical retina. Basel: Karger, 2012.

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C, Ho Allen, and Wills Eye Hospital (Philadelphia, Pa.), eds. Retina. New York: McGraw-Hill, Medical Pub. Division, 2003.

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Sharon, Fekrat, Moshfeghi Darius, and Eliott Dean, eds. Curbside consultation in retina: 49 clinical questions. Thorofare, NJ: SLACK, 2010.

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Hollyfield, Joe G., R. E. Anderson, and Matthew M. LaVail. Retinal degenerative diseases and experimental therapy. New York: Kluwer Academic/Plenum Publishers, 1999.

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Schepens, Charles L. Schepens' Retinal detachment and allied diseases. 2nd ed. Boston: Butterworth-Heinemann, 2000.

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Regillo, Carl D. Retina and vitreous. San Francisco, CA: American Academy of Ophthalmology, 2011.

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Anderson, Robert E., Matthew M. LaVail, and Joe G. Hollyfield, eds. Degenerative Diseases of the Retina. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1897-6.

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Book chapters on the topic "Retina Diseases"

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Liu, Xuyang, Jia Ma, and Ningli Wang. "Retina." In Advances in Visual Science and Eye Diseases, 5–10. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-2502-1_1.

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Hussein, Mohamed, and David K. Coats. "Infectious Diseases of the Pediatric Retina." In Pediatric Retina, 361–407. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12041-1_16.

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Storti, Federica, and Christian Grimm. "Active Cholesterol Efflux in the Retina and Retinal Pigment Epithelium." In Retinal Degenerative Diseases, 51–55. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27378-1_9.

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Han, Ian C. "Combined Hamartoma of the Retina and Retinal Pigment Epithelium." In Manual of Retinal Diseases, 181–84. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20460-4_37.

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Greenberg, Jacquie, Rene Goliath, Joyce Tombran-Tink, Gerald Chader, and Rajkumar Ramesar. "Growth Factors In The Retina." In Degenerative Retinal Diseases, 291–94. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5933-7_31.

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Karlstetter, Marcus, and Thomas Langmann. "Microglia in the Aging Retina." In Retinal Degenerative Diseases, 207–12. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-3209-8_27.

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Barben, Maya, Ana Bordonhos, Marijana Samardzija, and Christian Grimm. "Hypoxia-Regulated MicroRNAs in the Retina." In Retinal Degenerative Diseases, 413–17. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27378-1_68.

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Kato, S., Z. Y. Zhou, K. Sugawara, Y. Yasui, N. Takizawa, K. Sugitani, and K. Mawatari. "Ischemic Neuronal Death in the Fish Retina." In Degenerative Retinal Diseases, 199–204. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5933-7_23.

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Lahne, Manuela, and David R. Hyde. "Interkinetic Nuclear Migration in the Regenerating Retina." In Retinal Degenerative Diseases, 587–93. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_78.

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Yan, Naihong, Ke Ma, Jia Ma, Wei Chen, Yun Wang, Guiqun Cao, Dominic Man-Kit Lam, and Xuyang Liu. "Profiling MicroRNAs Differentially Expressed in Rabbit Retina." In Retinal Degenerative Diseases, 203–9. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1399-9_23.

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Conference papers on the topic "Retina Diseases"

1

Greenstein, Vivienne C., and Donald C. Hood. "A Test of the Decreased Responsiveness Hypothesis in Retinitis Pigmentosa." In Noninvasive Assessment of Visual Function. Washington, D.C.: Optica Publishing Group, 1985. http://dx.doi.org/10.1364/navf.1985.tua2.

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The most fundamental deficit attributable to retinal disease is a reduction in sensitivity to light. Recently we suggested a simple physiological basis for this sensitivity loss (Hood and Greenstein, 1982, Greenstein et al., 1982.). Based upon psychophysical experiments performed on patients with a variety of retinal diseases we hypothesized that in the diseased retina all retinal cells are less responsive to light. That is because of anoxia, or decreased metabolic activity, or some other factor, retinal cells respond to all light intensities with a fraction of the response produced in a non-diseased retina. In fact, much of our data suggest that a simple form of this explanation can be applied to the retinal diseases we studied. It is not surprising that decreased cellular responsiveness occurs in a disease like diabetic retinopathy; it is surprising that the loss in foveal sensitivity found in a group of patients with retinitis pigmentosa (RP) was consistent with this explanation (Greenstein et al. 1984). If sensitivity loss in RP can be attributed entirely to decreased responsiveness then the effects of adding adapting lights are quantitatively predictable. In this paper this hypothesis is tested by collecting foveal data at two levels of steady adaptation on a selected group of RP patients.
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Petrig, Benno L., and Charles E. Riva. "Towards Computer-Assisted Clinical Retinal Laser Doppler Velocimetry." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/navs.1987.wc5.

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The retina is among the few tissues in the human body where blood circulation can be observed directly and noninvasively. This has facilitated a detailed description of the morphological changes of the retinal vasculature caused by many ocular and systemic diseases. Despite the accessibility of the retinal vasculature and the obvious importance of blood flow, quantitative data on the retinal hemodynamics in the normal and diseased retina is not available to the clinician. Assessments of "normal" or "low" flow based on fluorescein angiography remain qualitative and the fluorescein dye dilution technique has had limited success in providing a quantitative measure of retinal blood flow.
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Daley, 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.

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Acquired loss of color vision is associated with diseases which produce vascular complications that affect the eye.1,2 In particular, the early loss of color vision associated with diabetes mellitus initially influences the blue-sensitive mechanism. Generally, as the disease progresses, loss of green vision becomes evident, and finally, red vision is involved.3 The patho-physiological mechanisms which produce the visual loss appear to be related to optical and neural changes within the eye.4,5 The optical loss may be caused by light scattering produced by plasma proteins which leak into the retina through an altered blood-retinal barrier.4,5
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Burns, Stephen A., Shuang Wu, Ann E. Eisner, and Francois Delori. "Reflectometric Measurement of Human Cone Photoreceptor Directionality." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/vsia.1995.sac2.

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The photoreceptors of the human retina are normally aligned such that their long axis points toward the center of the pupil (Stiles; Enoch and Laties). This alignment probably serves several functions. It optimizes sensitivity to light entering the center of the pupil, it decreases sensitivity to intraocular stray light, and may improve the resolution of the eye by apodizing the pupil. Cone photoreceptor alignment is affected by a number of retinal diseases (Enoch, Smith and Pokorny), and has been shown to be related to exudative maculopathy (Smith et al). However, clinical investigation of the relation between photoreceptor alignment and retinal disease has been impeded both by the difficulty of the measurement techniques available and the large investment of patient time required to make measurements.
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Caruso, Rafael C., Muriel I. Kaiser-Kupfer, Malina A. Drews-Bankiewicz, and David L. Valle. "Measurements of the Stiles-Crawford Effect and of Increment Thresholds in Patients with Gyrate Atrophy of the Choroid and Retina." In Ophthalmic and Visual Optics. Washington, D.C.: Optica Publishing Group, 1993. http://dx.doi.org/10.1364/ovo.1993.osaa.4.

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As the Stiles-Crawford (S-C) effect of the first kind depends on the directional sensitivity of photoreceptors, it can be used in clinical research to identify and quantify photoreceptor involvement in retinal diseases. In this report, we describe abnormalities of foveal cone directional sensitivity and foveal cone thresholds in patients with gyrate atrophy of the choroid and retina (GA).
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Breton, Michael E., Graham E. Quinn, Sara S. Keene, Janet C. Dahmen, and Alexander J. Brucker. "Analysis of ERG Parameters in Central Retinal Vein Occlusion." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/navs.1988.wa1.

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Effective treatment of the complications resulting from an ischemic condition such as central retinal vein occlusion (CRVO) may depend on the accuracy of early diagnosis. In CRVO, relative ischemia of a significant proportion of retina has been associated with ocular morbidity in the form of rubeosis iridis and neovascular glaucoma (1,2,3). Fluorescein angiography (FA) has been used routinely to determine the degree of retinal ischemia in CRVO as in other occlusive vascular diseases of the retina. However, FA interpretation, based on non-quantitative visual judgements, may lack sufficient sensitivity to detect early ischemic changes (4). The purposes of this report are: 1) to characterize the ERG parameters for CRVO and fellow eyes as to their ability to identify functionally distinct sub-groups, and 2) to compare the ERG characterization of CRVO eyes to a variety of FA caracteristics.
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Zeimer, Ran, Theresa Guran, Mahnaz Shahidi, and Marek Mori. "Application of Targeted Dye Delivery to The Mapping of Retinal Hemodynamics." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/navs.1990.tua4.

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Since many diseases of the retina result in changes in retinal circulation, information on hemodynamics can be important in the diagnosis and the evaluation of current and new therapies. We are developing a method that would allow repeated mapping of the hemodynamics of the retinal macro- and micro-circulation. The method, named targeted dye delivery, consists of encapsulating a fluorescent dye in temperature sensitive liposomes, injecting them systemically and releasing a bolus of dye in a targeted retinal vessel by a light pulse from an argon laser. We report here on the evaluation of the method in the study of retinal hemodynamics of a primate.
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Meriaudeau, Fabrice. "Keynote speech 3: Computer aided diagnosis for retina related diseases." In 2015 IEEE International Conference on Signal and Image Processing Applications (ICSIPA). IEEE, 2015. http://dx.doi.org/10.1109/icsipa.2015.7412151.

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Johnson, Mary A., Julian Procope, and Patricia M. Quinlan. "Electroretinographic Oscillatory Potentials and Their Role in Predicting Treatable Complications in Patients with Central Retinal Vein Occlusion." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/navs.1990.mc3.

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Oscillatory potentials (OPs) are small electroretinographic (ERG) wavelets that occur on the rising phase of the ERG b-wave. Thought to originate as a feedback circuit involving the bipolar, amacrine and possibly ganglion cell layers of the retina1, the potential clinical utility of OPs in diseases that preferentially affect the inner retina has long been acknowledged.2 Recently, OPs were shown to be much more sensitive predictors of the development of high risk characteristics in diabetic retinopathy than were fundus features graded using the ETDRS (Early Treatment of Diabetic Retinopathy Study) classification scheme3.
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Shahidi, Mahnaz, Richard Land, Richard S. Weinhaus, D. Max Snodderly, and Ran Zeimer. "Comparison Between Measurements of Retinal Thickness Made Noninvasively in Vivo and by Microscopy in Vitro." In Ophthalmic and Visual Optics. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/ovo.1991.thd2.

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In many ocular diseases the retinal thickness is altered due to edema or atrophy. We have developed a method to measure the retinal thickness and thus provide earlier diagnosis and improve therapy monitoring. The application in humans has provided encouraging results. (1,2) To establish the method further, comparison between in vivo and in vitro thickness measurements in the same eye are desirable. The layers from which light is reflected and detected by the in vivo method can be identified and more information about the presence of tissue distortions arising from the in vitro method during preparation can be acquired. We present the comparison between locally measured thickness values in a cynomolgus monkey and measurements made by light microscopy of the whole mounted retina.
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Reports on the topic "Retina Diseases"

1

Stevens, Brianna. Retinal Changes Associated with Alzheimer's Disease. Ames (Iowa): Iowa State University, January 2020. http://dx.doi.org/10.31274/cc-20240624-1231.

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Zilliox, Patricia. Inherited Retinal Degenerative Disease Clinical Trial Network. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada581282.

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Zilliox, Patricia. Inherited Retinal Degenerative Disease Clinical Trials Network. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada618254.

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Rose, Stephen. Inherited Retinal Degenerative Disease Clinical Trial Network. Addendum. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada602848.

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Skutnik, Bolesh J. Diode Pumped Frequency Doubled ND:Yag Laser for the Treatment of Glaucoma and Retinal Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada408804.

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Skutnik, Bolesh J. Diode Pumped Frequency Doubled ND:YAG Laser for the Treatment of Glaucoma and Retinal Disease. Fort Belvoir, VA: Defense Technical Information Center, November 2002. http://dx.doi.org/10.21236/ada409052.

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Li, Ting, Shudan Ge, Wei Zheng, Chao Luan, Xingtong Liu, Zongxiu Luo, Qi Zhao, and Lulu Xie. Effectiveness and safety of panretinal photocoagulation combined with intravitreous ranibizumab for patients with type 2 proliferative diabetic retinopathy：A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0048.

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Review question / Objective: Our study aims to synthesise results from randomised controlled trials to assess the effectiveness and safety of PRP combined with intravitreous ranibizumab for T2PDR. Condition being studied: Diabetic retinopathy (DR) is the most common complication of diabetes mellitus, which will seriously affect the quality of life of patients and bring great burden to patients’ families and society. DR is one of the most important diseases of blindness in people aged 20 to 60 years worldwide. Nearly 15% of diabetic patients with a disease duration of more than 5 years were combined with DR.The prevalence of vision threatening diabetic retinopathy in the United States is 4.4 percent. Worldwide, the prevalence is estimated at 10.2%.At present, the treatment methods for type 2 proliferative diabetic retinopathy (T2PDR), at home and abroad mainly include retinal laser photocoagulation and intravitreal injection of vascular endothelial growth factor (VEGF) inhibitors.
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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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Dawson, William O., and Moshe Bar-Joseph. Creating an Ally from an Adversary: Genetic Manipulation of Citrus Tristeza. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7586540.bard.

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Citrus is one of the major agricultural crops common to Israel and the United States, important in terms of nutrition, foreign exchange, and employment. The economy of both citrus industries have been chronically plagued by diseases caused by Citrus tristeza virus (CTV). The short term solution until virus-resistant plants can be used is the use of mild strain cross-protection. We are custom designing "ideal" protecting viruses to immunize trees against severe isolates of CTV by purposely inoculating existing endangered trees and new plantings to be propagated as infected (protected) citrus budwood. We crossed the substantial technological hurdles necessary to accomplish this task which included developing an infectious cDNA clone which allows in vitro manipulation of the virus and methods to then infect citrus plants. We created a series of hybrids between decline-inducing and mild CTV strains, tested them in protoplasts, and are amplifying them to inoculate citrus trees for evaluation and mapping of disease determinants. We also extended this developed technology to begin engineering transient expression vectors based on CTV as tools for genetic improvement of tree crops, in this case citrus. Because of the long periods between genetic transformation and the ultimate assay of mature tree characteristics, there is a great need for an effective system that allows the expression or suppression of target genes in fruiting plants. Virus-based vectors will greatly expedite progress in citrus genetic improvement. We characterized several components of the virus that provides necessary information for designing virus-based vectors. We characterized the requirements of the 3 ’-nontranslated replication promoter and two 3 ’-ORF subgenomic (sg) mRNA controller elements. We discovered a novel type of 5’-terminal sgRNAs and characterized the cis-acting control element that also functions as a strong promoter of a 3 ’-sgRNA. We showed that the p23 gene controls negative-stranded RNA synthesis and expression of 3 ’ genes. We identified which genes are required for infection of plants, which are host range determinants, and which are not needed for plant infection. We continued the characterization of native dRNA populations and showed the presence of five different classes including class III dRNAs that consists of infectious and self-replicating molecules and class V dRNAs that contain all of the 3 ’ ORFs, along with class IV dRNAs that retain non-contiguous internal sequences. We have constructed and tested in protoplasts a series of expression vectors that will be described in this proposal.
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Kelly, Luke. Policy and Administrative Barriers to IDPs Accessing Basic Services. Institute of Development Studies (IDS), July 2021. http://dx.doi.org/10.19088/k4d.2021.112.

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Literature shows that IDPs struggle to access services, which has an impact on their ability to live healthy and fulfilling lives. In the field of health, IDPs frequently have worse outcomes than both host community and refugees. This rapid literature review finds evidence of a number of policy and administrative barriers to access of services for internally displaced persons (IDPs). IDPs remain citizens of the countries in which they are displaced, and the national authorities retain responsibility for meeting their basic rights. However, their displacement, loss of livelihoods and assets, lack of documentation, as well as discrimination against them, lack of protection under international law, lack of policy to address their needs, poor services and conflict or disaster conditions, can all make it more difficult for IDPs to access basic services than non-displaced citizens. There is relatively little literature systematically addressing the issue of administrative and policy barriers to service access among IDPs. Much of the literature discusses IDPs alongside refugees (who have a different legal status and access to different national and international support), or discusses the whole range of difficulties facing IDPs but does not focus on administrative or policy barriers. The literature frequently does not compare IDPs and other citizens and service users. Nevertheless, policy and administrative barriers are discussed, ranging from analysis of international instruments on IDPs to documentation procedures in particular countries. Much of the literature shows the prevalence of disease, lack of school attendance, limited provision of services etc. faced by IDPs, but does not discuss the policy and administrative barriers in detail.
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