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Glaucoma 2.0: neuroprotection, neuroregeneration, neuroenhancement. Ophthalmology. 2012;119(5):979–86.\n• Cho KS, Chen DF. Promoting optic nerve regeneration in adult mice with pharmaceutical approach. Neurochem Res. 2008;33(10):2126–33. Study demonstrating the importance of glial cell modulation using pharmacological compounds in order to enhance nerve regeneration in a model of glaucoma.\nLevin LA. Neuroprotection and regeneration in glaucoma. Ophthalmology clinics of North America. 2005;18(4):585–596vii.\nWeinreb RN. Glaucoma neuroprotection: What is it? Why is it needed? Can J Ophthalmol. 2007;42(3):396–8.\nGonzalez-Cordero A, et al. Photoreceptor precursors derived from three-dimensional embryonic stem cell cultures integrate and mature within adult degenerate retina. Nat Biotechnol. 2013;31(8):741–7.\nLakowski J, et al. Transplantation of photoreceptor precursors isolated via a cell surface biomarker panel from embryonic stem cell-derived self-forming retina. Stem Cells. 2015;33(8):2469–82.\nLamba DA, Gust J, Reh TA. Transplantation of human embryonic stem cell-derived photoreceptors restores some visual function in Crx-deficient mice. Cell Stem Cell. 2009;4(1):73–9.\n•• Lamba DA, Karl MO, Ware CB, Reh TA. Efficient generation of retinal progenitor cells from human embryonic stem cells. Proc Natl Acad Sci USA. 2006;103(34):12769–74. This paper was the first to describe retinal cell differentiation from human embryonic stem cells.\n•• Meyer JS, et al. Optic vesicle-like structures derived from human pluripotent stem cells facilitate a customized approach to retinal disease treatment. Stem cells. 2011;29(8):1206–18. This study was among the first to describe the differentiation of RGCs from hPSCs, particularly from highly enriched populations of optic vesicle-like structures. Furthermore, this study was also among the first to demonstrate the ability to model retinal degeneration in vitro with these cells.\n•• Meyer JS, et al. Modeling early retinal development with human embryonic and induced pluripotent stem cells. Proc Natl Acad Sci USA. 2009;106(39):16698–703. This study was the first to describe minimal and defined media components that allowed for cell intrinsic differentiation into retinal cells.\nNakano T, et al. Self-formation of optic cups and storable stratified neural retina from human ESCs. Cell Stem Cell. 2012;10(6):771–85.\nOsakada F, et al. Toward the generation of rod and cone photoreceptors from mouse, monkey and human embryonic stem cells. Nat Biotechnol. 2008;26(2):215–24.\nOsakada F, et al. In vitro differentiation of retinal cells from human pluripotent stem cells by small-molecule induction. J Cell Sci. 2009;122(Pt 17):3169–79.\nWest EL, et al. Defining the integration capacity of embryonic stem cell-derived photoreceptor precursors. Stem cells. 2012;30(7):1424–35.\nAl-Shamekh S, Goldberg JL. Retinal repair with induced pluripotent stem cells. Transl Res. 2014;163(4):377–86.\nJin ZB, Takahashi M. Generation of retinal cells from pluripotent stem cells. Prog Brain Res. 2012;201:171–81.\nSluch VM, Zack DJ. Stem cells, retinal ganglion cells and glaucoma. Dev Ophthalmol. 2014;53:111–21.\nKuehn MH, Fingert JH, Kwon YH. Retinal ganglion cell death in glaucoma: mechanisms and neuroprotective strategies. Ophthalmol clin North Am. 2005;18(3):383–395vi.\nMoore DL, Goldberg JL. Four steps to optic nerve regeneration. J Neuroophthalmol. 2010;30(4):347–60.\nQuigley HA, Broman AT. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol. 2006;90(3):262–7.\nTham YC, et al. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology. 2014;121(11):2081–90.\nCarelli V, et al. Retinal ganglion cell neurodegeneration in mitochondrial inherited disorders. Biochim Biophys Acta. 2009;1787(5):518–28.\nNewman NJ. Treatment of hereditary optic neuropathies. Nature reviews. Neurology. 2012;8(10):545–56.\nYu-Wai-Man P, Votruba M, Moore AT, Chinnery PF. Treatment strategies for inherited optic neuropathies: past, present and future. Eye. 2014;28(5):521–37.\nBerdahl JP, Allingham RR. Intracranial pressure and glaucoma. Curr Opin Ophthalmol. 2010;21(2):106–11.\nCohen LP, Pasquale LR. Clinical characteristics and current treatment of glaucoma. Cold Spring Harb Perspect Med. 2014;4(6):a017236.\nRasmussen CA, Kaufman PL. The trabecular meshwork in normal eyes and in exfoliation glaucoma. J Glaucoma. 2014;23(8 Suppl 1):S15–9.\nKowing D, Messer D, Slagle S, Wasik A. Programs to optimize adherence in glaucoma. Optometry. 2010;81(7):339–50.\nMcKinnon SJ, Goldberg LD, Peeples P, Walt JG, Bramley TJ. Current management of glaucoma and the need for complete therapy. Am J Manag Care. 2008;14(1 Suppl):S20–7.\nSambhara D, Aref AA. Glaucoma management: relative value and place in therapy of available drug treatments. Ther Adv Chronic Dis. 2014;5(1):30–43.\nZhang K, Zhang L, Weinreb RN. Ophthalmic drug discovery: novel targets and mechanisms for retinal diseases and glaucoma. Nat Rev Drug Discov. 2012;11(7):541–59.\nBagga H, Liu JH, Weinreb RN. Intraocular pressure measurements throughout the 24 h. Curr Opin Ophthalmol. 2009;20(2):79–83.\nGrippo TM, et al. Twenty-four-hour pattern of intraocular pressure in untreated patients with ocular hypertension. Invest Ophthalmol Vis Sci. 2013;54(1):512–7.\nWilensky JT. The role of diurnal pressure measurements in the management of open angle glaucoma. Curr Opin Ophthalmol. 2004;15(2):90–2.\nJohnson TV, Bull ND, Martin KR. Neurotrophic factor delivery as a protective treatment for glaucoma. Exp Eye Res. 2011;93(2):196–203.\nMartin KR, et al. Gene therapy with brain-derived neurotrophic factor as a protection: retinal ganglion cells in a rat glaucoma model. Invest Ophthalmol Vis Sci. 2003;44(10):4357–65.\nPease ME, et al. Effect of CNTF on retinal ganglion cell survival in experimental glaucoma. Invest Ophthalmol Vis Sci. 2009;50(5):2194–200.\nFrank L, Wiegand SJ, Siuciak JA, Lindsay RM, Rudge JS. Effects of BDNF infusion on the regulation of TrkB protein and message in adult rat brain. Exp Neurol. 1997;145(1):62–70.\nMeyer-Franke A, et al. Depolarization and cAMP elevation rapidly recruit TrkB to the plasma membrane of CNS neurons. Neuron. 1998;21(4):681–93.\nChen H, Weber AJ. Brain-derived neurotrophic factor reduces TrkB protein and mRNA in the normal retina and following optic nerve crush in adult rats. Brain Res. 2004;1011(1):99–106.\nCapowski EE, et al. Loss of MITF expression during human embryonic stem cell differentiation disrupts retinal pigment epithelium development and optic vesicle cell proliferation. Hum Mol Genet. 2014;23(23):6332–44.\nLamba DA, et al. Generation, purification and transplantation of photoreceptors derived from human induced pluripotent stem cells. PLoS One. 2010;5(1):e8763.\nMellough CB, Sernagor E, Moreno-Gimeno I, Steel DH, Lako M. Efficient stage-specific differentiation of human pluripotent stem cells toward retinal photoreceptor cells. Stem cells. 2012;30(4):673–86.\nOhlemacher SK, Iglesias CL, Sridhar A, Gamm DM, Meyer JS. Generation of highly enriched populations of optic vesicle-like retinal cells from human pluripotent stem cells. Current protocols in stem cell biology. 2015;32:1h.8.1–8.20.\nPhillips MJ, et al. Blood-derived human iPS cells generate optic vesicle-like structures with the capacity to form retinal laminae and develop synapses. Invest Ophthalmol Vis Sci. 2012;53(4):2007–19.\nReichman S, et al. From confluent human iPS cells to self-forming neural retina and retinal pigmented epithelium. Proc Natl Acad Sci USA. 2014;111(23):8518–23.\nSridhar A, Steward MM, Meyer JS. Nonxenogeneic growth and retinal differentiation of human induced pluripotent stem cells. Stem Cells Transl Med. 2013;2(4):255–64.\n• Tucker BA, et al. Duplication of TBK1 stimulates autophagy in iPSC-derived retinal cells from a patient with normal tension glaucoma. J Stem Cell Res Ther. 2014;3(5):161. One of the few papers that attempts to address disease modeling from hPSC-derived RGC-like cells.\n• Zhong X, et al. Generation of three-dimensional retinal tissue with functional photoreceptors from human iPSCs. Nat Commun. 2014;5:4047. Through the three-dimensional differentiation and organization of retinal cells from hPSCs, the authors are able to demonstrate a yield of Brn3-positive RGCs with the correct localization within retinal neuropsheres.\nJin ZB, et al. Modeling retinal degeneration using patient-specific induced pluripotent stem cells. PLoS One. 2011;6(2):e17084.\nSchwarz N, et al. Translational read-through of the RP2 Arg120stop mutation in patient iPSC-derived retinal pigment epithelium cells. Hum Mol Genet. 2015;24(4):972–86.\nCarr AJ, et al. Protective effects of human iPS-derived retinal pigment epithelium cell transplantation in the retinal dystrophic rat. PLoS One. 2009;4(12):e8152.\nHu Y, et al. A novel approach for subretinal implantation of ultrathin substrates containing stem cell-derived retinal pigment epithelium monolayer. Ophthalmic Res. 2012;48(4):186–91.\nNakagawa M, et al. Generation of induced pluripotent stem cells without Myc from mouse and human fibroblasts. Nat Biotechnol. 2008;26(1):101–6.\n• Takahashi K, et al. Induction of pluripotent stem cells from adult human fibroblasts by defined factors. Cell. 2007;131(5):861–72. One of the first two papers to describe the induction of pluripotency from human somatic cells. This method really revolutionized the ability to study early human development and to now model diseases using patient-specific cells.\nYu J, et al. Human induced pluripotent stem cells free of vector and transgene sequences. Science. 2009;324(5928):797–801.\n• Yu J, et al. Induced pluripotent stem cell lines derived from human somatic cells. Science. 2007;318(5858):1917–20. This paper was also the first to describe the induction of pluripotency in human somatic cells. The two seminal studies were announced on the same day.\nHirami Y, et al. Generation of retinal cells from mouse and human induced pluripotent stem cells. Neurosci Lett. 2009;458(3):126–31.\nBuchholz DE, et al. Derivation of functional retinal pigmented epithelium from induced pluripotent stem cells. Stem cells. 2009;27(10):2427–34.\nVugler A, et al. Elucidating the phenomenon of HESC-derived RPE: anatomy of cell genesis, expansion and retinal transplantation. Exp Neurol. 2008;214(2):347–61.\nDingwell KS, Holt CE, Harris WA. The multiple decisions made by growth cones of RGCs as they navigate from the retina to the tectum in Xenopus embryos. J Neurobiol. 2000;44(2):246–59.\nErskine L, Herrera E. The retinal ganglion cell axon’s journey: insights into molecular mechanisms of axon guidance. Dev Biol. 2007;308(1):1–14.\nErskine L, Herrera E. Connecting the retina to the brain. ASN Neuro. 2014;6(6):1759091414562107.\nWilliams SE, Mason CA, Herrera E. The optic chiasm as a midline choice point. Curr Opin Neurobiol. 2004;14(1):51–60.\nChambers SM, et al. Combined small-molecule inhibition accelerates developmental timing and converts human pluripotent stem cells into nociceptors. Nat Biotechnol. 2012;30(7):715–20.\nKoehler KR, Mikosz AM, Molosh AI, Patel D, Hashino E. Generation of inner ear sensory epithelia from pluripotent stem cells in 3D culture. Nature. 2013;500(7461):217–21.\nShlens J, Rieke F, Chichilnisky E. Synchronized firing in the retina. Curr Opin Neurobiol. 2008;18(4):396–402.\nVelte TJ, Masland RH. Action potentials in the dendrites of retinal ganglion cells. J Neurophysiol. 1999;81(3):1412–7.\n•• Maekawa Y, et al. Optimized culture system to induce neurite outgrowth from retinal ganglion cells in three-dimensional retinal aggregates differentiated from mouse and human embryonic stem cells. Curr Eye Res. 2015;16:1–11. The authors attempt considerable characterization of neurite outgrowth from the hPSC-derived RGCs in this study. Alongside classic RGC markers the authors also identified RGCs using additional protein markers further delineating cell fate.\n•• Riazifar H, Jia Y, Chen J, Lynch G, Huang T. Chemically induced specification of retinal ganglion cells from human embryonic and induced pluripotent stem cells. Stem Cells Transl Med. 2014;3(4):424–32. Cells differentiated in this study were characterized with more extensive RGC markers and the authors make first attempts at analyzing the cells functionality by whole-cell recording.\n•• Tanaka T, et al. Generation of retinal ganglion cells with functional axons from human induced pluripotent stem cells. Sci Rep. 2015;5:8344. This study shows more extensive characterization of RGC differentiated from hPSCs and touches upon functionality of the cells generated.\nMarchetto MC, Brennand KJ, Boyer LF, Gage FH. Induced pluripotent stem cells (iPSCs) and neurological disease modeling: progress and promises. Hum Mol Genet. 2011;20(R2):R109–15.\nMerkle FT, Eggan K. Modeling human disease with pluripotent stem cells: from genome association to function. Cell Stem Cell. 2013;12(6):656–68.\nMinegishi Y, et al. Enhanced optineurin E50 K-TBK1 interaction evokes protein insolubility and initiates familial primary open-angle glaucoma. Hum Mol Genet. 2013;22(17):3559–67.\nHeilker R, Traub S, Reinhardt P, Scholer HR, Sterneckert J. iPS cell derived neuronal cells for drug discovery. Trends Pharmacol Sci. 2014;35(10):510–9.\nKo HC, Gelb BD. Concise review: drug discovery in the age of the induced pluripotent stem cell. Stem Cells Transl Med. 2014;3(4):500–9.\nSchadt EE, Buchanan S, Brennand KJ, Merchant KM. Evolving toward a human-cell based and multiscale approach to drug discovery for CNS disorders. Front Pharmacol. 2014;5:252.\nJeffery G, Levitt JB, Cooper HM. Segregated hemispheric pathways through the optic chiasm distinguish primates from rodents. Neuroscience. 2008;157(3):637–43.\nNeveu MM, Jeffery G. Chiasm formation in man is fundamentally different from that in the mouse. Eye. 2007;21(10):1264–70.\nSchmidt KG, Bergert H, Funk RH. Neurodegenerative diseases of the retina and potential for protection and recovery. Curr Neuropharmacol. 2008;6(2):164–78.",{"EN":115},"Retinal ganglion cells (RGCs) are highly specialized neuronal cells located in the innermost layer of the retina and serve to relay visual information to the brain, with their axons collectively forming the optic nerve. Loss or damage to the RGCs results in visual impairment and ultimately blindness. Several diseases affect the RGCs exclusively, the most common being glaucoma. Even though the mechanisms of glaucoma are not fully understood, some common treatments can delay cell death. Pharmacological intervention or laser therapy is thought to reduce the intraocular pressure and therefore reduce cell damage, but ultimately these therapies are often transient and stop working. Additional strategies to rescue RGCs and prevent their loss are being explored. Human pluripotent stem cells (hPSCs), including both embryonic and induced pluripotent stem cells, serve as an effective in vitro model of retinal development and repair. In addition, RGCs differentiated from hPSCs can also provide an unlimited source of transplantable cells for use in cell replacement strategies. This review addresses some of the technical and clinical issues and concerns with generating bone fide RGCs in vitro. We also outline the potential applications of hPSC-derived RGCs as a useful tool in disease modeling and drug screening in order to advance knowledge of optic neuropathies.",{"EN":117},"Human Pluripotent Stem Cell-Derived Retinal Ganglion Cells: Applications for the Study and Treatment of Optic Neuropathies",{"VOID":119},"10.1007\u002Fs40135-015-0081-9","PUBLICATION","VERIFIED","Auto Verify","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40135-015-0081-9",[125,141],{"id":126,"sortIndex":19,"researcher":18,"roles":127,"affiliations":129,"properties":138},"e29fa86d-1cfe-4008-b70d-51623bcceed7",[128],"AUTHOR",[130],{"id":18,"sortIndex":19,"affiliation":131,"properties":18},{"id":132,"createTime":133,"updateTime":133,"relativeEntities":134,"slug":18,"properties":135,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"949e8775-7d6e-438b-8b8c-e45d0ec30d31","2024-01-11T17:10:36.627+00:00",[],{"title":136},{"VI":137},"Department of Biology, SL306, Indiana University-Purdue University Indianapolis, Indianapolis, USA",{"title":139},{"VI":140},"Jessica A. Cooke",{"id":142,"sortIndex":97,"researcher":18,"roles":143,"affiliations":144,"properties":170},"a3d4a446-a2ff-4435-a9f8-74af932cab2a",[128],[145,155,165],{"id":146,"sortIndex":95,"affiliation":147,"properties":154},"37a3bd98-8f7e-4fe4-978a-7ef6d82d97de",{"id":148,"createTime":149,"updateTime":149,"relativeEntities":150,"slug":18,"properties":151,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"8b24ae4e-2118-4d9a-bbb1-0fe59c1497d6","2024-01-03T04:41:09.458+00:00",[],{"title":152},{"VI":153},"Stark Neurosciences Research Institute, Indiana University, Indianapolis, USA",{},{"id":156,"sortIndex":97,"affiliation":157,"properties":164},"3613e49b-9900-48be-affa-3f4c1c8a8d37",{"id":158,"createTime":159,"updateTime":159,"relativeEntities":160,"slug":18,"properties":161,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"c4d47347-0826-434a-8726-9723e5427b80","2024-01-18T05:36:27.071+00:00",[],{"title":162},{"VI":163},"Department of Medical and Molecular Genetics, Indiana University, Indianapolis, USA",{},{"id":18,"sortIndex":19,"affiliation":166,"properties":18},{"id":132,"createTime":133,"updateTime":133,"relativeEntities":167,"slug":18,"properties":168,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":169},{"VI":137},{"title":171},{"VI":172},"Jason S. Meyer","ARTICLE",{"url":123,"publisher":175,"properties":202},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":176,"slug":10,"properties":177,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":180,"manageAffiliations":181,"indexDatabases":182,"url":92,"thumbnailPath":18,"statistic":197,"gsStatistic":18,"type":100,"analyzePriority":18},[],{"issn":178,"title":179},{"VOID":13},{"EN":15},[],[],[183,190],{"id":74,"indexDatabase":184,"url":89,"indexYears":18,"academicFieldIds":189,"indexDatabaseRanking":18},{"id":76,"createTime":77,"updateTime":78,"relativeEntities":185,"label":186,"description":187,"key":85,"publicationTags":188,"standard":18},[],{"EN":81,"VI":81},{"VI":83,"EN":84},[87,88],[91],{"id":55,"indexDatabase":191,"url":68,"indexYears":69,"academicFieldIds":196,"indexDatabaseRanking":72},{"id":57,"createTime":58,"updateTime":59,"relativeEntities":192,"label":193,"description":194,"key":65,"publicationTags":195,"standard":18},[],{"EN":62,"VI":62},{"EN":62,"VI":64},[67],[71],{"impactFactor":19,"impactFactorByYear":198,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":95,"totalPublicationByYear":199,"totalCitation":19,"totalCitationByYear":200,"totalCitationPerPublication":19,"totalCitationPerPublicationByYear":201,"hindexLast5Year":19,"hindex":19},{},{"2018":97,"2019":97},{},{},{"volume":203,"pages":205},{"VOID":204},"3",{"VOID":206},"200-206","2015-08-07",2015,false,{"id":211,"createTime":212,"updateTime":213,"relativeEntities":214,"slug":215,"properties":216,"entityType":120,"verifyStatus":121,"verifyTime":213,"verifyNote":122,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":225,"fullTextUrl":18,"authors":226,"publicationType":173,"publisherRelationship":295,"citationCount":18,"citationInfo":18,"publishDate":328,"publishYear":329,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":209},"56b8bfbb-e554-40a1-abab-0563000336e8","2023-12-27T04:00:23.211+00:00","2025-02-10T23:59:04.878+00:00",[],"Extraocular-Muscle-Repair-and-Regeneration",{"references":217,"abstract":219,"title":221,"doi":223},{"VOID":218},"Van Campenhout A, Molenaers G. Localization of the motor endplate zone in human skeletal muscles of the lower limb: anatomical guidelines for injection with botulinum toxin. Dev Med Child Neurol. 2011;53:108–19.\nChow RS, Medri MK, Martin DC, Leekam RN, Agur AM, McKee NH. Sonographic studies of human soleus and gastrocnemius muscle architecture: gender variability. Eur J Appl Physiol. 2000;82:236–44.\nGauthier GF, Lowey S. Distribution of myosin isoenzymes among skeletal muscle fiber types. J Cell Biol. 1979;81:10–25.\nMcLoon LK, Willoughby CL, Andrade FH. Extraocular muscles: structure and function. In: Craniofacial muscles: a new framework for understanding the effector side of craniofacial muscles. Eds: LK McLoon, F Andrade. Springer, 2012; Chapter 3; pp. 31–88.\nKupfer C. Motor innervation of extraocular muscle. J Physiol. 1960;153:522–6.\nJacoby J, Chiarandini DJ, Stefani E. Electrical properties and innervation of fibers in the orbital layer of rat extraocular muscles. J Neurophysiol. 1989;61:116–25.\nDavidowitz J, Philips G, Breinin GM. Organization of the orbital surface layer in rabbit superior rectus. Invest Ophthalmol Vis Sci. 1977;16:711–29.\nMcLoon LK, Rios L, Wirtschafter JD. Complex three-dimensional patterns of myosin isoform expression: differences between and within specific extraocular muscles. J Muscle Res Cell Motil. 1999;20:771–83.\nWieczorek DF, Periasamy M, Butler-Browne GS, Whalen RG, Nadal-Ginard B. Co-expression of multiple myosin heavy chain genes, in addition to a tissue-specific one, in extraocular musculature. J Cell Biol. 1985;10:618–29.\nMcLoon LK, Park H, Kim JH, Pedrosa-Domellöf F, Thompson LV. A continuum of myofibers in adult rabbit extraocular muscle: force, shortening velocity, and patterns of myosin heavy chain co-localization. J Appl Physiol. 2011;111:1178–89.\nClose RI, Ar L. Dynamic properties of inferior rectus muscle of the rat. J Physiol. 1974;236:259–70.\nFuchs AF, Binder MD. Fatigue resistance of human extraocular muscles. J Neurophysiol. 1988;60:1874–95.\nPorter JD, Khanna S, Kaminski HJ, Rao JS, Merriam AP, Richmonds CR, Leahy P, Li J, Andrade FH. Extraocular muscle is defined by a fundamentally distinct gene expression profile. Proc Natl Acad Sci USA. 2001;98:12062–7.\nFraterman S, Zeiger U, Khurana TS, Rubinstein NA, Wilm M. Combination of OFFGEL fractionation and label-free quantitation facilitated proteomics of extraocular muscle. Proteomics. 2007;7:3404–16.\nTajbakhsh S, Rocancout D, Cossu G, Buckingham M. Redefining the genetic hierarchies controlling skeletal myogenesis: Pax-3 and myf-5 act upstream of MyoD. Cell. 1997;89:127–38.\nDiehl AG, Zareparsi S, Qian M, Khanna R, Angeles R, Gage PJ. Extraocular muscle morphogenesis and gene expression are regulated by Pitx2 gene dose. Invest Ophthalmol Vis Sci. 2006;47:1785–93.\nZhou Y, Cheng G, Dieter L, Hjalt TA, Andrade FH, Stahl JS, Kaminski HJ. An altered phenotype in a conditional knockout of Pitx2 in extraocular muscle. Invest Ophthalmol Vis Sci. 2009;50:4531–41.\nZhou Y, Liu D, Kaminski HJ. Pitx2 regulates myosin heavy chain isoform expression and multi-innervation in extraocular muscle. J Physiol. 2011;589:4601–14.\nMauro A. Satellite cell of skeletal muscle fibers. J Biophys Biochem Cytol. 1961;9:493–5.\nSeale P, Sabourin LA, Girgis-Garbardo A, Mansouri A, Gruss P, Rudnicki MA. Pax7 is required for the specification of myogenic satellite cells. Cell. 2000;102:777–86.\n•• Keefe AC, Lawson JA, Flygare SD, Fox ZD, Colasanto MP, Mathew SJ, Yandell M, Kardon G. Muscle stem cells contribute to myofibers in sedentary adult mice. Nat Commun. 2015;6:7087. Pax7 lineage tracing in adult skeletal muscles\n•• Pawlikowski B, Pulliam C, Betta ND, Kardon G, Olwin B. Pervasive satellite cell contribution to uninjured adult muscle fibers. Skelet Muscle. 2015;5:42. doi:10.1186\u002Fs13395-015-0067. Pax7 lineage tracing in adult skeletal muscles\nMcLoon LK, Wirtschafter JD. Activated satellite cells in extraocular muscles of normal adult monkeys and humans. Invest Ophthalmol Vis Sci. 2003;44:1927–32.\n• McDonald AA, Kunz MD, McLoon LK. Dystrophic changes in extraocular muscles after gamma irradiation in mdx:utrophin(+\u002F−) mice. PLoS One. 2014;9(1):e86424. Demonstration of a radiation resistant myogenic precursor cell in extraocular muscle.\n• Kallestad KM, Hebert SL, McDonald AA, Daniel ML, Cu SR, McLoon LK. Sparing of the extraocular muscle in aging and muscular dystrophies: a myogenic precursor cell hypothesis. Exp Cell Res. 2011;317:873–5. Study demonstrating an enriched population of muscle precursor cells in extraocular muscle in the mdx mouse\nLindström M, Tjust AE, PedrosaDomellöf F. Pax7-positive cells\u002Fsatellite cells in human extraocular muscles. Invest Ophthalmol Vis Sci. 2015;56:6132–43.\nStuelsatz P, Shearer A, Li Y, Muir LA, Ieronimakis N, Shen QW, Kirillova I, Yablonka-Reuveni Z. Extraocular muscle satellite cells are high performance myo-engines retaining efficient regeneration capacity in dystrophin deficiency. Dev Biol. 2015;397:31–44.\n• Nogueira JM, Hawrot K, Sharpe C, Noble A, Wood WM, Jorge EC, Goldhamer DJ, Kardon G, Dietrich S. The emergence of Pax7-expressing muscle stem cells during vertebrate head muscle development. Front Aging Neurosci. 2015;7:62. Study showing that Pax7 is not expressed early in cranial muscle development\nKuang S, Charge SB, Seale P, Huh M, Rudnicki MA. Distinct roles for Pax7 and Pax3 in adult regenerative myogenesis. J Cell Biol. 2006;172:103–13.\n•• Hebert SL, Daniel ML, McLoon LK. The role of Pitx2 in maintaining the phenotype of myogenic precursor cells in the extraocular muscles. PLoS One. 2013;8(3):e58405. Study showing Pitx2-positive myogenic precursor cells in the extraocular muscles\nGage PJ, Zacharias AL. Signaling “cross-talk” is integrated by transcription factors in the development of the anterior segment of the eye. Dev Dyn. 2009;238:2149–62.\nShih HP, Gross MK, Kioussi C. Muscle development: forming the head and trunk muscles. Acta Histochem. 2008;110:97–108.\nAsakura A, Seale P, Girgis-Gabardo A, Rudnicki MA. Myogenic specification of side population cells in skeletal muscle. J Cell Biol. 2002;159:123–34.\nPacheco-Pinedo EC, Budak MT, Zeiger U, Jorgensen LH, Bogdanovich S, Schroder HD, Rubinstein NA, Khurana TS. Transcriptional and functional differences in stem cell populations isolated from extraocular and limb muscles. Physiol Genomics. 2009;37:35–42.\nBildsoe H, Loebel DA, Jones VJ, Hor AC, Braithwaite AW, Chen YT, Behringer RR, Tam PP. The mesenchymal architecture of the cranial mesoderm of mouse embryos is disrupted by the loss of Twist1 function. Dev Biol. 2013;374:295–307.\nVincentz JW, Barnes RM, Rodgers R, Firulli BA, Conway SJ, Firulli AB. An absence of Twist1 results in aberrant cardiac neural crest morphogenesis. Dev Biol. 2008;320:131–9.\nMatt N, Ghyselinck NB, Pellerin I, Dupe V. Impairing retinoic acid signaling in the neural crest cells is sufficient to alter entire eye morphogenesis. Dev Biol. 2008;320:1401–48.\n•• Bohnsack BL, Gallina D, Thompson H, Kasprick DS, Lucarellie MJ, Dootz G, Nelson C, McGonnell IM, Kahana A. Development of extraocular muscles requires early signals from periocular neural crest and the developing eye. Arch Ophthalmol. 2011;129:1030–41. Study showing that neural crest cells control early extraocular muscle development\nLiu N, Garry GA, Li S, Bezprozvannava S, Sanchez-Ortiz E, Chen B, Shelton JM, Jaichander P, Dabbel-Duby R, Olson EN. A Twist2-dependent progenitor cell contributes to adult skeletal muscle. Nat Cell Biol. 2017;19:202–13.\n•• Formicola L, Marazzi G, Sassoon DA. The extraocular muscle stem cell niche is resistant to ageing and disease. Front Aging Neurosci. 2014;6:328. Study of the unique properties of the stem cell niche in extraocular muscles\n• Saera-Vila A, Kasprick DS, Junttila TL, Grzegorski SJ, Louie KW, Chiaria EF, Kish PE, Kahana A. Myocyte dedifferentiation derives extraocular muscle regeneration in adult zebrafish. Invest Ophthalmol Vis Sci. 2015;56:4977–93. Study of the processes used for regeneration of extraocular muscle in zebrafish\nGovindan M, Mohney BG, Diehl NN, Burke JP. Incidence and types of childhood exotropia: a population-based study. Ophthalmology. 2005;112:104–8.\nGreenberg AR, Mohney BG, Diehl NN, Burke JP. Incidence and types of childhood esotropia: a population-based study. Ophthalmology. 2007;114:170–4.\nLudwig IH. Scar remodeling after strabismus surgery. Trans Am Ophthalmol Soc. 1999;97:583–651.\nTinley C, Evans S, McGrane D, Quinn A. Single medial rectus muscle advancement in stretched scar consecutive exotropia. J AAPOS. 2010;14:120–3.\nNelson LB, Ervin-Mulvey LD, Calhoun JH, Harley RD, Keisler MS. Surgical management for abnormal head posture in nystagmus: the augmented modified Kestenbaum procedure. Brit J Ophthalmol. 1984;68:796–800.\nVroman DT, Hutchinson AK, Saunders RA, Wilson ME. Two-muscle surgery for congenital esotropia: rate of reoperation in patients with small versus large angles of deviation. J AAPOS. 2000;4:267–70.\n• Pineles SL, Ela-Dalman N, Zvansky AG, Yu F, Rosenbaum AL. Long-term results of the surgical management of intermittent exotropia. J AAPOS. 2010;14:298–304. Examination of the efficacy of surgical management of strabismus\nLivir-Rallatos G, Gunton KB, Calhoun JH. Surgical results for large-angle exotropia. J AAPOS. 2002;6:77–80.\nChristiansen SP, Soulsby ME, Seifen EE. Effect of antagonist weakening on developed tension in cat extraocular muscle. Invest Ophthalmol Vis Sci. 1995;36:2547–50.\nChristiansen SP, Madhat M, Baker L, Baker R. Fiber hypertrophy in rat extraocular muscle following lateral rectus resection. J Pedatri Ophthalmol Strabismus. 1988;25:167–71.\nChristiansen SP, McLoon LK. The effect of resection on satellite cell activity in rabbit extraocular muscle. Invest Ophthalmol Vis Sci. 2006;47:605–13.\nChristiansen SP, Antunes-Forschini RS, McLoon LK. Effects of recession versus tenotomy surgery without recession in adult rabbit extraocular muscle. Invest Ophthalmol Vis Sci. 2010;51:5646–56.\nShin SY, Park DJ. Expression of four growth factors in recessed extraocular muscles of rabbits. Ophthalmic Surg Lasers Imaging. 2006;37:129–37.\n• Wang L, Nelson LB. One muscle strabismus surgery. Curr Opin Ophthalmol. 2010;21:335–40. Examination of the efficacy of one muscle surgical treatment of strabismus\nBrin MR. Botulinum toxin: chemistry, pharmacology, toxicity, and immunology. Muscle Nerve Suppl. 1997;6:S61–91.\nHassan SM, Jennekens FGI, Veldman H. Botulinum toxin-induced myopathy in the rat. Brain. 1995;118:533–45.\nPinter MJ, Van den Noven S, Muccio D, Wallace N. Axotomy-like changes in cat motoneuron electrical properties elicited by botulinum toxin depend on the complete elimination of neuromuscular transmission. J Neurosci. 1991;11:657–66.\nPorter JD, Strebeck S, Capra NF. Botulinum-induced changes in monkey eyelid muscle. Comparison with changes seen in extraocular muscle. Arch Ophthalmol. 1991;109:396–404.\nSpencer RF, McNeer KW. Botulinum toxin paralysis of adult monkey extraocular muscle: structural alterations in orbital, singly innervated muscle fibers. Arch Ophthalmol. 1987;105:1703–11.\nKrancj BS, Sketelj J, D’Albis A, Erzen I. Long-term changes in myosin heavy chain composition after botulinum toxin a injection into rat medial rectus muscle. Invest Ophthalmol Vis Sci. 2001;42:3158–64.\nCroes SA, Baryshnikova LM, Kaluskar SS, von Bartheld CS. Acute and long-term effects of botulinum neurotoxin on the function and structure of developing extraocular muscles. Neurobiol Dis. 2007;25:649–64.\nUgalde I, Christiansen SP, McLoon LK. Botulinum toxin treatment of extraocular muscles in rabbits results in increased myofiber remodeling. Invest Ophthalmol Vis Sci. 2005;46:4114–20.\n• Liu W, Wei-LaPierre L, Klose A, Dirksen RT, Chakkalakal JV. Inducible depletion of adult skeletal muscle stem cells impairs the regeneration of neuromuscular junctions. elife. 2015;27:4. doi:10.7554\u002FeLife.09221. Demonstration that myogenic precursor cells are critical for the regeneration of neuromuscular junctions after injury\nFoster AH, Carlson BM. Myotoxicity of local anesthetics and regeneration of the damaged muscle fibers. AnesthAnalg. 1980;59:727–36.\nRainin EA, Carlson BM. Postoperative diplopia and ptosis. A clinical hypothesis based on the myotoxicity of local anesthetics. Arch Ophthalmol. 1985;103:1337–9.\nGuyton DL. Strabismic complications from local anesthetics. Semin Ophthalmol. 2008;23:298–301.\nCarlson BM, Emerick S, Komorowski TE, Rainin EA, Shepard BM. Extraocular muscle regeneration in primates. Local anesthetic induced lesions. Ophthalmology. 1992;99:582–9.\nZhang C, Phamonvaechavan P, Rajan A, Poon DY, Topcu-Yilmaz P, Guyton D. Concentration-dependent bupivacaine myotoxicity in rabbit extraocular muscle. J AAPOS. 2010;14:323–7.\nPorter JD, Edney DP, McMahon EJ, Burns LA. Extraocularmyotoxicity of the retrobulbar anesthetic bupivacaine hydrochloride. Invest Ophthalmol Vis Sci. 1988;29:163–74.\nIrving EL, Arshinoff SA, Samis W, Lillakas L, Lui B, Laporte JT, Steinbach MJ. Effect of retrobulbar injection of lidocaine on saccadic velocities. J Cataract Refract Surg. 2004;30:350–6.\nScott AB, Miller JM, Shieh KR. Treating strabismus by injecting the agonist muscle with bupivacaine and the antagonist with botulinum toxin. Trans Am Ophthalmol Soc. 2009;107:104–9.\nKarpati G, Carpenter S. Small-caliber skeletal muscle fibers do not suffer deleterious consequences of dystrophic gene expression. Am J Med Genet. 1986;25:653–8.\nAndrade FH, Porter JD, Kaminski HJ. Eye muscle sparing by the muscular dystrophies: lessons to be learned? Microsc Res Tech. 2000;48:192–203.\n• Benítez-Temiño B, Davis-López de Carrizosa MA, Morcuende SR, Matarredona ER, de la Cruz RR, Pastor AM. Functional diversity of neurotrophin actions on the oculomotor system. Int J Molec Sci. 2016;17:pii.E2016. Review of the role played by neurotrophic factors in the function of the ocular motor system\nMcLoon LK, Christiansen SP. Increasing extraocular muscle strength with insulin-like growth factor II. Invest Ophthalmol Vis Sci. 2003;44:3866–72.\nFeng C, von Bartheld CS. Expression of insulin-like growth factor 1 isoforms in the rabbit oculomotor system. Growth Hormon IGF Res. 2011;21:228–32.\nDavis-López de Carrizosa MA, Morado-Díaz CJ, Tena JJ, Benítez-Temiño B, Pecero ML, Morcuende SR, de la Cruz RR, Pastor AM. Complementary actions of BDNF and neurotrophin-3 on the firing patterns and synaptic composition of motoneurons. J Neurosci. 2009;29:575–87.\n• Willoughby CL, Fleuriet J, Walton MM, Mustari MJ, McLoon LK. Adaptation of slow myofibers: the effect of sustained BDNF treatment of extraocular muscles in infant nonhuman primates. Invest Ophthalmol Vis Sci. 2015;56:3467–83. Study looking at the effect of exogenous treatment with brain derived neurotrophic factor on the infant monkey extraocular muscle\n• Agarwal AB, Feng CY, Altick AL, Quilici DR, Wen D, Johnson LA, von Bartheld CS. Altered protein composition and gene expression in strabismic human extraocular muscles and tendons. Invest Ophthalmol Vis Sci. 2016;57:5576–85. Analysis of genes that are down- or up-regulated in muscles from strabismic subjects\n• Harandi VM, Lindquist S, Kolan SS, Brännström T, Liu JX. Analysis of neurotrophic factors in limb and extraocular muscles of mouse model of amyotrophic lateral sclerosis. PLoS One. 2014;9(10):e109833. Demonstration of the role of neurotrophic factors in the differential effects of amyotrophic lateral sclerosis on extraocular and limb muscles\nSteljes TP, Kinoshita Y, Wheeler EF, Oppenheim RW, von Bartheld CS. Neurotrophic factor regulation of developing avian oculomotor neurons: differential effects of BDNF and GDNF. J Neurobiol. 1999;41:295–315.\nChen J, von Bartheld CS. Role of exogenous and endogenous trophic factors in the regulation of extraocular muscle strength during development. Invest Ophthalmol Vis Sci. 2004;45:3538–45.\nPorter JD, Hauser KF. Survival of extraocular muscle in long-term organotypic culture: differential influence of appropriate and inappropriate motoneurons. Dev Biol. 1993;160:39–50.\nMcLoon LK, Andrade FH. Comparison of craniofacial muscles: a unifying hypothesis. In: Craniofacial muscles: a new framework for understanding the effector side of craniofacial muscles. Eds: LK McLoon, F Andrade. Springer, 2012; Chapter 17. pp. 325–335.",{"EN":220},"The goal of this review is to summarize the unique regenerative milieu within mature mammalian extraocular muscles (EOMs). This will aid in understanding disease propensity for and sparing of EOMs in skeletal muscle diseases as well as the recalcitrance of the EOM to injury. The EOMs continually remodel throughout life and contain an extremely enriched number of myogenic precursor cells that differ in number and functional characteristics from those in limb skeletal muscle. The EOMs also contain a large population of Pitx2-positive myogenic precursor cells that provide the EOMs with many of their unusual biological characteristics, such as myofiber remodeling and skeletal muscle disease sparing. This environment provides for rapid and efficient remodeling and regeneration after various types of injury. In addition, the EOMs show a remarkable ability to respond to perturbations of single muscles with coordinated changes in the other EOMs that move in the same plane. These data will inform ophthalmologists as they work toward developing new treatments for eye movement disorders, new approaches for repair after nerve or direct EOM injury, as well as suggest potential explanations for the unusual disease propensity and disease-sparing characteristics of human EOM.",{"EN":222},"Extraocular Muscle Repair and Regeneration",{"VOID":224},"10.1007\u002Fs40135-017-0141-4","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40135-017-0141-4",[227,254,283],{"id":228,"sortIndex":97,"researcher":18,"roles":229,"affiliations":230,"properties":251},"9a31e9bc-95bd-4521-8094-83739cffe93c",[128],[231,241],{"id":232,"sortIndex":97,"affiliation":233,"properties":240},"ea63412c-c34d-4181-ba7c-ac7c95333544",{"id":234,"createTime":235,"updateTime":235,"relativeEntities":236,"slug":18,"properties":237,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"b0c8c5c3-f5c3-4a04-add0-bc5323e11d2f","2023-12-11T07:51:12.059+00:00",[],{"title":238},{"VI":239},"Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, USA",{},{"id":18,"sortIndex":19,"affiliation":242,"properties":18},{"id":243,"createTime":244,"updateTime":245,"relativeEntities":246,"slug":247,"properties":248,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"51073a70-03f7-48e5-b26f-e45ec82217b2","2024-01-05T11:38:15.760+00:00","2025-02-04T07:23:51.003+00:00",[],"Stem-Cell-Institute-University-of-Minnesota-Minneapolis-USA",{"title":249},{"VI":250},"Stem Cell Institute, University of Minnesota, Minneapolis, USA",{"title":252},{"VI":253},"Krysta R. Fitzpatrick",{"id":255,"sortIndex":95,"researcher":18,"roles":256,"affiliations":257,"properties":280},"97c8d5dd-dadf-4d77-8fdc-9fee808939fb",[128],[258,268,275],{"id":259,"sortIndex":95,"affiliation":260,"properties":267},"f7a0a3e4-007f-48a9-92f3-562cf8c36db7",{"id":261,"createTime":262,"updateTime":262,"relativeEntities":263,"slug":18,"properties":264,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"7e6b8b29-e1a4-461d-9379-cd3615929576","2023-11-30T00:18:08.502+00:00",[],{"title":265},{"VI":266},"Department of Neuroscience, University of Minnesota, Minneapolis, USA",{},{"id":269,"sortIndex":97,"affiliation":270,"properties":274},"24410b8f-d9db-46e4-872a-6f495937d6dd",{"id":234,"createTime":235,"updateTime":235,"relativeEntities":271,"slug":18,"properties":272,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":273},{"VI":239},{},{"id":18,"sortIndex":19,"affiliation":276,"properties":18},{"id":243,"createTime":244,"updateTime":245,"relativeEntities":277,"slug":247,"properties":278,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":279},{"VI":250},{"title":281},{"VI":282},"Linda K. McLoon",{"id":284,"sortIndex":19,"researcher":18,"roles":285,"affiliations":286,"properties":292},"58fe9212-1040-439d-850b-6e2927d1a934",[128],[287],{"id":18,"sortIndex":19,"affiliation":288,"properties":18},{"id":243,"createTime":244,"updateTime":245,"relativeEntities":289,"slug":247,"properties":290,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":291},{"VI":250},{"title":293},{"VI":294},"Mayank Verma",{"url":225,"publisher":296,"properties":323},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":297,"slug":10,"properties":298,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":301,"manageAffiliations":302,"indexDatabases":303,"url":92,"thumbnailPath":18,"statistic":318,"gsStatistic":18,"type":100,"analyzePriority":18},[],{"issn":299,"title":300},{"VOID":13},{"EN":15},[],[],[304,311],{"id":74,"indexDatabase":305,"url":89,"indexYears":18,"academicFieldIds":310,"indexDatabaseRanking":18},{"id":76,"createTime":77,"updateTime":78,"relativeEntities":306,"label":307,"description":308,"key":85,"publicationTags":309,"standard":18},[],{"EN":81,"VI":81},{"VI":83,"EN":84},[87,88],[91],{"id":55,"indexDatabase":312,"url":68,"indexYears":69,"academicFieldIds":317,"indexDatabaseRanking":72},{"id":57,"createTime":58,"updateTime":59,"relativeEntities":313,"label":314,"description":315,"key":65,"publicationTags":316,"standard":18},[],{"EN":62,"VI":62},{"EN":62,"VI":64},[67],[71],{"impactFactor":19,"impactFactorByYear":319,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":95,"totalPublicationByYear":320,"totalCitation":19,"totalCitationByYear":321,"totalCitationPerPublication":19,"totalCitationPerPublicationByYear":322,"hindexLast5Year":19,"hindex":19},{},{"2018":97,"2019":97},{},{},{"volume":324,"pages":326},{"VOID":325},"5",{"VOID":327},"207-215","2017-06-16",2017,{"id":331,"createTime":332,"updateTime":333,"relativeEntities":334,"slug":335,"properties":336,"entityType":120,"verifyStatus":121,"verifyTime":349,"verifyNote":122,"syncStatus":17,"languages":18,"translateLanguages":350,"viewCount":19,"primaryUrl":352,"fullTextUrl":18,"authors":353,"publicationType":173,"publisherRelationship":391,"citationCount":18,"citationInfo":18,"publishDate":423,"publishYear":329,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":209},"13f41937-55cd-4e30-a886-611b6e495930","2024-01-02T04:53:12.028+00:00","2025-02-12T23:58:50.464+00:00",[],"Regenerative-Medicine-in-the-Cornea",{"references":337,"abstract":339,"title":342,"doi":345,"keywords":347},{"VOID":338},"Nishida T, Saika S, Morishige N. Cornea and Sclera: Anatomy and Physiology. In: Mannis MJ, Holland EJ, editors. Cornea. 4th ed.: Elsevier; 2016. p. 1–22.\nSack RA, Nunes I, Beaton A, Morris C. Host-defense mechanism of the ocular surfaces. Biosci Rep. 2001;21:463–80.\nLambiase A, Rama P, Aloe L, Bonini S. Management of neurotrophic keratopathy. Curr Opin Ophthalmol. 1999;10:270–6.\nJonas JB, Holbach L. Central corneal thickness and thickness of the lamina cribrosa in human eyes. I nvest Ophthalmol Vis Sci. 2005;46:1275–9.\nTan D. From penetrating to lamellar: the evolution of keratoplasty. Cataract & refractive surgery today europe 2013.\nGain P, Jullienne R, He Z, Aldossary M, Acquart S, Cognasse F, et al. Global survey of corneal transplantation and eye banking. JAMA Ophthalmol. 2015;134:167–73.\nWorld Health Organisation. Causes of blindness and visual impairment. http:\u002F\u002Fwww.who.int\u002Fblindness\u002Fcauses\u002Fen\u002F.\nBorderie VM, Boelle PY, Touzeau O, Allouch C, Boutboul S, Laroche L. Predicted long-term outcome of corneal transplantation. Ophthalmology. 2009;116:2354–60.\nKammerdiener LL, Speiser JL, Aquavella JV, Harissi-Dagher M, Dohlman CH, Chodosh J, et al. Protective effect of soft contact lenses after Boston keratoprosthesis. Br J Ophthalmol. 2016;100:549–52.\nCrnej A, Omoto M, Dohlman TH, Dohlman CH, Dana R. Corneal inflammation after miniature keratoprosthesis implantation. Invest Ophthalmol Vis Sci. 2014;56:185–9.\nJacob JT, Rochefort JR, Bi J, Gebhardt BM. Corneal epithelial cell growth over tethered-protein\u002Fpeptide surface-modified hydrogels. J Biomed Mater Res B Appl Biomater. 2005;72:198–205.\nWallace C, Jacob JT, Stoltz A, Bi J, Bundy K. Corneal epithelial adhesion strength to tethered-protein\u002Fpeptide modified hydrogel surfaces. J Biomed Mater Res A. 2005;72:19–24.\nGeorge A, Pitt WG. Comparison of corneal epithelial cellular growth on synthetic cornea materials. Biomaterials. 2002;23:1369–73.\nBruining MJ, Pijpers AP, Kingshott P, Koole LH. Studies on new polymeric biomaterials with tunable hydrophilicity, and their possible utility in corneal repair surgery. Biomaterials. 2002;23:1213–9.\nLegeais JM, Renard G. A second generation of artificial cornea (Biokpro II). Biomaterials. 1998;19:1517–22.\nAucoin L, Griffith CM, Pleizier G, Deslandes Y, Sheardown H. Interactions of corneal epithelial cells and surfaces modified with cell adhesion peptide combinations. J Biomater Sci Polym Ed. 2002;13:447–62.\nJacob JT, Rochefort JR, Bi J, Gebhardt BM. Corneal epithelial cell growth over tethered-protein\u002Fpeptide surface-modified hydrogels. J Biomed Mater Res B Appl Biomater. 2004;72:198–205.\nKlenkler BJ, Griffith M, Becerril C, West-Mays JA, Sheardown H. EGF-grafted PDMS surfaces in artificial cornea applications. Biomaterials. 2005;26:7286–96.\nMyung D, Koh W, Bakri A, Zhang F, Marshall A, Ko J, et al. Design and fabrication of an artificial cornea based on a photolithographically patterned hydrogel construct. Biomed Microdevices. 2007;9:911–22.\nParke-Houben R, Fox CH, Zheng LL, Waters DJ, Cochran JR, Ta CN, et al. Interpenetrating polymer network hydrogel scaffolds for artificial cornea periphery. J Mater Sci Mater Med. 2015;26:107.\nEuropean Medicines Agency. Holoclar. European Medicines Agency. 2016. http:\u002F\u002Fwww.ema.europa.eu\u002Fema\u002Findex.jsp?curl=pages\u002Fmedicines\u002Fhuman\u002Fmedicines\u002F002450\u002Fhuman_med_001844.jsp&mid=WC0b01ac058001d124. Accessed 2017–03-02 2017.\n•• Rama P, Bonini S, Lambiase A, Golisano O, Paterna P, De Luca M, et al. Autologous fibrin-cultured limbal stem cells permanently restore the corneal surface of patients with total limbal stem cell deficiency. Transplantation. 2001;72:1478–85. Clinical trial of Holoclar ATMP which has recently been approved for clinical use\nSangwan VS, Basu S, MacNeil S, Balasubramanian D. Simple limbal epithelial transplantation (SLET): a novel surgical technique for the treatment of unilateral limbal stem cell deficiency. Br J Ophthalmol. 2012;96:931–4.\n•• Basu S, Sureka SP, Shanbhag SS, Kethiri AR, Singh V. Sangwan VS. simple Limbal epithelial transplantation: long-term clinical outcomes in 125 cases of unilateral chronic ocular surface burns. Ophthalmology. 2016;123:1000–10. doi:10.1016\u002Fj.ophtha.2015.12.042. Clinical trial of new surgical procedure for stem-cell grafting\nZhao Y, Ma L. Systematic review and meta-analysis on transplantation of ex vivo cultivated limbal epithelial stem cell on amniotic membrane in limbal stem cell deficiency. Cornea. 2015;34:592–600.\nNakamura T, Endo K, Cooper LJ, Fullwood NJ, Tanifuji N, Tsuzuki M, et al. The successful culture and autologous transplantation of rabbit oral mucosal epithelial cells on amniotic membrane. Invest Ophthalmol Vis Sci. 2003;44:106–16.\nNishida K, Yamato M, Hayashida Y, Watanabe K, Yamamoto K, Adachi E, et al. Corneal reconstruction with tissue-engineered cell sheets composed of autologous oral mucosal epithelium. N Engl J Med. 2004;351:1187–96.\nNakamura T, et al. Transplantation of cultivated autologous oral mucosal epithelial cells in patients with severe ocular surface disorders. Br J Ophthalmol. 2004;88:1280–4.\nInatomi T, Nakamura T, Kojyo M, Koizumi N, Sotozono C, Kinoshita S. Ocular surface reconstruction with combination of cultivated autologous oral mucosal epithelial transplantation and penetrating keratoplasty. Am J Ophthalmol. 2006;142:757–64.\nNakamura T, Takeda K, Inatomi T, Sotozono C, Kinoshita S. Long-term results of autologous cultivated oral mucosal epithelial transplantation in the scar phase of severe ocular surface disorders. Br J Ophthalmol. 2010;95:942–6.\nSotozono C, Inatomi T, Nakamura T, Koizumi N, Yokoi N, Ueta M, et al. Visual improvement after cultivated oral mucosal epithelial transplantation. Ophthalmology. 2012;120:193–200.\nSotozono C, Inatomi T, Nakamura T, Koizumi N, Yokoi N, Ueta M, et al. Cultivated oral mucosal epithelial transplantation for persistent epithelial defect in severe ocular surface diseases with acute inflammatory activity. Acta Ophthalmol. 2014;92:e447–53.\nDobrowolski D, Orzechowska-Wylegala B, Wowra B, Wroblewska-Czajka E, Grolik M, Szczubialka K, et al. Cultivated oral mucosa epithelium in ocular surface reconstruction in Aniridia patients. Biomed Res Int. 2015;2015:281870.\n• Chen SC, Telinius N, Lin HT, Huang MC, Lin CC, Chou CH, et al. Use of fish scale-derived biocornea to seal full-thickness corneal perforations in pig models. PLoS One. 2015;10:e0143511. doi:10.1371\u002Fjournal.pone.0143511.eCollection 2015. Animal trial of decellularized fish scale for corneal perforations\nvan Essen TH, Lin CC, Hussain AK, Maas S, Lai HJ, Linnartz H, et al. A fish scale-derived collagen matrix as artificial cornea in rats: properties and potential. Invest Ophthalmol Vis Sci. 2013;54:3224–33.\nDeshpande P, Ramachandran C, Sangwan VS, Macneil S. Cultivation of limbal epithelial cells on electrospun poly (lactide-co-glycolide) scaffolds for delivery to the cornea. Methods Mol Biol. 2013;1014:179–85.\nDeshpande P, Ramachandran C, Sefat F, Mariappan I, Johnson C, McKean R, et al. Simplifying corneal surface regeneration using a biodegradable synthetic membrane and limbal tissue explants. Biomaterials. 2013;34:5088–106.\nBasu S, Hertsenberg AJ, Funderburgh ML, Burrow MK, Mann MM, Du Y, et al. Human limbal biopsy-derived stromal stem cells prevent corneal scarring. Sci Transl Med. 2014;6:266ra172.\nProulx S, d'Arc Uwamaliya J, Carrier P, Deschambeault A, Audet C, Giasson CJ, et al. Reconstruction of a human cornea by the self-assembly approach of tissue engineering using the three native cell types. Mol Vis. 2010;16:2192–201.\nKaramichos D, Rich CB, Hutcheon AE, Ren R, Saitta B, Trinkaus-Randall V, et al. Self-assembled matrix by umbilical cord stem cells. J Funct Biomater. 2011;2:213–29.\nBoulze Pankert M, Goyer B, Zaguia F, Bareille M, Perron MC, Liu X, et al. Biocompatibility and functionality of a tissue-engineered living corneal stroma transplanted in the feline eye. Invest Ophthalmol Vis Sci. 2014;55:6908–20.\nSyed-Picard FN, Du Y, Hertsenberg AJ, Palchesko R, Funderburgh ML, Feinberg AW et al. Scaffold-free tissue engineering of functional corneal stromal tissue. J Tissue Eng Regen Med. 2016.\nUzunalli G, Soran Z, Erkal TS, Dagdas YS, Dinc E, Hondur AM, et al. Bioactive self-assembled peptide nanofibers for corneal stroma regeneration. Acta Biomater. 2014;10:1156–66.\nGouveia RM, Jones RR, Hamley IW, Connon CJ. The bioactivity of composite Fmoc-RGDS-collagen gels. Biomater Sci. 2014;2:1222–9.\nGouveia RM, Hamley IW, Connon CJ. Bio-fabrication and physiological self-release of tissue equivalents using smart peptide amphiphile templates. J Mater Sci Mater Med. 2015;26:242.\nGouveia RM, Castelletto V, Hamley IW, Connon CJ. New self-assembling multifunctional templates for the biofabrication and controlled self-release of cultured tissue. Tissue Eng Part A. 2015;21:1772–84.\n• Walter MN, Dehsorkhi A, Hamley IW, Connon CJ. Supra-molecular assembly of a lumican-derived peptide amphiphile enhances its collagen-stimulating activity. Biomater Sci. 2016;4:346–54. doi:10.1039\u002Fc5bm00428d. Development of a new peptide ampiphile that self-assembles into nanotape\nDaoud YJ, Smith R, Smith T, Akpek EK, Ward DE, Stark WJ. The intraoperative impression and postoperative outcomes of gamma-irradiated corneas in corneal and glaucoma patch surgery. Cornea. 2011;30:1387–91.\nZhang MC, Liu X, Jin Y, Jiang DL, Wei XS, Xie HT. Lamellar keratoplasty treatment of fungal corneal ulcers with acellular porcine corneal stroma. Am J Transplant. 2015;15:1068–75.\n•• Buznyk O, Pasyechnikova N, Islam MM, Iakymenko S, Fagerholm P, Griffith M. Bioengineered corneas grafted as alternatives to human donor corneas in three high-risk patients. Clin Transl Sci. 2015;8:558–62. doi:10.1111\u002Fcts.1229310.1111\u002Fcts.12293. Clinical trial of collagen-based artificial cornea in high-risk patients\nBuznyk O, Pasyechnikova N, Islam MM, Iakymenko S, Fagerholm P, Griffith M. Bioengineered corneas grafted as alternatives to human donor corneas in three high-risk patients. Clin Transl Sci. 2015;8:558–62.\nIslam MM, Cepla V, He C, Edin J, Rakickas T, Kobuch K, et al. Functional fabrication of recombinant human collagen-phosphorylcholine hydrogels for regenerative medicine applications. Acta Biomater. 2015;12:70–80.\nO'Leary LER, Fallas JA, Bakota EL, Kang MK, Hartgerink JD. Multi-hierarchical self-assembly of a collagen mimetic peptide from triple helix to nanofibre and hydrogel. Nat Chem. 2011;3:821–8.\nIslam MM, Ravichandran R, Olsen D, Ljunggren MK, Fagerholm P, Lee CJ, et al. Self-assembled collagen-like-peptide implants as alternatives to human donor corneal transplantation. RSC Adv. 2016;6:55745–9.\nWu J, Rnjak-Kovacina J, Du Y, Funderburgh ML, Kaplan DL, Funderburgh JL. Corneal stromal bioequivalents secreted on patterned silk substrates. Biomaterials. 2014;35:3744–55.\nWang S, Ghezzi CE, Gomes R, Pollard RE, Funderburgh JL, Kaplan DL. In vitro 3D corneal tissue model with epithelium, stroma, and innervation. Biomaterials. 2017;112:1–9.\nHazra S, Nandi S, Naskar D, Guha R, Chowdhury S, Pradhan N, et al. Non-mulberry silk fibroin biomaterial for corneal regeneration. Sci Rep. 2016;6:21840.\nGuan L, Ge H, Tang X, Su S, Tian P, Xiao N, et al. Use of a silk fibroin-chitosan scaffold to construct a tissue-engineered corneal stroma. Cells Tissues Organs. 2013;198:190–7.",{"EN":340,"VI":341},"Corneal disease affects 12.7 million individuals globally, and the current gold standard therapy using a human donor cornea (HDC) in low-risk patients or keratoprosthesis in high-risk patients is prone to graft rejection. New techniques are currently being investigated to regenerate corneal tissue to provide a more effective treatment for corneal blindness. Research into corneal regeneration falls broadly into three categories: cell-based therapies using autografts or allografts expanded in culture, material-based therapies that provide fully synthetic scaffolds, and cell-biomaterial composites that combine both strategies. Progress has been made developing tissue-specific solutions and multilayer grafts to target specific types of corneal disease. All three classes of therapies have shown progress. The recent European approval of “Holoclar” composite autografts and the phase I clinical trials of fully synthetic corneas demonstrate that research in this field is being actively translated into clinical practice.","Bệnh giác mạc ảnh hưởng đến 12,7 triệu người trên toàn cầu, và liệu pháp tiêu chuẩn hiện tại sử dụng giác mạc từ người hiến tặng (HDC) ở những bệnh nhân có nguy cơ thấp hoặc keratoprosthesis ở những bệnh nhân có nguy cơ cao dễ bị từ chối ghép. Các kỹ thuật mới hiện đang được nghiên cứu nhằm tái tạo mô giác mạc để cung cấp một phương pháp điều trị hiệu quả hơn cho tình trạng mù giác mạc. Nghiên cứu về sự tái tạo giác mạc chủ yếu được chia thành ba phân loại: liệu pháp dựa trên tế bào sử dụng ghép tự thân hoặc ghép đồng loại được mở rộng trong môi trường nuôi cấy, liệu pháp dựa trên vật liệu cung cấp khung hình thái hoàn toàn nhân tạo, và các hợp chất tế bào-vật liệu kết hợp cả hai chiến lược. Đã có những tiến bộ trong việc phát triển các giải pháp đặc hiệu cho mô và các ghép đa lớp nhằm mục tiêu vào các loại bệnh giác mạc cụ thể. Tất cả ba loại liệu pháp đều đã cho thấy sự tiến bộ. Việc phê duyệt gần đây của châu Âu đối với ghép tự thân composite “Holoclar” và các thử nghiệm lâm sàng giai đoạn I về giác mạc hoàn toàn nhân tạo cho thấy nghiên cứu trong lĩnh vực này đang được dịch sang thực hành lâm sàng một cách tích cực.",{"EN":343,"VI":344},"Regenerative Medicine in the Cornea","Y học tái sinh trong giác mạc",{"VOID":346},"10.1007\u002Fs40135-017-0140-5",{"VI":348},"giác mạc, y học tái sinh, liệu pháp tế bào, ghép đồng loại, khung nhân tạo, khung đa lớp","2025-02-05T19:20:53.720+00:00",[351],"VI","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40135-017-0140-5",[354,369],{"id":355,"sortIndex":19,"researcher":18,"roles":356,"affiliations":357,"properties":366},"75330339-8455-4f1f-9615-933cedc371eb",[128],[358],{"id":18,"sortIndex":19,"affiliation":359,"properties":18},{"id":360,"createTime":361,"updateTime":361,"relativeEntities":362,"slug":18,"properties":363,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"58a546f1-23b6-4969-a9b7-968cd64da46d","2024-01-02T04:53:12.053+00:00",[],{"title":364},{"VI":365},"Direction de la Recherche, Hôpital Maisonneuve-Rosemont, Montréal, Canada",{"title":367},{"VI":368},"Fiona C. Simpson",{"id":370,"sortIndex":97,"researcher":18,"roles":371,"affiliations":372,"properties":388},"32d3288d-a010-46c2-8b2e-0e1e6ad44aa3",[128],[373,383],{"id":374,"sortIndex":97,"affiliation":375,"properties":382},"8e22c282-716c-41ae-9bd7-0e74b54dd8a7",{"id":376,"createTime":377,"updateTime":377,"relativeEntities":378,"slug":18,"properties":379,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"dcc6a5f9-dbdb-4d1d-b2e5-984786155ab3","2024-01-02T04:53:12.058+00:00",[],{"title":380},{"VI":381},"Department of Ophthalmology, Université de Montréal, Montréal, Canada",{},{"id":18,"sortIndex":19,"affiliation":384,"properties":18},{"id":360,"createTime":361,"updateTime":361,"relativeEntities":385,"slug":18,"properties":386,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":387},{"VI":365},{"title":389},{"VI":390},"May Griffith",{"url":352,"publisher":392,"properties":419},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":393,"slug":10,"properties":394,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":397,"manageAffiliations":398,"indexDatabases":399,"url":92,"thumbnailPath":18,"statistic":414,"gsStatistic":18,"type":100,"analyzePriority":18},[],{"issn":395,"title":396},{"VOID":13},{"EN":15},[],[],[400,407],{"id":74,"indexDatabase":401,"url":89,"indexYears":18,"academicFieldIds":406,"indexDatabaseRanking":18},{"id":76,"createTime":77,"updateTime":78,"relativeEntities":402,"label":403,"description":404,"key":85,"publicationTags":405,"standard":18},[],{"EN":81,"VI":81},{"VI":83,"EN":84},[87,88],[91],{"id":55,"indexDatabase":408,"url":68,"indexYears":69,"academicFieldIds":413,"indexDatabaseRanking":72},{"id":57,"createTime":58,"updateTime":59,"relativeEntities":409,"label":410,"description":411,"key":65,"publicationTags":412,"standard":18},[],{"EN":62,"VI":62},{"EN":62,"VI":64},[67],[71],{"impactFactor":19,"impactFactorByYear":415,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":95,"totalPublicationByYear":416,"totalCitation":19,"totalCitationByYear":417,"totalCitationPerPublication":19,"totalCitationPerPublicationByYear":418,"hindexLast5Year":19,"hindex":19},{},{"2018":97,"2019":97},{},{},{"volume":420,"pages":421},{"VOID":325},{"VOID":422},"187-192","2017-05-22",{"id":425,"createTime":426,"updateTime":427,"relativeEntities":428,"slug":429,"properties":430,"entityType":120,"verifyStatus":121,"verifyTime":427,"verifyNote":122,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":439,"fullTextUrl":18,"authors":440,"publicationType":173,"publisherRelationship":470,"citationCount":18,"citationInfo":18,"publishDate":503,"publishYear":504,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":209},"6a18fc44-2d89-4819-a195-a486111ce7df","2024-02-17T15:26:09.008+00:00","2025-01-24T23:57:36.400+00:00",[],"The-Immune-System-and-AMD",{"references":431,"abstract":433,"title":435,"doi":437},{"VOID":432},"Sahu A, Lambris JD. Structure and biology of complement protein C3, a connecting link between innate and acquired immunity. Immunol Rev. 2001;180:35–48.\nJohnson LV, et al. Complement activation and inflammatory processes in Drusen formation and age related macular degeneration. Exp Eye Res. 2001;73(6):887–96.\nAnderson DH, et al. A role for local inflammation in the formation of drusen in the aging eye. Am J Ophthalmol. 2002;134(3):411–31.\nGehrs KM, et al. Age-related macular degeneration–emerging pathogenetic and therapeutic concepts. Ann Med. 2006;38(7):450–71.\nVogt SD, et al. Distribution of complement anaphylatoxin receptors and membrane-bound regulators in normal human retina. Exp Eye Res. 2006;83(4):834–40.\nMullins RF, et al. Drusen associated with aging and age-related macular degeneration contain proteins common to extracellular deposits associated with atherosclerosis, elastosis, amyloidosis, and dense deposit disease. Faseb J. 2000;14(7):835–46.\nAnderson DH, et al. Characterization of beta amyloid assemblies in drusen: the deposits associated with aging and age-related macular degeneration. Exp Eye Res. 2004;78(2):243–56.\nNozaki M, et al. Drusen complement components C3a and C5a promote choroidal neovascularization. Proc Natl Acad Sci USA. 2006;103(7):2328–33.\nRichardson AJ, et al. A tag-single nucleotide polymorphisms approach to the vascular endothelial growth factor-A gene in age-related macular degeneration. Mol Vis. 2007;13:2148–52.\nHageman GS, et al. A common haplotype in the complement regulatory gene factor H (HF1\u002FCFH) predisposes individuals to age-related macular degeneration. Proc Natl Acad Sci USA. 2005;102(20):7227–32.\nEdwards AO, et al. Complement factor H polymorphism and age-related macular degeneration. Science. 2005;308(5720):421–4.\nHaines JL, et al. Complement factor H variant increases the risk of age-related macular degeneration. Science. 2005;308(5720):419–21.\nKlein RJ, et al. Complement factor H polymorphism in age-related macular degeneration. Science. 2005;308(5720):385–9.\nClark SJ, et al. H384 allotypic variant of factor H associated with age-related macular degeneration has different heparin-binding properties from the non-disease-associated form. J Biol Chem. 2006;281(34):24713–20.\nGold B, et al. Variation in factor B (BF) and complement component 2 (C2) genes is associated with age-related macular degeneration. Nat Genet. 2006;38(4):458–62.\nYates JR, et al. Complement C3 variant and the risk of age-related macular degeneration. N Engl J Med. 2007;357(6):553–61.\n•• van de Ven JP, et al. A functional variant in the CFI gene confers a high risk of age-related macular degeneration. Nat Genet. 2013;45(7):813–7. This paper identifies a missense mutation in the CFI gene that is highly associated with AMD (OR = 22.20). The specific mutation leads to decreased expression of CFI which can cause unregulated alternative complement activation.\nMaloney SC, et al. Choroidal neovascular membranes express toll-like receptor 3. Ophthalmic Res. 2010;44(4):237–41.\nHaines JL, et al. Functional candidate genes in age-related macular degeneration: significant association with VEGF, VLDLR, and LRP6. Invest Ophthalmol Vis Sci. 2006;47(1):329–35.\nRohrer B, et al. Eliminating complement factor D reduces photoreceptor susceptibility to light-induced damage. Invest Ophthalmol Vis Sci. 2007;48(11):5282–9.\n• Do DV, et al. A phase ia dose-escalation study of the anti-factor d monoclonal antibody fragment fcfd4514s in patients with geographic atrophy. Retina. 2013. This is the Phase I study for a novel anti-complement factor D antibody which is now is advanced clinical trials for the treatment of geographic atrophy.\nRegillo CD, Lampalizumab (Anti-factor D) In patients with geographic atrophy: The MAHALO Phase II Results in 2013 Annual Meeting of the American Academy of Ophthalmology. 2013. New Orleans, LA.\nMiller DM, et al. The association of prior cytomegalovirus infection with neovascular age-related macular degeneration. Am J Ophthalmol. 2004;138(3):323–8.\nKalayoglu MV, et al. Identification of Chlamydia pneumoniae within human choroidal neovascular membranes secondary to age-related macular degeneration. Graefes Arch Clin Exp Ophthalmol. 2005;243(11):1080–90.\nRobman L, et al. Exposure to Chlamydia pneumoniae infection and age-related macular degeneration: the Blue Mountains Eye Study. Invest Ophthalmol Vis Sci. 2007;48(9):4007–11.\nKumar MV, et al. Innate immunity in the retina: Toll-like receptor (TLR) signaling in human retinal pigment epithelial cells. J Neuroimmunol. 2004;153(1–2):7–15.\nKleinman ME, et al. Sequence- and target-independent suppression of angiogenesis by siRNA. Nature. 2008;452(7187):591–7.\nKwak N, et al. VEGF is major stimulator in model of choroidal neovascularization. Invest Ophthalmol Vis Sci. 2000;41(10):3158–64.\nEdwards AO, et al. Toll-like receptor polymorphisms and age-related macular degeneration. Invest Ophthalmol Vis Sci. 2008;49(4):1652–9.\nZhou P, et al. Toll-like receptor 3 C1234T may protect against geographic atrophy through decreased dsRNA binding capacity. Faseb J. 2011;25(10):3489–95.\nYang Z, et al. Toll-like receptor 3 and geographic atrophy in age-related macular degeneration. N Engl J Med. 2008;359(14):1456–63.\n• Klein ML, et al. Progression of geographic atrophy and genotype in age-related macular degeneration. Ophthalmology. 2010;117(8):1554–9, 1559 e1. In this longitudinal progression study, patients with geographic atrophy were analyzed for rate of RPE cell loss and association with various SNPs in complement and innate immune pathways.\nCho Y, et al. Toll-like receptor polymorphisms and age-related macular degeneration: replication in three case-control samples. Invest Ophthalmol Vis Sci. 2009;50(12):5614–8.\nArbour NC, et al. TLR4 mutations are associated with endotoxin hyporesponsiveness in humans. Nat Genet. 2000;25(2):187–91.\nZareparsi S, et al. Toll-like receptor 4 variant D299G is associated with susceptibility to age-related macular degeneration. Hum Mol Genet. 2005;14(11):1449–55.\nKaur I, et al. Analysis of CFH, TLR4, and APOE polymorphism in India suggests the Tyr402His variant of CFH to be a global marker for age-related macular degeneration. Invest Ophthalmol Vis Sci. 2006;47(9):3729–35.\n• Yu Y, et al. Common variants near FRK\u002FCOL10A1 and VEGFA are associated with advanced age-related macular degeneration. Hum Mol Genet. 2011;20(18):3699–709. This paper identified 7 new genes associated with AMD in a large collaborative GWAS.\nZhao L, et al. Common variant in VEGFA and response to anti-VEGF therapy for neovascular age-related macular degeneration. Curr Mol Med. 2013;13(6):929–34.\nKleinman ME, et al. Short-interfering RNAs induce retinal degeneration via TLR3 and IRF3. Mol Ther. 2012;20(1):101–8.\nMurakami Y, et al. Programmed necrosis, not apoptosis, is a key mediator of cell loss and DAMP-mediated inflammation in dsRNA-induced retinal degeneration. Cell Death Differ. 2013;21(2):270–7.\n•• Kaneko H, et al. DICER1 deficit induces Alu RNA toxicity in age-related macular degeneration. Nature. 2011;471(7338):325–30. A major advance in the pathogenesis of geographic atrophy is revealed in the studies conducted in this paper relating to the identification of endogenous RNAs that are toxic to the RPE.\n• Tarallo V, et al. DICER1 loss and Alu RNA induce age-related macular degeneration via the NLRP3 inflammasome and MyD88. Cell. 2012;149(4):847–59. This is a follow-up study to the discovery of Alu RNA induced RPE degeneration in geographic atrophy demonstrating critical involvement of the inflammasome that is NLRP3 dependent.\nPenfold PL, et al. Immunological and aetiological aspects of macular degeneration. Prog Retin Eye Res. 2001;20(3):385–414.\nPenfold PL, et al. Autoantibodies to retinal astrocytes associated with age-related macular degeneration. Graefes Arch Clin Exp Ophthalmol. 1990;228(3):270–4.\nKubicka-Trzaska A, et al. Circulating antiretinal antibodies predict the outcome of anti-VEGF therapy in patients with exudative age-related macular degeneration. Acta Ophthalmol. 2012;90(1):e21–4.\n• Hollyfield JG, et al. Oxidative damage-induced inflammation initiates age-related macular degeneration. Nat Med. 2008;14(2):194–8. A new angle on AMD was introduced in this study which reports on an antigenic protein modification known as carboxyethylpyrrole (CEP) leads the formation of anti-retinal antibodies, retinal toxicity and resultant cell death in AMD.\nGu X, et al. Carboxyethylpyrrole protein adducts and autoantibodies, biomarkers for age-related macular degeneration. J Biol Chem. 2003;278(43):42027–35.\nSakurai E, et al. Macrophage depletion inhibits experimental choroidal neovascularization. Invest Ophthalmol Vis Sci. 2003;44(8):3578–85.\nTsutsumi C, et al. The critical role of ocular-infiltrating macrophages in the development of choroidal neovascularization. J Leukoc Biol. 2003;74(1):25–32.\nGrossniklaus HE, et al. Histopathologic and ultrastructural features of surgically excised subfoveal choroidal neovascular lesions: submacular surgery trials report no. 7. Arch Ophthalmol. 2005;123(7):914–21.\nHuang H, et al. VEGF receptor blockade markedly reduces retinal microglia\u002Fmacrophage infiltration into laser-induced CNV. PLoS One. 2013;8(8):e71808.\nTsutsumi-Miyahara C, et al. The relative contributions of each subset of ocular infiltrated cells in experimental choroidal neovascularisation. Br J Ophthalmol. 2004;88(9):1217–22.\nAmbati J, et al. An animal model of age-related macular degeneration in senescent Ccl-2- or Ccr-2-deficient mice. Nat Med. 2003;9(11):1390–7.\n• Apte RS, et al. Macrophages inhibit neovascularization in a murine model of age-related macular degeneration. PLoS Med. 2006;3(8):e310. An pioneering study into the anti-angiogenic effects of macrophages in a laser-induced model of choroidal neovascularization and macrophage class switching depending on gene expression profiling and cell subtype.\nDuffield JS. The inflammatory macrophage: a story of Jekyll and Hyde. Clin Sci (Lond). 2003;104(1):27–38.\nKelly J, et al. Senescence regulates macrophage activation and angiogenic fate at sites of tissue injury in mice. J Clin Invest. 2007;117(11):3421–6.\n• Espinosa-Heidmann DG, et al. Bone marrow transplantation transfers age-related susceptibility to neovascular remodeling in murine laser-induced choroidal neovascularization. Invest Ophthalmol Vis Sci. 2013;54(12):7439–49. Further foundational work on the effects of aging on bone-marrow cell function and circulating immune cell properties in an animal model of choroidal neovascularization.\nWang VM, et al. Suggestive association between PLA2G12A single nucleotide polymorphism rs2285714 and response to anti-vascular endothelial growth factor therapy in patients with exudative age-related macular degeneration. Mol Vis. 2012;18:2578–85.\nSchick JH, et al. A whole-genome screen of a quantitative trait of age-related maculopathy in sibships from the Beaver Dam Eye Study. Am J Hum Genet. 2003;72(6):1412–24.\nYu Y, et al. Association of variants in the LIPC and ABCA1 genes with intermediate and large drusen and advanced age-related macular degeneration. Invest Ophthalmol Vis Sci. 2011;52(7):4663–70.\nCombadiere C, et al. CX3CR1-dependent subretinal microglia cell accumulation is associated with cardinal features of age-related macular degeneration. J Clin Invest. 2007;117(10):2920–8.\nTuo J, et al. Murine ccl2\u002Fcx3cr1 deficiency results in retinal lesions mimicking human age-related macular degeneration. Invest Ophthalmol Vis Sci. 2007;48(8):3827–36.\nTuo J, et al. The involvement of sequence variation and expression of CX3CR1 in the pathogenesis of age-related macular degeneration. Faseb J. 2004;18(11):1297–9.\nGeissmann F, Jung S, Littman DR. Blood monocytes consist of two principal subsets with distinct migratory properties. Immunity. 2003;19(1):71–82.\nMaller J, et al. Common variation in three genes, including a noncoding variant in CFH, strongly influences risk of age-related macular degeneration. Nat Genet. 2006;38(9):1055–9.\nKortvely E, et al. ARMS2 is a constituent of the extracellular matrix providing a link between familial and sporadic age-related macular degenerations. Invest Ophthalmol Vis Sci. 2010;51(1):79–88.",{"EN":434},"Age-related macular degeneration is a complex, multifactorial disease that has yet to be completely understood. Significant efforts in the basic and clinical sciences have unveiled numerous areas that appear to be critical in the pathogenesis of this disease. The alternative complement pathway, immune cell activation, and autoimmunity are all emerging as important themes in the suspected immunological origins of this disease. Advancement toward a complete understanding of these processes is important in the development of new techniques for disease monitoring and treatment.",{"EN":436},"The Immune System and AMD",{"VOID":438},"10.1007\u002Fs40135-013-0037-x","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40135-013-0037-x",[441,458],{"id":442,"sortIndex":19,"researcher":18,"roles":443,"affiliations":444,"properties":455},"523c0807-4dc6-4421-842c-a6f55a3d4162",[128],[445],{"id":18,"sortIndex":19,"affiliation":446,"properties":18},{"id":447,"createTime":448,"updateTime":449,"relativeEntities":450,"slug":451,"properties":452,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"fce75203-0d8d-4dcd-b517-f007f932c191","2023-12-25T18:31:08.019+00:00","2024-10-09T12:40:18.836+00:00",[],"Department-of-Ophthalmology-and-Visual-Sciences-University-of-Kentucky-Lexington-USA",{"title":453},{"VI":454},"Department of Ophthalmology and Visual Sciences, University of Kentucky, Lexington, USA",{"title":456},{"VI":457},"Paul A. Frederick",{"id":459,"sortIndex":97,"researcher":18,"roles":460,"affiliations":461,"properties":467},"7505c02b-fa2e-4e48-93b9-025a4beb4591",[128],[462],{"id":18,"sortIndex":19,"affiliation":463,"properties":18},{"id":447,"createTime":448,"updateTime":449,"relativeEntities":464,"slug":451,"properties":465,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":466},{"VI":454},{"title":468},{"VI":469},"Mark E. Kleinman",{"url":439,"publisher":471,"properties":498},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":472,"slug":10,"properties":473,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":476,"manageAffiliations":477,"indexDatabases":478,"url":92,"thumbnailPath":18,"statistic":493,"gsStatistic":18,"type":100,"analyzePriority":18},[],{"issn":474,"title":475},{"VOID":13},{"EN":15},[],[],[479,486],{"id":74,"indexDatabase":480,"url":89,"indexYears":18,"academicFieldIds":485,"indexDatabaseRanking":18},{"id":76,"createTime":77,"updateTime":78,"relativeEntities":481,"label":482,"description":483,"key":85,"publicationTags":484,"standard":18},[],{"EN":81,"VI":81},{"VI":83,"EN":84},[87,88],[91],{"id":55,"indexDatabase":487,"url":68,"indexYears":69,"academicFieldIds":492,"indexDatabaseRanking":72},{"id":57,"createTime":58,"updateTime":59,"relativeEntities":488,"label":489,"description":490,"key":65,"publicationTags":491,"standard":18},[],{"EN":62,"VI":62},{"EN":62,"VI":64},[67],[71],{"impactFactor":19,"impactFactorByYear":494,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":95,"totalPublicationByYear":495,"totalCitation":19,"totalCitationByYear":496,"totalCitationPerPublication":19,"totalCitationPerPublicationByYear":497,"hindexLast5Year":19,"hindex":19},{},{"2018":97,"2019":97},{},{},{"volume":499,"pages":501},{"VOID":500},"2",{"VOID":502},"14-19","2014-01-30",2014,{"id":506,"createTime":507,"updateTime":508,"relativeEntities":509,"slug":510,"properties":511,"entityType":120,"verifyStatus":121,"verifyTime":508,"verifyNote":122,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":520,"fullTextUrl":18,"authors":521,"publicationType":173,"publisherRelationship":618,"citationCount":18,"citationInfo":18,"publishDate":651,"publishYear":652,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":209},"713d5dff-a5b8-4cf7-9026-b0b8959b7bb3","2023-12-07T00:49:15.847+00:00","2024-12-26T23:55:06.259+00:00",[],"Management-Strategies-to-Reduce-Risk-of-Postoperative-Infections",{"references":512,"abstract":514,"title":516,"doi":518},{"VOID":513},"Mino De Kaspar H, Ta CN, Froehlich SJ, et al. Prospective study of risk factors for conjunctival bacterial contamination in patients undergoing intraocular surgery. Eur J Ophthalmol. 2009;19:717–22.\nMino de Kaspar H, Shriver EM, Nguyen EV, et al. Risk factors for antibiotic-resistant conjunctival bacterial flora in patients undergoing intraocular surgery. Graefes Arch Clin Exp Ophthalmol. 2003;241:730–3.\nMontan PG, Koranyi G, Setterquist HE, et al. Endophthalmitis after cataract surgery: risk factors relating to technique and events of the operation and patient history: a retrospective case–control study. Ophthalmology. 1998;105:2171–7.\n•• Friling E, Lundstrom M, Stenevi U, Montan P. Six-year incidence of endophthalmitis after cataract surgery: Swedish national study. J Cataract Refract Surg. 2013;39:15–21. A comprehensive study of all cataract surgeries performed in Sweden showing a decrease in the endophthalmitis rate after the universal adoption of cefuroxime intracameral antibiotic administration after cataract surgery.\nHatch WV, Cernat G, Wong D, et al. Risk factors for acute endophthalmitis after cataract surgery: a population-based study. Ophthalmology. 2009;116:425–30.\nCiulla TA, Starr MB, Masket S. Bacterial endophthalmitis prophylaxis for cataract surgery: an evidence-based update. Ophthalmology. 2002;109:13–24.\nBarreau G, Mounier M, Marin B, et al. Intracameral cefuroxime injection at the end of cataract surgery to reduce the incidence of endophthalmitis: French study. J Cataract Refract Surg. 2012;38:1370–5.\nRomero-Aroca P, Mendez-Marin I, Salvat-Serra M, et al. Results at seven years after the use of intracameral cefazolin as an endophthalmitis prophylaxis in cataract surgery. BMC Ophthalmol. 2012;12:2.\nEndophthalmitis Study Group, European Society of Cataract & Refractive Surgeons. Prophylaxis of postoperative endophthalmitis following cataract surgery results of the ESCRS multicenter study and identification of risk factors. J Cataract Refract Surg. 2007;33:978–88.\nGarcia-Saenz MC, Arias-Puente A, Rodriguez-Caravaca G, Banuelos JB. Effectiveness of intracameral cefuroxime in preventing endophthalmitis after cataract surgery ten-year comparative study. J Cataract Refract Surg. 2010;36:203–7.\n• Tan CS, Wong HK, Yang FP. Epidemiology of postoperative endophthalmitis in an Asian population: 11-year incidence and effect of intracameral antibiotic agents. J Cataract Refract Surg. 2012;38:425–30. First Asian study to demonstrate a reduction in endophthalmitis rates after the universal adoption of intracameral cefazolin administration after cataract surgery in Tan Tock Seng Hospital, Singapore.\n•• Shorstein NH, Winthrop KL, Herrinton LJ. Decreased postoperative endophthalmitis rate after institution of intracameral antibiotics in a northern California eye department. J Cataract Refract Surg. 2013;39:8–14. The first US study to demonstrate a reduction in endophthalmitis rates after the universal adoption of intracameral antibiotic administration after cataract surgery in the Kaiser Permanente patients in northern California.\nGoldberg RA, Flynn HW, Jr., Isom RF, et al. An outbreak of Streptococcus endophthalmitis after intravitreal injection of bevacizumab. Am J Ophthalmol. 2012;153(2):204–8 e1.\n• Gungel H, Eren MH, Pinarci EY, et al. An outbreak of Fusarium solani endophthalmitis after cataract surgery in an eye training and research hospital in Istanbul. Mycoses. 2011;54:e767–74. A study demonstrating the danger of using compounded medications as 9 patients developed devastating endophthalmitis likely in the setting of contaminated cefuroxime.\n•• Wykoff CC, Parrott MB, Flynn HW, Jr., et al. Nosocomial acute-onset postoperative endophthalmitis at a university teaching hospital (2002–2009). Am J Ophthalmol. 2010;150:392–8 e2. A retrospective study reporting the lowest rate of endophthalmitis in the literature, achieved without the use of intracameral antibiotics.\nTa CN, Chang RT, Singh K, et al. Antibiotic resistance patterns of ocular bacterial flora: a prospective study of patients undergoing anterior segment surgery. Ophthalmology. 2003;110:1946–51.\nGarcia-Arumi J, Fonollosa A, Sararols L, et al. Topical anesthesia: possible risk factor for endophthalmitis after cataract extraction. J Cataract Refract Surg. 2007;33:989–92.\nMiller JJ, Scott IU, Flynn HW Jr, et al. Acute-onset endophthalmitis after cataract surgery (2000–2004): incidence, clinical settings, and visual acuity outcomes after treatment. Am J Ophthalmol. 2005;139:983–7.\nNagaki Y, Hayasaka S, Kadoi C, et al. Bacterial endophthalmitis after small-incision cataract surgery. Effect of incision placement and intraocular lens type. J Cataract Refract Surg. 2003;29:20–6.\nColleaux KM, Hamilton WK. Effect of prophylactic antibiotics and incision type on the incidence of endophthalmitis after cataract surgery. Can J Ophthalmol. 2000;35:373–8.\nMcDonnell PJ, Taban M, Sarayba M, et al. Dynamic morphology of clear corneal cataract incisions. Ophthalmology. 2003;110:2342–8.\nTaban M, Rao B, Reznik J, et al. Dynamic morphology of sutureless cataract wounds—effect of incision angle and location. Surv Ophthalmol. 2004;49 Suppl 2:S62–72.\nWallin T, Parker J, Jin Y, et al. Cohort study of 27 cases of endophthalmitis at a single institution. J Cataract Refract Surg. 2005;31:735–41.\nPacker M, Chang DF, Dewey SH, et al. Prevention, diagnosis, and management of acute postoperative bacterial endophthalmitis. J Cataract Refract Surg. 2011;37:1699–714.\nErnest PH, Kiessling LA, Lavery KT. Relative strength of cataract incisions in cadaver eyes. J Cataract Refract Surg. 1991;17(Suppl):668–71.\nMollan SP, Gao A, Lockwood A, et al. Postcataract endophthalmitis: incidence and microbial isolates in a United Kingdom region from 1996 through 2004. J Cataract Refract Surg. 2007;33:265–8.\nNg JQ, Morlet N, Bulsara MK, Semmens JB. Reducing the risk for endophthalmitis after cataract surgery: population-based nested case-control study: endophthalmitis population study of Western Australia sixth report. J Cataract Refract Surg. 2007;33:269–80.\nLundstrom M, Wejde G, Stenevi U, et al. Endophthalmitis after cataract surgery: a nationwide prospective study evaluating incidence in relation to incision type and location. Ophthalmology. 2007;114:866–70.\nFrancis IC, Roufas A, Figueira EC, et al. Endophthalmitis following cataract surgery: the sucking corneal wound. J Cataract Refract Surg. 2009;35:1643–5.\n• Fukuda S, Kawana K, Yasuno Y, Oshika T. Wound architecture of clear corneal incision with or without stromal hydration observed with 3-dimensional optical coherence tomography. Am J Ophthalmol. 2011;151:413–9 e1. A study demonstrating the transient nature of the effect of stromal wound hydration in clear corneal incisions.\nMasket S, Sarayba M, Ignacio T, Fram N. Femtosecond laser-assisted cataract incisions: architectural stability and reproducibility. J Cataract Refract Surg. 2010;36:1048–9.\n• Luz RA, Padoveze MC, Falabella P, et al. Risk factors for postoperative endophthalmitis caused by Pseudomonas aeruginosa: Possible role of environment. Am J Infect Control. 2013. A study suggesting that the operating room environment may play a role in the risk of post-cataract endophthalmitis.\nLou B, Lin X, Luo L, et al. Residual lens cortex material: potential risk factor for endophthalmitis after phacoemulsification cataract surgery. J Cataract Refract Surg. 2013;39:250–7.\n•• Simaroj P, Kompreyarat S, Santanirand P, Lekhanont K. Anterior chamber contamination during phacoemulsification after povidone-iodine application. J Med Assoc Thai. 2012;95:689–92. A study demonstrating that anterior chamber bacterial contamination can occur even after the application of povidone-iodine.\nTaravella MJ, Davidson R, Erlanger M, et al. Characterizing the learning curve in phacoemulsification. J Cataract Refract Surg. 2011;37:1069–75.\nLee JS, Hou CH, Yang ML, et al. A different approach to assess resident phacoemulsification learning curve: analysis of both completion and complication rates. Eye (Lond). 2009;23:683–7.\nRamappa M, Majji AB, Murthy SI, et al. An outbreak of acute post-cataract surgery Pseudomonas sp. endophthalmitis caused by contaminated hydrophilic intraocular lens solution. Ophthalmology. 2012;119:564–70.\nAkcakaya AA, Sargin F, Erbil HH, et al. A cluster of acute-onset postoperative endophthalmitis over a 1-month period: investigation of an outbreak caused by uncommon species. Br J Ophthalmol. 2011;95:481–4.\nPinna A, Usai D, Sechi LA, et al. An outbreak of post-cataract surgery endophthalmitis caused by Pseudomonas aeruginosa. Ophthalmology. 2009;116:2321–6 e1-4.\nJambulingam M, Parameswaran SK, Lysa S, et al. A study on the incidence, microbiological analysis and investigations on the source of infection of postoperative infectious endophthalmitis in a tertiary care ophthalmic hospital: an 8-year study. Indian J Ophthalmol. 2010;58:297–302.\n• Das T, Hussain A, Naduvilath T, et al. Case control analyses of acute endophthalmitis after cataract surgery in South India associated with technique, patient care, and socioeconomic status. J Ophthalmol. 2012;2012:298459. A study emphasizing that patient factors such as post-surgical hygiene may play a role in the risk of endophthalmitis.\n•• Zahid S, Musch DC, Niziol LM, Lichter PR. Risk of endophthalmitis and other long-term complications of trabeculectomy in the Collaborative Initial Glaucoma Treatment Study (CIGTS). Am J Ophthalmol. 2013;155:674–80, 80 e1. A prospective study evaluating the risks of endophthalmitis after trabeculectomy.\nAlwitry A, King AJ. Surveillance of late-onset bleb leak, blebitis and bleb-related endophthalmitis—a UK incidence study. Graefes Arch Clin Exp Ophthalmol. 2012;250:1231–6.\nKuang TM, Lin YC, Liu CJ, et al. Early and late endophthalmitis following trabeculectomy in a Chinese population. Eur J Ophthalmol. 2008;18:66–70.\nWilkins M, Indar A, Wormald R. Intra-operative mitomycin C for glaucoma surgery. Cochrane Database Syst Rev. 2005;1:CD002897.\nAl-Torbak AA, Al-Shahwan S, Al-Jadaan I, et al. Endophthalmitis associated with the Ahmed glaucoma valve implant. Br J Ophthalmol. 2005;89:454–8.\nKeay L, Gower EW, Cassard SD, et al. Postcataract surgery endophthalmitis in the United States: analysis of the complete 2003 to 2004 Medicare database of cataract surgeries. Ophthalmology. 2012;119:914–22.\nFreeman EE, Roy-Gagnon MH, Fortin E, et al. Rate of endophthalmitis after cataract surgery in quebec, Canada, 1996–2005. Arch Ophthalmol. 2010;128:230–4.\nMelo GB, Bispo PJ, Regatieri CV, et al. Incidence of endophthalmitis after cataract surgery (2002–2008) at a Brazilian university-hospital. Arq Bras Oftalmol. 2010;73:505–7.",{"EN":515},"Postoperative infections, although rare, are still of great concern to the ophthalmologist. The incidence of post-cataract endophthalmitis is low, with a range of 0.28 per 1,000 to 2.99 per 1,000. In addition to intraoperative considerations such as poor wound construction, vitreous loss, topical anesthesia, and prolonged surgical time, other risk factors include preoperative factors such as a diseased ocular surface and systemic immunosuppression. Potential methods of reducing risk of endophthalmitis after anterior segment surgery are discussed and available literature is summarized. ",{"EN":517},"Management Strategies to Reduce Risk of Postoperative Infections",{"VOID":519},"10.1007\u002Fs40135-013-0021-5","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs40135-013-0021-5",[522,538,561,580,599],{"id":523,"sortIndex":524,"researcher":18,"roles":525,"affiliations":526,"properties":535},"a0079b37-f9b5-4158-8b2e-0b1fd19b2530",4,[128],[527],{"id":18,"sortIndex":19,"affiliation":528,"properties":18},{"id":529,"createTime":530,"updateTime":530,"relativeEntities":531,"slug":18,"properties":532,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"cbcb4f49-1082-40eb-89c9-c98937059973","2024-01-10T18:15:07.372+00:00",[],{"title":533},{"VI":534},"Bascom Palmer Eye Institute, University of Miami, Miami, USA",{"title":536},{"VI":537},"Harry W. Flynn",{"id":539,"sortIndex":540,"researcher":18,"roles":541,"affiliations":542,"properties":558},"26c99060-8ef7-4041-bf22-2a02d5c51797",3,[128],[543,551],{"id":18,"sortIndex":19,"affiliation":544,"properties":18},{"id":545,"createTime":546,"updateTime":546,"relativeEntities":547,"slug":18,"properties":548,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"40a3f6e4-f494-4e49-92cf-5584b0e6b5af","2023-12-07T00:49:15.859+00:00",[],{"title":549},{"VI":550},"Miami Veterans Administration Medical Center, Miami, USA",{"id":552,"sortIndex":97,"affiliation":553,"properties":557},"2cd8d189-8011-4c12-9cf3-6a474962eaa4",{"id":529,"createTime":530,"updateTime":530,"relativeEntities":554,"slug":18,"properties":555,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":556},{"VI":534},{},{"title":559},{"VI":560},"Ninel Z. Gregori",{"id":562,"sortIndex":95,"researcher":18,"roles":563,"affiliations":564,"properties":577},"f43bee0c-8ae2-491d-bb09-91c6d5728f44",[128],[565,570],{"id":18,"sortIndex":19,"affiliation":566,"properties":18},{"id":545,"createTime":546,"updateTime":546,"relativeEntities":567,"slug":18,"properties":568,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":569},{"VI":550},{"id":571,"sortIndex":97,"affiliation":572,"properties":576},"1c081445-486c-4fb1-98f7-a4cb350f1a91",{"id":529,"createTime":530,"updateTime":530,"relativeEntities":573,"slug":18,"properties":574,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":575},{"VI":534},{},{"title":578},{"VI":579},"Sarah R. Wellik",{"id":581,"sortIndex":97,"researcher":18,"roles":582,"affiliations":583,"properties":596},"f2355813-071d-4e7f-8d27-8d33a89f1510",[128],[584,589],{"id":18,"sortIndex":19,"affiliation":585,"properties":18},{"id":545,"createTime":546,"updateTime":546,"relativeEntities":586,"slug":18,"properties":587,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":588},{"VI":550},{"id":590,"sortIndex":97,"affiliation":591,"properties":595},"cea78cf1-f247-4ac7-b5ff-1d7949edf004",{"id":529,"createTime":530,"updateTime":530,"relativeEntities":592,"slug":18,"properties":593,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":594},{"VI":534},{},{"title":597},{"VI":598},"Raquel Goldhardt",{"id":600,"sortIndex":19,"researcher":18,"roles":601,"affiliations":602,"properties":615},"59b6e612-37d6-4269-b363-4b488b90e6b3",[128],[603,610],{"id":604,"sortIndex":97,"affiliation":605,"properties":609},"e7ec11f6-8b7c-4faf-91aa-8079840a30e2",{"id":529,"createTime":530,"updateTime":530,"relativeEntities":606,"slug":18,"properties":607,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":608},{"VI":534},{},{"id":18,"sortIndex":19,"affiliation":611,"properties":18},{"id":545,"createTime":546,"updateTime":546,"relativeEntities":612,"slug":18,"properties":613,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":614},{"VI":550},{"title":616},{"VI":617},"Anat Galor",{"url":520,"publisher":619,"properties":646},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":620,"slug":10,"properties":621,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":624,"manageAffiliations":625,"indexDatabases":626,"url":92,"thumbnailPath":18,"statistic":641,"gsStatistic":18,"type":100,"analyzePriority":18},[],{"issn":622,"title":623},{"VOID":13},{"EN":15},[],[],[627,634],{"id":74,"indexDatabase":628,"url":89,"indexYears":18,"academicFieldIds":633,"indexDatabaseRanking":18},{"id":76,"createTime":77,"updateTime":78,"relativeEntities":629,"label":630,"description":631,"key":85,"publicationTags":632,"standard":18},[],{"EN":81,"VI":81},{"VI":83,"EN":84},[87,88],[91],{"id":55,"indexDatabase":635,"url":68,"indexYears":69,"academicFieldIds":640,"indexDatabaseRanking":72},{"id":57,"createTime":58,"updateTime":59,"relativeEntities":636,"label":637,"description":638,"key":65,"publicationTags":639,"standard":18},[],{"EN":62,"VI":62},{"EN":62,"VI":64},[67],[71],{"impactFactor":19,"impactFactorByYear":642,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":95,"totalPublicationByYear":643,"totalCitation":19,"totalCitationByYear":644,"totalCitationPerPublication":19,"totalCitationPerPublicationByYear":645,"hindexLast5Year":19,"hindex":19},{},{"2018":97,"2019":97},{},{},{"volume":647,"pages":649},{"VOID":648},"1",{"VOID":650},"161-168","2013-08-18",2013,{"id":654,"createTime":655,"updateTime":656,"relativeEntities":657,"slug":658,"properties":659,"entityType":120,"verifyStatus":121,"verifyTime":656,"verifyNote":122,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":668,"fullTextUrl":18,"authors":669,"publicationType":173,"publisherRelationship":714,"citationCount":18,"citationInfo":18,"publishDate":746,"publishYear":504,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":209},"ed9563cf-058c-4249-8343-75344e92eff8","2023-12-20T20:45:12.932+00:00","2024-12-05T23:52:24.593+00:00",[],"Development-of-Retinal-Amacrine-Cells-and-Their-Dendritic-Stratification",{"references":660,"abstract":662,"title":664,"doi":666},{"VOID":661},"Masland RH. The neuronal organization of the retina. Neuron. 2012;76(2):266–80.\n• Masland RH. The fundamental plan of the retina. Nat Neurosci. 2001;4(9):877–86. This article describes the diversity of retinal neurons and its association with function.\nMasland RH. Neuronal diversity in the retina. Curr Opin Neurobiol. 2001;11(4):431–6.\nLivesey FJ, Cepko CL. Vertebrate neural cell-fate determination: lessons from the retina. Nat Rev Neurosci. 2001;2(2):109–18.\nMasland RH. The tasks of amacrine cells. Vis Neurosci. 2012;29(1):3–9.\n• MacNeil MA, Masland RH. Extreme diversity among amacrine cells: implications for function. Neuron. 1998;20(5):971–82. This article describes the morphological diversity among amacrine cells and explores the functions of amacrine interneurons.\nVaney DI. Morphological identification of serotonin-accumulating neurons in the living retina. Science. 1986;233(4762):444–6.\nVaney DI. Territorial organization of direction-selective ganglion cells in rabbit retina. J Neurosci. 1994;14(11 Pt 1):6301–16.\nVaney DI, Gynther IC, Young HM. Rod-signal interneurons in the rabbit retina: 2. AII amacrine cells. J Comp Neurol. 1991;310(2):154–69.\n• MacNeil MA, et al. The shapes and numbers of amacrine cells: matching of photofilled with golgi-stained cells in the rabbit retina and comparison with other mammalian species. J Comp Neurol. 1999;413(2):305–26. This article provides a thorough classification of amacrine cells based on their dendritic stratification.\nWassle H, Grunert U, Rohrenbeck J. Immunocytochemical staining of AII-amacrine cells in the rat retina with antibodies against parvalbumin. J Comp Neurol. 1993;332(4):407–20.\n• Haverkamp S, Wassle H. Immunocytochemical analysis of the mouse retina. J Comp Neurol. 2000;424(1):1–23. Using immunohistochemistry, this report classifies amacrine interneurons based on neurotransmitters or neuropeptides they express.\nHaverkamp S, Wassle H. Characterization of an amacrine cell type of the mammalian retina immunoreactive for vesicular glutamate transporter 3. J Comp Neurol. 2004;468(2):251–63.\nMenger N, Pow DV, Wassle H. Glycinergic amacrine cells of the rat retina. J Comp Neurol. 1998;401(1):34–46.\nStrettoi E, Masland RH. The organization of the inner nuclear layer of the rabbit retina. J Neurosci. 1995;15(1 Pt 2):875–88.\n• Kay JN, et al. Neurod6 expression defines new retinal amacrine cell subtypes and regulates their fate. Nat Neurosci. 2011;14(8):965–72. An excellent reference describing the development and characterization of nGnG (neither glycinergic nor GABAergic) amacrine cells.\nHaverkamp S, Kolb H, Cuenca N. Morphological and neurochemical diversity of neuronal nitric oxide synthase-positive amacrine cells in the turtle retina. Cell Tissue Res. 2000;302(1):11–9.\nOh SJ, et al. Distribution and synaptic connectivity of neuropeptide Y-immunoreactive amacrine cells in the rat retina. J Comp Neurol. 2002;446(3):219–34.\nPang JJ, Gao F, Wu SM. Light responses and morphology of bNOS-immunoreactive neurons in the mouse retina. J Comp Neurol. 2010;518(13):2456–74.\nSinclair JR, Nirenberg S. Characterization of neuropeptide Y-expressing cells in the mouse retina using immunohistochemical and transgenic techniques. J Comp Neurol. 2001;432(3):296–306.\nEglen SJ, et al. Dopaminergic amacrine cells in the inner nuclear layer and ganglion cell layer comprise a single functional retinal mosaic. J Comp Neurol. 2003;466(3):343–55.\nRice DS, Curran T. Disabled-1 is expressed in type AII amacrine cells in the mouse retina. J Comp Neurol. 2000;424(2):327–38.\nYeo JY, Lee ES, Jeon CJ. Parvalbumin-immunoreactive neurons in the inner nuclear layer of zebrafish retina. Exp Eye Res. 2009;88(3):553–60.\nLee EJ, et al. AII amacrine cells in the distal inner nuclear layer of the mouse retina. J Comp Neurol. 2006;494(4):651–62.\nJohnson J, et al. Vesicular glutamate transporter 3 expression identifies glutamatergic amacrine cells in the rodent retina. J Comp Neurol. 2004;477(4):386–98.\n• Voinescu PE, Kay JN, Sanes JR. Birthdays of retinal amacrine cell subtypes are systematically related to their molecular identity and soma position. J Comp Neurol. 2009;517(5):737–50. This report details the developmental time line of a number of amacrine cell subtypes.\nTaylor WR, Smith RG. The role of starburst amacrine cells in visual signal processing. Vis Neurosci. 2012;29(1):73–81.\nSinclair JR, Jacobs AL, Nirenberg S. Selective ablation of a class of amacrine cells alters spatial processing in the retina. J Neurosci. 2004;24(6):1459–67.\nMeng S, et al. Targeting retinal dopaminergic neurons in tyrosine hydroxylase-driven green fluorescent protein transgenic zebrafish. Mol Vis. 2008;14:2475–83.\nVielma AH, Retamal MA, Schmachtenberg O. Nitric oxide signaling in the retina: what have we learned in two decades? Brain Res. 2012;1430:112–25.\nDemb JB, Singer JH. Intrinsic properties and functional circuitry of the AII amacrine cell. Vis Neurosci. 2012;29(1):51–60.\nGrimes WN, et al. Genetic targeting and physiological features of VGLUT3+ amacrine cells. Vis Neurosci. 2011;28(5):381–92.\nYamagata M, Weiner JA, Sanes JR. Sidekicks: synaptic adhesion molecules that promote lamina-specific connectivity in the retina. Cell. 2002;110(5):649–60.\nYamagata M, Sanes JR. Dscam and Sidekick proteins direct lamina-specific synaptic connections in vertebrate retina. Nature. 2008;451(7177):465–9.\nFuerst PG, et al. Neurite arborization and mosaic spacing in the mouse retina require DSCAM. Nature. 2008;451(7177):470–4.\nMatsuoka RL, et al. Transmembrane semaphorin signalling controls laminar stratification in the mammalian retina. Nature. 2011;470(7333):259–63.\nMatsuoka RL, et al. Class 5 transmembrane semaphorins control selective mammalian retinal lamination and function. Neuron. 2011;71(3):460–73.\nZhang Y, et al. The expression of irx7 in the inner nuclear layer of zebrafish retina is essential for a proper retinal development and lamination. PLoS ONE. 2012;7(4):e36145.\nCantrup R, et al. Cell-type specific roles for PTEN in establishing a functional retinal architecture. PLoS ONE. 2012;7(3):e32795.\nMarquardt T, et al. Pax6 is required for the multipotent state of retinal progenitor cells. Cell. 2001;105(1):43–55.\nOron-Karni V, et al. Dual requirement for Pax6 in retinal progenitor cells. Development. 2008;135(24):4037–47.\nOrieux G, et al. Involvement of Bcl-2-associated transcription factor 1 in the differentiation of early-born retinal cells. J Neurosci. 2014;34(4):1530–41.\nLin YP, et al. Sox2 plays a role in the induction of amacrine and Muller glial cells in mouse retinal progenitor cells. Invest Ophthalmol Vis Sci. 2009;50(1):68–74.\nLi S, et al. Foxn4 controls the genesis of amacrine and horizontal cells by retinal progenitors. Neuron. 2004;43(6):795–807.\n• Ohsawa R, Kageyama R. Regulation of retinal cell fate specification by multiple transcription factors. Brain Res. 2008;1192:90–8. An excellent review that details the role of specific transcription factors during the development of amacrine cell types and subtypes.\nIslam MM, et al. Meis1 regulates Foxn4 expression during retinal progenitor cell differentiation. Biol Open. 2013;2(11):1125–36.\nInoue T, et al. Math3 and NeuroD regulate amacrine cell fate specification in the retina. Development. 2002;129(4):831–42.\nFujitani Y, et al. Ptf1a determines horizontal and amacrine cell fates during mouse retinal development. Development. 2006;133(22):4439–50.\nNakhai H, et al. Ptf1a is essential for the differentiation of GABAergic and glycinergic amacrine cells and horizontal cells in the mouse retina. Development. 2007;134(6):1151–60.\nDullin JP, et al. Ptf1a triggers GABAergic neuronal cell fates in the retina. BMC Dev Biol. 2007;7:110.\nMo Z, et al. Role of the Barhl2 homeobox gene in the specification of glycinergic amacrine cells. Development. 2004;131(7):1607–18.\nDing Q, et al. BARHL2 differentially regulates the development of retinal amacrine and ganglion neurons. J Neurosci. 2009;29(13):3992–4003.\nElshatory Y, et al. Expression of the LIM-homeodomain protein Isl1 in the developing and mature mouse retina. J Comp Neurol. 2007;503(1):182–97.\nElshatory Y, et al. Islet-1 controls the differentiation of retinal bipolar and cholinergic amacrine cells. J Neurosci. 2007;27(46):12707–20.\nFeng L, et al. Requirement for Bhlhb5 in the specification of amacrine and cone bipolar subtypes in mouse retina. Development. 2006;133(24):4815–25.\nHuang L, et al. Bhlhb5 is required for the subtype development of retinal amacrine and bipolar cells in mice. Dev Dyn. 2014;243(2):279–89.\nDuquette PM, et al. Loss of LMO4 in the retina leads to reduction of GABAergic amacrine cells and functional deficits. PLoS ONE. 2010;5(10):e13232.\nCherry TJ, et al. NeuroD factors regulate cell fate and neurite stratification in the developing retina. J Neurosci. 2011;31(20):7365–79.\nJin K, et al. Early B-cell factors are required for specifying multiple retinal cell types and subtypes from postmitotic precursors. J Neurosci. 2010;30(36):11902–16.",{"EN":663},"The mammalian retina contains multiple neurons, each of which contributes differentially to visual processing. Of these retinal neurons, amacrine cells have recently come to prime light since they facilitate majority of visual processing that takes place in the retina. Amacrine cells are also the most diverse group of neurons in the retina, classified majorly based on the neurotransmitter type they express and morphology of their dendritic arbors. Currently, little is known about the molecular basis contributing to this diversity during development. Amacrine cells also contribute to most of the synapses in the inner plexiform layer and mediate visual information input from bipolar cells onto retinal ganglion cells. In this review, we will describe the current understanding of amacrine cell and cell subtype development. Furthermore, we will address the molecular basis of retinal lamination at the inner plexiform layer. Overall, our review will provide a developmental perspective of amacrine cell subtype classification and their dendritic stratification.",{"EN":665},"Development of Retinal Amacrine Cells and Their Dendritic Stratification",{"VOID":667},"10.1007\u002Fs40135-014-0048-2","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40135-014-0048-2",[670,695],{"id":671,"sortIndex":19,"researcher":18,"roles":672,"affiliations":673,"properties":692},"518f118c-3f99-454e-bac6-ac544002ccd2",[128],[674,682],{"id":18,"sortIndex":19,"affiliation":675,"properties":18},{"id":676,"createTime":677,"updateTime":677,"relativeEntities":678,"slug":18,"properties":679,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"8a539035-4554-4e01-bd5c-47637eff653d","2023-12-20T20:44:30.474+00:00",[],{"title":680},{"VI":681},"Department of Ophthalmology and Flaum Eye Institute, University of Rochester, Rochester, USA",{"id":683,"sortIndex":97,"affiliation":684,"properties":691},"31e87a3d-48ce-4641-add9-7f866a5d0fb7",{"id":685,"createTime":686,"updateTime":686,"relativeEntities":687,"slug":18,"properties":688,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"91b04fca-c521-4adb-9ece-aad466433a2e","2024-01-22T14:01:59.272+00:00",[],{"title":689},{"VI":690},"Department of Neurobiology and Anatomy, University of Rochester, Rochester, USA",{},{"title":693},{"VI":694},"Revathi Balasubramanian",{"id":696,"sortIndex":97,"researcher":18,"roles":697,"affiliations":698,"properties":711},"04f85e6d-7167-419d-a6e2-205d56ca3c24",[128],[699,704],{"id":18,"sortIndex":19,"affiliation":700,"properties":18},{"id":676,"createTime":677,"updateTime":677,"relativeEntities":701,"slug":18,"properties":702,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":703},{"VI":681},{"id":705,"sortIndex":97,"affiliation":706,"properties":710},"e0ee775a-f9d6-45a0-aaca-73886af177fa",{"id":685,"createTime":686,"updateTime":686,"relativeEntities":707,"slug":18,"properties":708,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":709},{"VI":690},{},{"title":712},{"VI":713},"Lin Gan",{"url":668,"publisher":715,"properties":742},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":716,"slug":10,"properties":717,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":720,"manageAffiliations":721,"indexDatabases":722,"url":92,"thumbnailPath":18,"statistic":737,"gsStatistic":18,"type":100,"analyzePriority":18},[],{"issn":718,"title":719},{"VOID":13},{"EN":15},[],[],[723,730],{"id":74,"indexDatabase":724,"url":89,"indexYears":18,"academicFieldIds":729,"indexDatabaseRanking":18},{"id":76,"createTime":77,"updateTime":78,"relativeEntities":725,"label":726,"description":727,"key":85,"publicationTags":728,"standard":18},[],{"EN":81,"VI":81},{"VI":83,"EN":84},[87,88],[91],{"id":55,"indexDatabase":731,"url":68,"indexYears":69,"academicFieldIds":736,"indexDatabaseRanking":72},{"id":57,"createTime":58,"updateTime":59,"relativeEntities":732,"label":733,"description":734,"key":65,"publicationTags":735,"standard":18},[],{"EN":62,"VI":62},{"EN":62,"VI":64},[67],[71],{"impactFactor":19,"impactFactorByYear":738,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":95,"totalPublicationByYear":739,"totalCitation":19,"totalCitationByYear":740,"totalCitationPerPublication":19,"totalCitationPerPublicationByYear":741,"hindexLast5Year":19,"hindex":19},{},{"2018":97,"2019":97},{},{},{"volume":743,"pages":744},{"VOID":500},{"VOID":745},"100-106","2014-07-05",{"id":748,"createTime":749,"updateTime":750,"relativeEntities":751,"slug":752,"properties":753,"entityType":120,"verifyStatus":121,"verifyTime":762,"verifyNote":122,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":763,"fullTextUrl":18,"authors":764,"publicationType":173,"publisherRelationship":792,"citationCount":18,"citationInfo":18,"publishDate":824,"publishYear":329,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":209},"ce2fdef1-09c3-484a-82b6-58bc24f7e87e","2024-01-21T14:41:06.203+00:00","2024-06-30T23:52:12.065+00:00",[],"Refractive-IOL-Pipeline-Innovations-Predictions-and-Needs",{"references":754,"abstract":756,"title":758,"doi":760},{"VOID":755},"Ford J, Werner L, Mamalis N. Adjustable intraocular lens power technology. J Cataract Refract Surg. 2014;40(7):1205–23.\nMamalis N. Complications of foldable intraocular lenses requiring explantation or secondary intervention—1998 survey. J Cataract Refract Surg. 2000;26:766–22.\nMamalis N, Spencer TS. Complications of foldable intraocular lenses requiring explantation or secondary intervention—2000 survey update. J Cataract Refract Surg. 2001;27:1310–7.\nMamalis N, Davis B, Nilson CD, et al. Complications of foldable intraocular lenses requiring explantation or secondary intervention—2003 survey update. J Cataract Refract Surg. 2004;30(10):2209–18.\nMamalis N, Brubaker J, Davis D, et al. Complications of foldable intraocular lenses requiring explantation or secondary intervention—2007 survey update. J Cataract Refract Surg. 2008;34(9):1584–91.\n•• Nuzzi R, Tridico F. Comparison of visual outcomes, spectacles dependence and patient satisfaction of multifocal and accommodative intraocular lenses: innovative perspectives for maximal refractive-oriented cataract surgery. BMC Ophthalmol. 2017;17(1):12. This study compared three multifocal IOLs and one accommodative IOL, noting the AcrySof ReSTOR SN6AD1 provided the best outcomes across all distances, but that the Optoflex FIL611PV may be a more cost-effective option for patients who prioritize intermediate and near vision\nStudeny P, Krizova D, Urminsky J. Clinical experience with the WIOL-CF accommodative bioanalogic intraocular lens: Czech national observational registry. Eur J Ophthalmol. 2016;26(3):230–5.\nPallikaris IG, Portaliou DM, Kymionis GD, et al. Outcomes after accommodative bioanalogic intraocular lens implantation. J Refract Surg. 2014;30(6):402–6.\nKim YC, Kang KT, Yeo Y, et al. Consistent pattern in positional instability of polyfocal full-optics accommodative IOL. Int Ophthalmol 2016.\nKang KT, Kim YC. Dislocation of polyfocal full-optics accommodative intraocular lens after neodymium-doped yttrium aluminum garnet capsulotomy in vitrectomized eye. Indian J Ophthalmol. 2013;61(11):678–80.\nAlio JL, Simonov A, Plaza-Puche AB, et al. Visual outcomes and accommodative response of the Lumina accommodative intraocular lens. Am J Ophthalmol. 2016;164:37–48.\nVillegas EA, Alcon E, Mirabet S, et al. Extended depth of focus with induced spherical aberration in light-adjustable intraocular lenses. Am J Ophthalmol. 2014;157(1):142–9.\nSandoval HP, Donnenfeld ED, Kohnen T, et al. Modern laser in situ keratomileusis outcomes. J Cataract Refract Surg. 2016;42(8):1224–34.\nSolomon KD, Fernandez de Castro LE, Sandoval HP, et al. LASIK world literature review: quality of life and patient satisfaction. Ophthalmology. 2009;116(4):691–701.\nBrierley L. Refractive results after implantation of a light-adjustable intraocular lens in postrefractive surgery cataract patients. Ophthalmology. 2013;120(10):1968–72.\nHeinzelmann S, Hengerer FH, Maier P, et al. Is there an endothelial cell toxicity of light-adjustable lens UVA irradiation on the human corneal endothelium? Eur J Ophthalmol. 2012;22(Suppl 7):S57–61.\nWerner L, Chang W, Haymore J, et al. Retinal safety of the irradiation delivered to light-adjustable intraocular lenses evaluated in a rabbit model. J Cataract Refract Surg. 2010;36(8):1392–7.\nChayet A, Sandstedt C, Chang S, et al. Correction of myopia after cataract surgery with a light-adjustable lens. Ophthalmology. 2009;116(8):1432–5.\nVillegas EA, Alcon E, Rubio E, et al. Refractive accuracy with light-adjustable intraocular lenses. J Cataract Refract Surg. 2014;40(7):1075–84.e2.\nHengerer FH, Muller M, Dick HB, Conrad-Hengerer I. Clinical evaluation of macular thickness changes in cataract surgery using a light-adjustable intraocular lens. J Refract Surg. 2016;32(4):250–4.\nSales CS, Manche EE. Managing residual refractive error after cataract surgery. J Cataract Refract Surg. 2015;41(6):1289–99.\nDominguez-Vicent A, Esteve-Taboada JJ, Del Aguila-Carrasco AJ, et al. In vitro optical quality comparison between the Mini WELL Ready progressive multifocal and the TECNIS Symfony. Graefes Arch Clin Exp Ophthalmol. 2016;254(7):1387–97.\nCochener B, Concerto SG. Clinical outcomes of a new extended range of vision intraocular lens: International Multicenter Concerto Study. J Cataract Refract Surg. 2016;42(9):1268–75.\nAbbott Inc. TECNIS Symfony Extended Range of Vision IOLs DFU. Santa Ana, Calif. Abbott Medical Optics Inc.\nSchwiegerling J. Image quality analysis for an aspheric toric apodized diffractive intraocular lens using modulation transfer function testing. Invest Ophthalmol Vis Sci 2010;50:E-Abstract # 5727.\nSalman AG. Long-term visual performance of AT LISA 909M multifocal toric intraocular lenses. J Egypt Ophthal Soc. 2013;106(3):199–205.\nBellucci R, Bauer NJ, Daya SM, et al. Visual acuity and refraction with a diffractive multifocal toric intraocular lens. J Cataract Refract Surg. 2013;39(10):1507–18.\nFrieling-Reuss EH. Comparative analysis of the visual and refractive outcomes of an aspheric diffractive intraocular lens with and without toricity. J Cataract Refract Surg. 2013;39(10):1485–93.\nBrito P, Salgado-Borges J, Neves H, et al. Light-distortion analysis as a possible indicator of visual quality after refractive lens exchange with diffractive multifocal intraocular lenses. J Cataract Refract Surg. 2015;41(3):613–22.\nChang JS, Chan VK, Ng JC, Law AK. Visual performance after bilateral implantation of a four-haptic diffractive toric multifocal intraocular lens in high myopes. J Ophthalmol. 2016;2016:5320105.\nGruber E. Complications associated with spin-cast soft contact lenses. Ophthalmology. 1979;86(6):1124–9.\nGuan JJ, Kramer GD, MacLean K, et al. Optic replacement in a novel modular intraocular lens system. Clin Exp Ophthalmol. 2016;44(9):817–23.\nMacLean KD, Werner L, Kramer GD, et al. Evaluation of stability and capsular bag opacification of a new foldable adjustable intraocular lens. Clin Exp Ophthalmol. 2015;43(7):648–54.\nPortaliou DM, Grentzelos MA, Pallikaris IG. Multicomponent intraocular lens implantation: two-year follow-up. J Cataract Refract Surg. 2013;39(4):578–84.\nCarson D, Xu Z, Alexander E, et al. Optical bench performance of 3 trifocal intraocular lenses. J Cataract Refract Surg. 2016;42(9):1361–7.\n•• Cochener B, Vryghem J, Rozot P, et al. Clinical outcomes with a trifocal intraocular lens: a multicenter study. J Refract Surg. 2014;30(11):762–8. With 198 eyes (99 patients), this is one of the largest multicenter studies to date on a trifocal IOL, and details the advantages of adding a dedicated intermediate zone to two diffractive patterns. Advantages of the technology include good vision across distances and few reports of visual disturbances\nEsteve-Taboada JJ, Dominguez-Vicent A, Del Aguila-Carrasco AJ, et al. Effect of large apertures on the optical quality of three multifocal lenses. J Refract Surg. 2015;31(10):666–76.\n•• Jonker SM, Bauer NJ, Makhotkina NY, et al. Comparison of a trifocal intraocular lens with a +3.0 D bifocal IOL: results of a prospective randomized clinical trial. J Cataract Refract Surg. 2015;41(8):1631–40. One of the few studies comparing outcomes between bifocal and trifocal lenses (each implanted bilaterally in 28 patients). Mesopic contrast sensitivity was better in the bifocaul group, but spectacle independence was substantially higher in the trifocal group, and the defocus curve was better at intermediate vision with the trifocal\nCarballo-Alvarez J, Vazquez-Molini JM, Sanz-Fernandez JC, et al. Visual outcomes after bilateral trifocal diffractive intraocular lens implantation. BMC Ophthalmol. 2015;15:26.\nRuiz-Alcocer J, Madrid-Costa D, Garcia-Lazaro S, et al. Optical performance of two new trifocal intraocular lenses: through-focus modulation transfer function and influence of pupil size. Clin Experiment Ophthalmol. 2014;42(3):271–6.\nBilbao-Calabuig R, Llovet-Osuna F, Gonzalez-Lopez F, Beltran J. Nd:YAG capsulotomy rates with two trifocal intraocular lenses. J Refract Surg. 2016;32(11):748–52.\nLee S, Choi M, Xu Z, et al. Optical bench performance of a novel trifocal intraocular lens compared with a multifocal intraocular lens. Clin Ophthalmol. 2016;10:1031–8.\nKretz FT, Muller M, Gerl M, et al. Binocular function to increase visual outcome in patients implanted with a diffractive trifocal intraocular lens. BMC Ophthalmol. 2015;15:110.\nKretz FT, Breyer D, Diakonis VF, et al. Clinical outcomes after binocular implantation of a new trifocal diffractive intraocular lens. J Ophthalmol. 2015;2015:962891.\nRosa AM, Loureiro Silva MF, Lobo C, et al. Comparison of visual function after bilateral implantation of inferior sector-shaped near-addition and diffractive-refractive multifocal IOLs. J Cataract Refract Surg. 2013;39(11):1653–9.\nPlaza-Puche AB, Alio JL, Sala E, Mojzis P. Impact of low mesopic contrast sensitivity outcomes in different types of modern multifocal intraocular lenses. Eur J Ophthalmol. 2016;26(6):612–7.\n•• Garcia-Domene MC, Felipe A, Peris-Martinez C, et al. Image quality comparison of two multifocal IOLs: influence of the pupil. J Refract Surg. 2015;31(4):230–5. This details the effect on MTF in trifocal lenses at 3 different pupil diameters—3, 4, and 5mm. Having the varied diameter results is helpful in daily clinical practice\nde Wit DW, Diaz J, Moore TC, et al. Effect of position of near addition in an asymmetric refractive multifocal intraocular lens on quality of vision. J Cataract Refract Surg. 2015;41(5):945–55.\nChiam PJ, Quah SA. The refractive outcome of Toric Lentis Mplus implant in cataract surgery. Int J Ophthalmol. 2016;9(5):699–702.",{"EN":757},"The aim of this paper is to provide an overview of published literature evaluating new refractive intraocular lenses (IOLs). Six categories of refractive IOLs are either currently commercialized in various regions (notably Europe) or under investigation for the treatment of presbyopia. No single category has emerged as a clear market leader, re-emphasizing the need for surgeons to individualize their treatment approaches. The newest refractive IOLs provide good outcomes with minimal complications. However, the categories studied each have their own strengths and weaknesses. Despite advancements, there are still significant opportunities to meet the unmet refractive needs through additional research and development in intraocular lenses.",{"EN":759},"Refractive IOL Pipeline: Innovations, Predictions, and Needs",{"VOID":761},"10.1007\u002Fs40135-017-0150-3","2024-06-30T23:52:12.064+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40135-017-0150-3",[765,780],{"id":766,"sortIndex":19,"researcher":18,"roles":767,"affiliations":768,"properties":777},"ebf090f3-f710-48cc-b2ef-b6e083ec28d7",[128],[769],{"id":18,"sortIndex":19,"affiliation":770,"properties":18},{"id":771,"createTime":772,"updateTime":772,"relativeEntities":773,"slug":18,"properties":774,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"f23c640d-e61e-4108-958f-850702741127","2024-01-21T14:41:06.221+00:00",[],{"title":775},{"VI":776},"Commonwealth Eye Surgery, Lexington, USA",{"title":778},{"VI":779},"Gary N. 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Management of Tractional Retinal Detachments in Proliferative Diabetic Retinopathy",{"VOID":841},"10.1007\u002Fs40135-016-0096-x",[843],"EN","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs40135-016-0096-x",[846,865],{"id":847,"sortIndex":97,"researcher":18,"roles":848,"affiliations":849,"properties":860},"b20c34e4-8dc4-40f4-aa7d-fe66693702c0",[],[850],{"id":18,"sortIndex":19,"affiliation":851,"properties":18},{"id":852,"createTime":853,"updateTime":854,"relativeEntities":855,"slug":856,"properties":857,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"02d6619c-29de-4a6c-8fc4-c8e93d40bb2c","2024-04-13T11:37:23.439+00:00","2025-06-11T16:13:06.073+00:00",[],"Alkek-Eye-Center-Cullen-Eye-Institute-Baylor-College-of-Medicine-Houston-USA",{"title":858},{"EN":859},"Alkek Eye Center, Cullen Eye Institute, Baylor College of Medicine, Houston, 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Am J Ophthalmol. 2000;129:178–85.",{"doi":923},"10.1016\u002FS0002-9394(99)00322-0",{"id":18,"text":925,"url":18,"identifiers":926},"• Meleth AD, Carvounis PE. Outcomes of vitrectomy for tractional retinal detachment in diabetic retinopathy. Int Ophthalmol Clin. 2014;54(2):127–39. A great review paper on surgical management, complications, and outcomes of diabetic vitrectomy.",{"doi":927},"10.1097\u002FIIO.0000000000000021",{"id":18,"text":929,"url":18,"identifiers":930},"Charles S, Flinn CE. The natural history of diabetic extramacular tractional retinal detachment. Arch Ophthalmol. 1981;99(1):66–8.",{"doi":931},"10.1001\u002Farchopht.1981.03930010068003",{"id":18,"text":933,"url":18,"identifiers":934},"Diabetic Retinopathy Vitrectomy Study. Two-year course of visual acuity in severe proliferative diabetic retinopathy with conventional management. Diabetic Retinopathy Vitrectomy Study (DRVS) Report #1. Ophthalmology. 1985;92:492–502.",{"doi":935},"10.1016\u002FS0161-6420(85)34002-2",{"id":18,"text":937,"url":18,"identifiers":938},"Yang CM. Surgical treatment for diabetic retinopathy: 5-year experience. J Formos Med Assoc. 1998;97(7):477–84.",{},{"id":18,"text":940,"url":18,"identifiers":941},"Thompson JT, Auer CL, de Bustros S, Michels RG, et al. Prognostic indicators of success and failure in vitrectomy for diabetic retinopathy. Ophthalmology. 1986;93:290–5.",{"doi":942},"10.1016\u002FS0161-6420(86)33741-2",{"id":18,"text":944,"url":18,"identifiers":945},"Aaberg TM, Abrams GW. Changing indications and techniques for vitrectomy in management of complications of diabetic retinopathy. Ophthalmology. 1987;94:775–9.",{"doi":946},"10.1016\u002FS0161-6420(87)33528-6",{"id":18,"text":948,"url":18,"identifiers":949},"Hwang JC, Sharma AG, Elliott D. Fellow eye vitrectomy for proliferative diabetic retinopathy in an inner city population. Br J Ophthalmol. 2013;97:297–301.",{"doi":950},"10.1136\u002Fbjophthalmol-2012-302233",{"id":18,"text":952,"url":18,"identifiers":953},"Gündüz K, Bakri SJ. Management of proliferative diabetic retinopathy. Compr Ophthalmol Update. 2007;8(5):245–56.",{},{"id":18,"text":955,"url":18,"identifiers":956},"Williams DF, Williams GA, Hartz A, Mieler WF, et al. Results of vitrectomy for diabetic traction retinal detachment using the en bloc excision technique. Ophthalmology. 1989;96(6):752–8.",{"doi":957},"10.1016\u002FS0161-6420(89)32813-2",{"id":18,"text":959,"url":18,"identifiers":960},"Issa SA, Connor A, Habib M, Steel DH. Comparison of retinal breaks observed during 23 gauge transconjunctival vitrectomy versus conventional 20 gauge surgery for proliferative diabetic retinopathy. Clin Ophthalmol. 2011;20(5):109–14.",{"doi":961},"10.2147\u002FOPTH.S16414",{"id":18,"text":963,"url":18,"identifiers":964},"Park DH, Shin JP, Kim SY. Comparison of clinical outcomes between 23-gauge and 20-gauge vitrectomy in patients with proliferative diabetic retinopathy. Retina. 2010;30:1662–70.",{"doi":965},"10.1097\u002FIAE.0b013e3181d95261",{"id":18,"text":967,"url":18,"identifiers":968},"Kumar A, Duraipandi K, Gogia V, Sehra SV, et al. Comparative evaluation of 23- and 25-gauge microincision vitrectomy surgery in management of diabetic macular traction retinal detachment. Eur J Ophthalmol. 2014;24(1):107–13.",{"doi":969},"10.5301\u002Fejo.5000305",{"id":18,"text":971,"url":18,"identifiers":972},"Altan T, Acar N, Kapran Z, et al. Transconjunctival 25-gauge sutureless vitrectomy and silicone oil injection in diabetic tractional retinal detachment. Retina. 2008;28(9):1201–6.",{"doi":973},"10.1097\u002FIAE.0b013e3181853d3c",{"id":18,"text":975,"url":18,"identifiers":976},"Yamada K, Maeno T, Yamada M. Hybrid microincision vitrectomy surgery combined with 20-gauge silicone cannulas for use with 20-gauge horizontal scissors in diabetic tractional retinal detachment. Clin Ophthalmol. 2013;7:1559–63.",{"doi":977},"10.2147\u002FOPTH.S46486",{"id":18,"text":979,"url":18,"identifiers":980},"Oshima Y, Shima C, Wakabayashi T, et al. Microincision vitrectomy surgery and intravitreal bevacizumab as a surgical adjunct to treat diabetic traction retinal detachment. Ophthalmology. 2009;116:927–38.",{"doi":981},"10.1016\u002Fj.ophtha.2008.11.005",{"id":18,"text":983,"url":18,"identifiers":984},"Schoenberger SD, Miller DM, Riemann CD, et al. Outcomes of 25-gauge pars plana vitrectomy in the surgical management of proliferative diabetic retinopathy. Ophthalmol Surg Laser Imaging. 2011;42(6):474–80.",{"doi":985},"10.3928\u002F15428877-20110901-02",{"id":18,"text":987,"url":18,"identifiers":988},"Ozone D, Hirano Y, Ueda J, et al. 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DIY—smartphone slit-lamp adaptor. Journal MTM. 2014;3(1):16–22. \n                      https:\u002F\u002Fdoi.org\u002F10.7309\u002Fjmtm.3.1.4\n                      \n                    .",{"doi":1377},"10.7309\u002Fjmtm.3.1.4",{"id":18,"text":1379,"url":18,"identifiers":1380},"EyeWiki. Smart phoneography—how to take slit lamp photographs with an iPhone. Available at: \n                      http:\u002F\u002Feyewiki.aao.org\u002FSmart_Phoneography_How_to_\n                      \n                     take_slit_lamp_photographs_with_an_iPhone. Last Accessed 1 Oct 2017.",{},{"id":18,"text":1382,"url":18,"identifiers":1383},"Barsam A, Bhogal M, Morris S, Little B. Anterior segment slitlamp photography using the iPhone. J Cataract Refract Surg. 2010;36(7):1240–1. \n                      https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jcrs.2010.04.001\n                      \n                    .",{"doi":1384},"10.1016\u002Fj.jcrs.2010.04.001",{"id":18,"text":1386,"url":18,"identifiers":1387},"Lee WW. Slit lamp adapters turn smartphones into clinical cameras. Ophthalmology Web. Available at: \n                      http:\u002F\u002Fwww.ophthalmologyweb.com\u002FFeatured-\n                      \n                     Articles\u002F136817-Slit-Lamp-Adapters-turn-Smartphones-into-Clinical-Cameras\u002F. Last Accessed 1 Oct 2017.",{},{"id":18,"text":1389,"url":18,"identifiers":1390},"Gurram MM. Ophthalmic cell-phone imaging system: a costless imaging system. Can J Ophthalmol. 2013;48(5):135–9. \n                      https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jcjo.2013.06.007\n                      \n                    .",{"doi":1391},"10.1016\u002Fj.jcjo.2013.06.007",{"id":18,"text":1393,"url":18,"identifiers":1394},"WelchAllyn. iExaminer eye imaging for your iPhone. Available at: \n                      http:\u002F\u002Fwww.welchallyn.com\u002Fen\u002Fmicrosites\u002Fiexaminer.html\n                      \n                    . Last Accessed 1 Oct 2017.",{},{"id":18,"text":1396,"url":18,"identifiers":1397},"Russo A, Civili PS. A novel device to exploit the smartphone camera for fundus photography. J Ophthalmology. 2015;2015:1–5. \n                      https:\u002F\u002Fdoi.org\u002F10.1155\u002F2015\u002F823139\n                      \n                    .",{"doi":1398},"10.1155\u002F2015\u002F823139",{"id":18,"text":1400,"url":18,"identifiers":1401},"Russo A, Morescalchi F, Costagliola C, Delcassi L, Semeraro F. Comparison of smartphone ophthalmoscopy with slit-lamp biomicroscopy for grading diabetic retinopathy. Am J Ophthalmol. 2015;159(2):360–4. \n                      https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ajo.2014.11.008\n                      \n                    .",{"doi":1402},"10.1016\u002Fj.ajo.2014.11.008",{"id":18,"text":1404,"url":18,"identifiers":1405},"Navitsky C. The portable eye examination kit. Retina Today. 2013. Available at \n                      http:\u002F\u002Fretinatoday.com\u002F2013\u002F12\u002Fthe-portable-eye-examination-kit\n                      \n                    . Last Accessed 20 Sept 2017.",{},{"id":18,"text":1407,"url":18,"identifiers":1408},"Bastawrous A, Mathenge W, Peto T, Weiss HA, Rono H, Foster A, et al. The Nakuru eye disease cohort study: methodology & rationale. BMC Ophthalmol. 2014;14(1):60. \n                      https:\u002F\u002Fdoi.org\u002F10.1186\u002F1471-2415-14-60\n                      \n                    .",{"doi":1409},"10.1186\u002F1471-2415-14-60",{"id":18,"text":1411,"url":18,"identifiers":1412},"Bastawrous A, Giardini ME, Bolster NM, Peto T, Shah N, Livingstone IA, et al. Clinical validation of a smartphone-based adapter for optic disc imaging in Kenya. JAMA Ophthalmol. 2016;134(2):151–8. \n                      https:\u002F\u002Fdoi.org\u002F10.1001\u002Fjamaophthalmol.2015.4625\n                      \n                    .",{"doi":1413},"10.1001\u002Fjamaophthalmol.2015.4625",{"id":18,"text":1415,"url":18,"identifiers":1416},"Maamari R, Keenan J, Fletcher D, Margolis T. A mobile phone-based retinal camera for portable wide field imaging. Br J Ophthalmol. 2014;98(4):438–41. \n                      https:\u002F\u002Fdoi.org\u002F10.1136\u002Fbjophthalmol-2013-303797\n                      \n                    .",{"doi":1417},"10.1136\u002Fbjophthalmol-2013-303797",{"id":18,"text":1419,"url":18,"identifiers":1420},"Solanki K, Ramachandra C, Bhat S, Bhaskaranand M, Nittala MG, et al. EyeArt. Automated, high-throughput, image analysis for diabetic retinopathy screening. Invest Ophthalmol Vis Sci. 2015;56:1429.",{},{"id":18,"text":1422,"url":18,"identifiers":1423},"Rajalakshmi R, Arulmalar S, Usha M, Prathiba V, Kareemuddin KS, Anjana RM, et al. Validation of smartphone based retinal photography for diabetic retinopathy screening. PLoS One. 2015;10(9):e0138285. \n                      https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0138285\n                      \n                    .",{"doi":1424},"10.1371\u002Fjournal.pone.0138285",{"id":18,"text":1426,"url":18,"identifiers":1427},"• Lord RK, Shah VA, San-Filippo AN, Krishna R. Novel uses of smartphones in ophthalmology. Ophthalmology. 2010;117(6):1274–1274.e3. \n                      https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ophtha.2010.01.001\n                      \n                    . This letter was the first to report about the various use of smartphones as an educational tool in ophthalmology as well as its ability to capture images of the eye that can be shared digitally.",{"doi":1428},"10.1016\u002Fj.ophtha.2010.01.001",{"id":18,"text":1430,"url":18,"identifiers":1431},"• Bastawrous A. Smartphone fundoscopy. Ophthalmology. 2012;119(2):433–433.e2. \n                      https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ophtha.2011.11.014\n                      \n                    . This article was the first to describe using the camera’s flash as a coaxial light source and the smartphone as an indirect ophthalmoscope to capture retinal images.",{"doi":1432},"10.1016\u002Fj.ophtha.2011.11.014",{"id":18,"text":1434,"url":18,"identifiers":1435},"Ryan ME, Rajalakshmi R, Prathiba V, Anjana RM, Ranjani H, Narayan KMV, et al. Comparison Among Methods of Retinopathy Assessment (CAMRA) study: smartphone, nonmydriatic, and mydriatic photography. Ophthalmology. 2015;122(10):2038–43. \n                      https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ophtha.2015.06.011\n                      \n                    .",{"doi":1436},"10.1016\u002Fj.ophtha.2015.06.011",{"id":18,"text":1438,"url":18,"identifiers":1439},"Kim DY, Delori F, Mukai S. Smartphone photography safety. Ophthalmology. 2012;119(10):2200–1. \n                      https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ophtha.2012.05.005\n                      \n                    .",{"doi":1440},"10.1016\u002Fj.ophtha.2012.05.005",{"id":18,"text":1442,"url":18,"identifiers":1443},"Haddock LJ, Kim DY, Muka S. Simple, inexpensive technique for high-quality smartphone fundus photography in human and animal eyes. J Ophthalmol. 2013;2013:518479–5. \n                      https:\u002F\u002Fdoi.org\u002F10.1155\u002F2013\u002F518479\n                      \n                    .",{"doi":1444},"10.1155\u002F2013\u002F518479",{"id":18,"text":1446,"url":18,"identifiers":1447},"Myung D, Jais A, He L, Blumenkranz MS, Chang RT. 3D printed smartphone indirect lens adapter for rapid, high quality retinal imaging. J Mobile Tech Med. 2014;3(1):9–15. \n                      https:\u002F\u002Fdoi.org\u002F10.7309\u002Fjmtm.3.1.3\n                      \n                    .",{"doi":1448},"10.7309\u002Fjmtm.3.1.3",{"id":18,"text":1450,"url":18,"identifiers":1451},"Hong SC. 3D printable retinal imaging adapter for smartphones could go global. Graefes Arch Clin Exp Ophthalmol. 2015;253(10):1831–3. \n                      https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00417-015-3017-z\n                      \n                    .",{"doi":1452},"10.1007\u002Fs00417-015-3017-z",{"id":18,"text":1454,"url":18,"identifiers":1455},"Volk iNview fundus imaging: Available at: \n                      https:\u002F\u002Fvolk.com\u002Findex.php\u002Fvolk-products\u002Fophthalmic-cameras\u002Fvolk-inview\u002Finview.html\n                      \n                    . Last Accessed 20 Oct 2017.",{},{"id":18,"text":1457,"url":18,"identifiers":1458},"Ludwig CA, Murthy SI, Pappuru RR, Jais A, Myung DJ, Chang RT. A novel smartphone ophthalmic imaging adapter: user feasibility studies in Hyderabad, India. Indian J Ophthalmol. 2016;64(3):191–200. \n                      https:\u002F\u002Fdoi.org\u002F10.4103\u002F0301-4738.181742\n                      \n                    .",{"doi":1459},"10.4103\u002F0301-4738.181742",{"id":18,"text":1461,"url":18,"identifiers":1462},"Toy BC, Myung DJ, He L, Pan CK, Chang RT, Polkinhorne A, et al. Smartphone-based dilated fundus photography and near visual acuity testing as inexpensive screening tools to detect referral warranted diabetic eye disease. Retina. 2016;36(5):1000–8. \n                      https:\u002F\u002Fdoi.org\u002F10.1097\u002FIAE.0000000000000955\n                      \n                    .",{"doi":1463},"10.1097\u002FIAE.0000000000000955",{"id":18,"text":1465,"url":18,"identifiers":1466},"Sharma A, Subramaniam SD, Ramachandran KI, Lakshmikanthan C, Krishna S, Sundaramoorthy SK. Smartphone-based fundus camera device (MII Ret Cam) and technique with ability to image peripheral retina. Eur J Ophthalmol. 2016;26(2):142–4. \n                      https:\u002F\u002Fdoi.org\u002F10.5301\u002Fejo.5000663\n                      \n                    .",{"doi":1467},"10.5301\u002Fejo.5000663",{"id":18,"text":1469,"url":18,"identifiers":1470},"Suto S, Hiraoka T, Oshika T. Fluorescein fundus angiography with smartphone. Retina. 2014;34(1):203–5. \n                      https:\u002F\u002Fdoi.org\u002F10.1097\u002FIAE.0000000000000041\n                      \n                    .",{"doi":1471},"10.1097\u002FIAE.0000000000000041",{"id":18,"text":1473,"url":18,"identifiers":1474},"Wang A, Avallone J, Guyton DL. Head mounted digital camera for indirect ophthalmoscopy. Invest Ophthalmol Vis Sci. 2014;55:1606.",{},{"id":18,"text":1476,"url":18,"identifiers":1477},"Welch RJ, Nguyen QD. A novel approach to ophthalmic photography using a portable and versatile camera device. Invest Ophthalmol Vis Sci. 2015;56:4102.",{},{"id":18,"text":1479,"url":18,"identifiers":1480},"Hansen MB, Abràmoff MD, Folk JC, Mathenge W, Bastawrous A, Peto T. Results of automated retinal image analysis for detection of diabetic retinopathy from the Nakuru study. Kenya PLoS One. 2015;10(10):e0139148. \n                      https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0139148\n                      \n                    .",{"doi":1481},"10.1371\u002Fjournal.pone.0139148",{"id":18,"text":1483,"url":18,"identifiers":1484},"Maker MP, Noble J, Silva PS, Cavallerano JD, Murtha TJ, Sun JK, et al. Automated Retinal Imaging System (ARIS) compared with ETDRS protocol color stereoscopic retinal photography to assess level of diabetic retinopathy. Diabetes Technol Ther. 2012;14(6):515–22. \n                      https:\u002F\u002Fdoi.org\u002F10.1089\u002Fdia.2011.0270\n                      \n                    .",{"doi":1485},"10.1089\u002Fdia.2011.0270",{"id":18,"text":1487,"url":18,"identifiers":1488},"Tran K, Yates PA. Constructing a non-mydriatic point and shoot fundus camera for retinal screening. Invest Ophthalmol Vis Sci. 2012;53:3105.",{"doi":1489},"10.1167\u002Fiovs.12-10449",{"id":1491,"createTime":1492,"updateTime":1493,"relativeEntities":1494,"slug":1495,"properties":1496,"entityType":120,"verifyStatus":121,"verifyTime":1493,"verifyNote":122,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1505,"fullTextUrl":18,"authors":1506,"publicationType":173,"publisherRelationship":1535,"citationCount":18,"citationInfo":18,"publishDate":1567,"publishYear":652,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":209},"3587da27-489f-4188-a6d7-baf107b8022c","2024-01-18T00:43:10.454+00:00","2025-02-02T23:38:36.810+00:00",[],"OCT-in-the-Management-of-Diabetic-Macular-Edema",{"references":1497,"abstract":1499,"title":1501,"doi":1503},{"VOID":1498},"Ding J, Wong TY. Current epidemiology of diabetic retinopathy and diabetic macular edema. 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Randomized trial evaluating ranibizumab plus prompt or deferred laser or triamcinolone plus prompt laser for diabetic macular edema. Ophthalmology. 2010;117:1064–77.\nVirgili G, Menchini F, Dimastrogiovanni AF, Rapizzi E, Menchini U, Bandello F, Chiodini RG. Optical coherence tomography versus stereoscopic fundus photography or biomicroscopy for diagnosing diabetic macular edema: a systematic review. Invest Ophthalmol Vis Sci. 2007;48:4963–73.\nCatier A, Tadayoni R, Paques M, Erginay A, Haouchine B, Gaudric A, Massin P. Characterization of macular edema from various etiologies by optical coherence tomography. Am J Ophthalmol. 2005;140(2):200–6.\nMurakami T, Nishijima K, Akagi T, Uji A, Horii T, Ueda-Arakawa N, Muraoka Y, Yoshimura N. Optical coherence tomographic reflectivity of photoreceptors beneath cystoid spaces in diabetic macular edema. Invest Ophthalmol Vis Sci. 2012;53(3):1506–11.\n• Yohannan J, Bittencourt M, Sepah YJ, Hatef E, Sophie R, Moradi A, Liu H, Ibrahim M, Do DV, Coulantuoni E, Nguyen QD. Association of retinal sensitivity to integrity of photoreceptor inner\u002Fouter segment junction in patients with diabetic macular edema. Ophthalmology. 2013;120(6):1254–61. doi:10.1016\u002Fj.ophtha.2012.12.003.\nLee SN, Chhablani J, Chan CK, Wang H, Barteselli G, El-Emam S, Gomez ML, Kozak I, Cheng L, Freeman WR. Characterization of microaneurysm closure after focal laser photocoagulation in diabetic macular edema. Am J Ophthalmol. 2013;155(5):905–12.\nChen X, Zhang L, Sohn EH, Lee K, Niemeijer M, Chen J, Sonka M, Abràmoff MD. Quantification of external limiting membrane disruption caused by diabetic macular edema from SD-OCT. Invest Ophthalmol Vis Sci. 2012;53(13):8042–8.\nDiabetic Retinopathy Clinical Research Network, Bressler NM, Miller KM, Beck RW, Bressler SB, Glassman AR, Kitchens JW, Melia M, Schlossman DK. 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The relationship between foveal ischemia and spectral-domain optical coherence tomography findings in ischemic diabetic macular edema. Invest Ophthalmol Vis Sci. 2013;54(2):1080–5.\nChhablani JK, Kim JS, Cheng L, Kozak I, Freeman W. External limiting membrane as a predictor of visual improvement in diabetic macular edema after pars plana vitrectomy. Graefes Arch Clin Exp Ophthalmol. 2012;250(10):1415–20.\n• Kang SW, Park CY, HAM DI. The correlation between fluorescein angiographic and optical coherence tomographic features in clinically significant diabetic macular edema. Am J Ophthalmol. 2004;137(2):313–22.\nGallego-Pinazo R, Suelves-Cogollos AM, Dolz-Marco R, Arevalo JF, García-Delpech S, Mullor JL, Díaz-Llopis M. Macular laser photocoagulation guided by spectral-domain optical coherence tomography versus fluorescein angiography for diabetic macular edema. Clin Ophthalmol. 2011;5:613–7.\nQuerques G, Lattanzio R, Querques L, Del Turco C, Forte R, Pierro L, Souied EH, Bandello F. Enhanced depth imaging optical coherence tomography in type 2 diabetes. Invest Ophthalmol Vis Sci. 2012;53(10):6017–24.\nAdhi M, Duker JS. Optical coherence tomography—current and future applications. Curr Opin Ophthalmol. 2013;24(3):213–21.",{"EN":1500},"Diabetic macular edema (DME) is the most common cause of mild-to-moderate visual loss in diabetes. With the introduction of anti-vascular endothelial growth factor therapies in addition to the previously available medical and laser therapies, OCT has become the cornerstone in the diagnosis, monitoring, therapeutic selection, and gauging response to therapy in eyes with DME. A review of the recent literature shows numerous advancements in the way OCT scanning is used both to monitor DME and to guide the management of DME.",{"EN":1502},"OCT in the Management of Diabetic Macular Edema",{"VOID":1504},"10.1007\u002Fs40135-013-0019-z","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40135-013-0019-z",[1507,1523],{"id":1508,"sortIndex":19,"researcher":18,"roles":1509,"affiliations":1510,"properties":1520},"16224e75-9cd9-4bc2-89d5-f8f0871a6c65",[128],[1511],{"id":18,"sortIndex":19,"affiliation":1512,"properties":18},{"id":1513,"createTime":1514,"updateTime":1514,"relativeEntities":1515,"slug":1516,"properties":1517,"entityType":39,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"abe43473-8991-400d-9e41-30d7a698034f","2024-04-14T06:25:46.887+00:00",[],"New-England-Eye-Center-Tufts-Medical-Center-Tufts-University-School-of-Medicine-Boston-USA",{"title":1518},{"EN":1519},"New England Eye Center, Tufts Medical Center, Tufts University School of Medicine, Boston, USA",{"title":1521},{"VI":1522},"Nadia K. 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