bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibodies, MRI and unusual clinical features of NMO
Authors: DE SEZE J 
Published: August 2014

AbstractNeuromyelitis optica (NMO) is a rare disease including both optic neuritis and myelitis together or successively. Recently, a specific antibody named anti‐NMO has been discovered allowing a more precise diagnosis. This antibody is directed againbst abti‐AQP4 protein, a watter chanel protein. This discovery enlarged the spectrum of NMO to patients with recurrent optic neuritis and positive antibodies, now include in the NMO spectrum disorder (NMOSD). MRI frequently shows intense hypersignal of optic nerve and spinal cord with normal or atypical brain MRI for MS. NMO is frequently associated with other auto‐immune diseases such as Sjogren syndrome ou lupus. The outcome of the disease may be severe with blindness and para/tetraplegia implying that an intensive treatment should be propose as soon as the diagnosis has been made.
Tale of lysosome in RPE cells and in the pathogenesis of AMD
Authors: SINHA D 
Published: August 2014

AbstractIn RPE cells, the lysosomal system is a crucial regulator of both phagocytosis and autophagy. We have recently shown in the Nuc1 rat (a spontaneous mutation in the Cryba1 gene encoding for betaA3/A1‐crystallin) and in mice lacking betaA3/A1‐crystallin specifically in the RPE, that impaired lysosomal clearance decreases both autophagy and phagocytosis. This leads to the accumulation of lipofuscin within RPE cells, subretinal lesions in the posterior pole, and deposits between the RPE and Bruch’s membrane. It is likely that disturbances in the homeostasis of RPE cells, due to accumulation of undegraded intracellular material in the mice lacking betaA3/A1‐crystallin, trigger a para‐inflammatory response in an attempt to restore normal RPE function. Severe or prolonged impairment of lysosomal‐mediated clearance may also convert para‐inflammation to chronic inflammation, leading to retinal degeneration. Several studies support the hypothesis that the immune system is involved in the pathogenesis of AMD, in concert with, or in addition to, other factors. We have generated a genetically engineered mouse model that exhibits a slowly progressing form of AMD‐like pathology associated with inefficient lysosomal clearance.
Therapeutic approaches‐ aflibercept first french results of intravitreous aflibercept for active naïve polypoidal choroidal vasculopathy‐6 months follow up
Authors: DIRANI A , COSCAS F , COSCAS G , SEMOUN O , SOUIED E 
Published: August 2014

AbstractTo evaluate the anatomical and functional effect of intravitreous aflibercept (IAI) for the treatment of polypoidal choroidal vasculopathy (PCV) associated with exudative AMD, with a follow up of 3 months.This is a case series study that included 22 eyes with active PCV. All eyes were naive to treatment before inclusion in the study. The treatment protocol consisted of an induction phase of 3 IAI, then the injections were done every 2 months. A complete ophthalmologic workup was done for every patient and included: best corrected visual acuity (ETDRS scale), Fluorescein and Indocyanine Green Angiography, EDI‐OCT (Spectralis HRA+OCT®, Heidelberg engineering). All results were analyzed at inclusion and at 3 months.The mean age was 76.3 +/‐ 11.3. Male to female ratio was 1. The BCVA improved at 3 months (0.58 +/‐ 0.39logMAR vs 0.20±0.27 log MAR; p= 0.01). The patients gained a mean of 15 letters in the BCVA. No loss of BCVA was noted in any patient. The central macular thickness improved significantly from 376.77+/‐99.54 to 279.80±82.53 at 3 months (p= 0.043).The polyp’s regression started at one month after the first injection and was almost complete at 3 months. A significant improvement of retinal pigment epithelium detachment
Modulators for autophagy: implications for ageing and neurodegeneration
Authors: BEHL C 
Published: August 2014

AbstractAutophagy is a key player in the cellular proteostasis and a degradative pathway that sequesters and transports cytosolic cargo in autophagosomes to lysosomes. This process is dependent on complex membrane dynamics and its deregulation leads to a disturbance in proteostasis contributing to several diseases, including neurodegeneration. In addition to selective macroautophagy pathways such as the "Bag3‐mediated selective macroautophagy" different key regulator proteins control the canonical autophagy process. In an RNAi screen in C. elegans designed to identify novel modifiers of proteostasis, we isolated RBG1, the homolog of mammalian RAB3GAP1 and found that the RAB3GAP complex previously known to be involved in cellular endocytosis is required for basal and rapamycin‐induced autophagy. The analysis of such distinct key modulators of macroautophagy will help to understand the involvement of the degradation pathways in ageing and disease.
Autophagy in retina and axonal degeneration
Authors: BOYA P 
Published: August 2014

AbstractAutophagy is a catabolic pathway that degrades and recycles intracellular components inside lysosomes to maintain cell homeostasis. This pathway is essential to keep postmitic cells such are neurons free of garbaje and damaged cell components. There are several types of autophagy. During macroautophagy, simply called autophagy, parts of the cytosol and even entire organelles are engulfed in an autophagosome that will finally fuse with a lysosome where degradation will take place. In chaperone mediated autophagy (CMA) proteins harbouring a specific aminoacid sequence will be recognized by a chaperone Hsc70 and delivered inside lysosomes thanks to the lysosomal receptor LAMP‐2A. The role of autophagy in the physiology and pathology of the retina is just starting to be investigated. We have demonstrated the cytoprotective role of autophagy in a model of optic nerve axotomy in mice. We show that autophagy‐deficient animals have reduced number of surviving RGCs after ONT and that pharmacological induction of autophagy delays neuronal cell death. We have also observed a reduction in the levels of autophagy during retinal aging and Atg5 deficient animals in the retina show increased photoreceptor death and reduced scotopic vision. Unexpectedly CMA seems to increase in these conditions and we postulate that this is a compensatory response to sustain cell survival. Thus balance in autophagic pathways plays important roles to maintain retinal homestasis.
Autoimmunity and neuroprotection in glaucoma
Authors: GRUS F 
Published: August 2014

AbstractImmunoproteomics could play a significant role in glaucoma. There are many hints for an involvement of autoantibodies in the pathogenesis of the disease. This paper will address the changes in immunoreactivities in glaucoma pateints. If will further demonstrate the findings about immunological changes in human glaucomatous retinae and the possible involvement of cellular components. Furthermore, the paper will address the clinical use for diagnosis and new approaches to neuroprotection in future.
Electron microscopic evaluation of the surfaces of variable depth lenticules in SMILE cases
Authors: OSMAN I 
Published: August 2014

AbstractPurpose Evaluating lenticule surfaces using electron microscopy in deeper corneal layers and comparing them to the superficial ones. This aims at determining the possibility of preserving the stronger superficial layers in the cornea by removing deeper lenticules in SMILE cases while attaining the same visual results and with the same ease.Methods 40 eyes underwent SMILE refractive procedure using femtosecond laser by VisuMax ( Zeiss Meditech). 2 groups were used, one with lenticules at 100 µm and the other with lenticules at 160 µm. Lenticules were immediately processed (fixed, dehydrated, dried and mounted with gold coating). JSM‐5300 scanning electron microscope was used for observations.Results Deeper lenticules had more irregular surfaces and were more difficult to dissect. Comparing the central and peripheral thickness of lenticules to the intended thickness was significantly more accurate in the superficial group. The visual results of the two groups were comparable. Surface irregularities were resulting from the break of bridges between the femtosecond cavities.Conclusion Energy settings still needs further adjustment to be able to create deeper predictable lenticules in SMILE cases
New concepts concerning the neural mechanisms of infantile strabismus and amblyopia
Authors: TEN TUSSCHER M 
Published: August 2014

AbstractInfantile strabismus results in a loss of binocularity in the primary visual cortex. Beyond the primary visual cortex, the contralateral eye dominates while the temporal retinal signal appears to lose influence. This may either be caused by inadequate retinotopic matching between the nasal and temporal retinal signals (e.g. albinism or agenesis of the corpus callosum), or the result of a lack of normal sensory input. Dominance of the crossing retinal signal might also explain the motor characteristics of infantile esotropia (asymmetric OKN, latent nystagmus, DVD). Only a normal binocular cortical signal will predominate over the evolutionary older, originally non‐binocular, retinal projections to the superior colliculi (CS) and the accessory optic system (AOS). Amblyopia seems to be the result of active suppression by the crossing ganglion cells of the non‐amblyopic eye. Early‐onset monocular deprivation is thought to produce competitive imbalance for synaptic sites, which in turn results in a reduced proportion of functionally binocular neurons.Amblyopia treatment may aim at an optimal binocular balance and pharmacological treatment after the critical period.
Amblyopia treatment trials
Authors: HOLMES JM 
Published: August 2014

AbstractRecent randomized clinical trials and observational studies conducted by the Pediatric Eye Disease Investigator Group, and other research teams, have led to an evidence‐based approach for treating anisometropic and strabismic amblyopia. Starting spectacle correction first, as optical treatment alone, results in resolution of amblyopia in at least a quarter of children. Starting low intensity treatment is the next reasonable step, offering parents a choice between 2 hours a day of patching the fellow eye or atropine drops to the fellow eye at the weekend. If amblyopia does not completely respond to these low‐intensity approaches, then more intense patching is warranted, such as patching 6 to 8 hours a day or changing the spectacle lens to plano while using atropine to increase penalization. We also have evidence that treating older children (13‐17 years old) has merit, particularly if not previously offered treatment. But despite these advances in treatment of amblyopia, one of our ongoing challenges is that a proportion of children are still left with residual amblyopia, so we continue to investigate alternative approaches such as oral levodopa as an adjunct to patching and a new treatment approach based on binocularity.
Genome‐wide association studies for the identification of keratoconus susceptibility regions
Authors: HYSI P 
Published: August 2014

AbstractConsensus seems to be building that most diseases are of complex nature and the result of interaction of a polygenic architecture with the environment. A great deal on the genetic architecture of the disease can be learned from population‐based and family studies. This presentation will explore the influence of heritable factors over keratoconus as well as shared genetic elements that influence both abnormal cornea and other phenotypic anomalies of the eye.
Coming back to the basics – overview on therapeutic contact lenses and scleral lenses
Authors: MELY R 
Published: August 2014

AbstractScleral lenses were introduced at the end of the 19th century but these first glass blown shells had a very limited success related to the corneal hypoxia they induced after a short wearing time. Therapeutic contact lenses (TCL) did not become widespread until the introduction of hydrogel lenses in the 1960s. The availability of high gas permeable silicone hydrogel materials (1999) was a major breakthrough and these lenses are now the most popular TCL used in everyday practice. Thanks to a better understanding of the scleral shape and the availability of high gas permeable materials, scleral lenses have made a significant comeback in recent years. These lenses rest on the sclera and are designed not to touch the cornea, creating a reservoir filled with fluid that prevents any desiccation and mechanical irritation of the cornea. Sclerals are often the only effective non‐surgical treatment option in a wide range of severe ocular conditions, including graft‐versus‐host disease, pellucid marginal degeneration, Stevens‐Johnson syndrome, ocular cicatricial pemphigoïd, severe dry eye, non‐healing epithelial defects.Scleral lenses dramatically improve the visual acuity and the quality of life of these patients.
Macular edema
Authors: LOEWENSTEIN A 
Published: August 2014

AbstractDiabetic macular edema (ME) is a severe complication of diabetic retinopathy (DR). The increasing worldwide prevalence of DR is fueling sustained efforts in devising new ways to prevent as well as to diagnose diabetic ME at an early stage in order to allow effective management to preserve or restore patient’s visual acuity. The extant knowledge of the pathophysiology underlying ME points to an interplay among systemic factors, retinal vascular dysfunction, chronic inflammation, angiogenic hyperactivity that promotes permeability and other pathological changes at cellular level, all of which may contribute to the breakdown of the blood‐retina barrier and accumulation of extracellular fluid, with subsequent leakage and ME formation. We overview the signs and symptoms which may help diagnose the pathology at different stages (reduced visual acuity, leakage from microaneurysms and nonperfusion) by assessing the role of imaging modalities such as FA and OCT in detecting these pathological changes.
Steroids
Authors: KODJIKIAN L 
Published: August 2014

AbstractDiabetic macular edema (DME) is the most common cause of moderate vision loss in working‐age individuals in developed countries. Corticosteroids reduce expression of VEGF and other permeability, providing good rationale for their use in DME. The first steroid used was the triamcinolone by intravitreal injection. Efficacy was good but the adverse events were rather important (elevated intraocular pressure being the most common). Different steroids implant with sustained ocular delivery are available. The Fluocinolone Acetonide for Macular Edema (FAME) studies permitted to the ILUVIEN® implant (190 µg) has received its marketing authorization approval in different European countries. It is indicated for the treatment of vision impairment associated with chronic DME, considered insufficiently responsive to available therapies. Dexamethasone Intravitreal Implant (OZURDEX®) provided long‐term vision improvement, with a mean of 4.1 injections over 3 years (phase III MEAD study). Its label is not yet obtained (March 2014). It safety profile was better or equivalent than that of steroids currently used in clinical practice. In summary, two platforms for sustained steroids drug delivery are available in DME.
Clinical cases
Authors: CREUZOT‐GARCHER C 
Published: August 2014

AbstractClinical cases of diabetic retinopathy with or without diabetic macular edema will be discussed with the audience. These cases will define the role and the pros and cons of different therapeutic options. Cases with macula edema with proliferative diabetic retinopathy, without diabetic retinopathy in phakic or pseudophakic patients will be presented.
Neuroprotection in the real world
Authors: KURYSHEVA N 
Published: August 2014

AbstractGlaucoma causes vision loss through the degeneration of retinal ganglion cells and their axons. Lowering IOP does not necessarily stop degeneration. Therefore neuroprotection is directed at neurons independently of its effects on IOP [1]. As the topical ocular hypotensive treatment is the main option in glaucoma nowadays, the direct neuroprotective effect of hypotensive eye drops is important. It has been postulated that PG analogues may have an IOP independent neuroprotective effect at clinically available intracameral concentration [2]. In vivo experiments demonstrated the neuroprotective properties of betaxolol [3]. The recent study of LoGTS demonstrates that the α2 agonist brimonidine may have a beneficial effect on visual function independent of IOP lowering [4]. Our recent research revealed the high antioxidant activity of fixed combinations of carboanhydrase inhibitors with timolol [5]. References 1. Cheung W, Guo L, Cordeiro MF. Optom Vis Sci. 2008;85:406‐416. 2. Yamagishi R., et al. Exp. Eye Res. 2011;93:265‐270. 3.Osborne NN, et al. Brain Res. 1997;751:113–123. 4.Krupin T, et al. 2011;151(4):671– 681. 5.Kurysheva N.I., et al. Rus. Ophthalm. J. 2013;6(2):41 – 45.
Wavefront Aberrometry: from basics to daily practice
Authors: GICQUEL J 
Published: August 2014

AbstractQuality of vision is a new comprehensive set of measures that determines visual performance at near, far and in variable light conditions. Good vision is no longer defined by 20/20 vision. The necessity of evaluating vision beyond Snellen acuity has led clinicians and vision scientists to utilize contrast sensitivity, wavefront aberrometry and straylight measurement in most clinical trials related to vision. Recently,the advent of 3D movies and 3D TVs brought us new challenges regarding 3 3 Dimensional Quality of Vision. In this course, experts will share with you their experience on this new frontier of modern ophthalmology.
Cytokine gene expression and protein production in West Nile virus‐infected retinal pigment epithelium
Authors: MUNOZ‐ERAZO L , MADIGAN M , KING NJC 
Published: August 2014

AbstractPurpose To investigate if West Nile virus (WNV) infection of human retinal pigment epithelium (RPE) cells induces differential expression of mRNA and proteins for cytokines important for leucocyte recruitment (e.g. CCL5) and integrity of the outer blood retinal barrier (BRB) (e.g. TNF).Methods Primary human RPE cells (P3‐5) were cultured until a complete monolayer was observed, and then infected with 1, 5 or 10 plaque‐forming units (p.f.u.) of WNV (Sarafend) for 24, 48 and 72hrs. Supernatants were collected for Luminex‐based cytokine assay. RNA was prepared from cells and processed for real‐time (RT)‐PCR. Pro‐inflammatory, leucocyte recruitment and viral defense cytokines and chemokines were studied.Results CCL5, IL8, IL6 (pro‐inflammatory) and IFNB1 (anti‐viral) showed increases in mRNA expression from 24 h post‐infection (p.i.) and protein levels from 48h p.i. However in WNV‐infected RPE, protein levels of VEGF and TNF were similar to mock‐infected cells, despite significant increases in mRNA (TNF 24 h p.i., p <0.05; VEGF 48 h, p<0.01). Interestingly, CCL2 mRNA and protein showed no change in expression post‐WNV infection at 24, 48 and 72hConclusion We previously observed that WNV induced transepithelial electrical resistance (TEER) changes in human RPE (outer BRB) after 48 hours, although the mechanisms(s) remain unclear. Studies in mice show that both TNF and CCL2 are important for blood‐brain barrier integrity and leucocyte recruitment following WNV infection. Surprisingly we find little or no effect on TNF or CCL2 expression in WNV‐infected RPE, suggesting alternate mechanisms operate in RPE post‐viral infection. Funding‐ NFMRI and NHMRC
Advanced glycation end‐products induced activation of NFkB and its suppression by different neurotrophic factors
Authors: BIKBOVA G , OSHITARI T , YAMAMOTO S 
Published: August 2014

AbstractPurpose To determine the effect of high doses of AGEs on neurite regeneration in isolated rat retinas, and the regenerative effects of different neurotrophic factors.Methods Retinal explants of 4 adult SD rats were three‐dimensionally cultured in collagen gel, and incubated in: 1) serum free control culture media; 2) 100 μg/ml glucose‐AGE‐BSA, glycolaldehyde‐AGE‐BSA, glyceraldehyde‐AGE‐BSA media; 3) glucose, glycol, glycer+100 ng/ml neurotrophin 4 (NT‐4)media; 4) glucose, glycol, glycer+100 ng/ml hepatocyte growth factor (HGF) media; 5)glucose, glycol, glycer+100 ng/ml glial cell line derived neurotrophic factor (GDNF) media; or 6) glucose, glycol, glycer+100 ng/ml tauroursodeoxycholic acid (TUDCA) media. After 7 days, the number of regenerating neurites were counted under a phase‐contrast microscope. The explants were immunostained for NFkB transcription factor. Statistical analyses were performed by one‐way ANOVA.Results In retinas incubated with AGEs, the number of regenerating neurites were fewer than in control. Neurotrophic factors increased the number of neurites, but more significantly in the NT4 group. The number of NFkB immunopositive cells was higher in retinas exposed to AGEs than in control (53,2 ± 7,2% vs.31,6 ± 16,08%,P = 0,0146). Neurotrophic factors decreased the number of immunopositives cell, but more significantly in the NT4 group.Conclusion High dose AGEs induce activation of NFkB and NT4 significantly suppresses this activation and enhances neurite regeneration in isolated retinas compared with other neurotrophic factors such as HGF,GDNF,and TUDCA.
Focal venous hypertension as a pathophysiologic mechanism for port‐wine stains and the Sturge‐Weber syndrome
Authors: PARSA C 
Published: August 2014

AbstractPurpose To provide an in‐depth re‐examination of assumed causes of tissue hypertrophy, port‐wine stains and the Sturge‐Weber and related syndromes to support an alternative unifying pathophysiologic mechanism of venous dysplasia producing focal venous hypertension with attendant tissue responses and to propose a novel etiological hypothesis for the venous dysplasia in these syndromes with supportive evidence.Methods Data from twenty patients with port‐wine stains was collected prospectively by the author in an institutional referral‐based practice. The literature was searched using Medline.Results Newly obtained dermatologic, corneal pachymetry, fundus ophthalmoscopic, ocular and orbital venous Doppler ultrasonography, and magnetic resonance imaging findings in patients with the Sturge‐Weber syndrome or isolated port‐wine stains, along with published data, reveal diffusely thickened tissues and neural atrophy in all areas associated with venous congestion.Conclusion Contrary to traditional understanding, signs and symptoms in the Sturge‐Weber and related syndromes, including both congenital and acquired port‐wine stains are shown to arise from effects of localized primary venous dysplasia or acquired venous obstruction rather than neural dysfunction, differentiating these syndromes from actual phacomatoses. Effects of focal venous hypertension are transmitted to nearby areas via compensatory collateral venous channels in the above conditions. Conclusion: A novel underlying etiology—prenatal venous thrombo‐occlusion—may be responsible for the absence of veins with persistence and enlargement of collateral circulatory pathways with data in the literature backing this offshoot hypothesis. The mechanism for isolated pathologic tissue