bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mechanism of macular hole closure
Authors: REPPUCCI V 
Published: November 2013

AbstractPurpose: To outline the mechanism of closure in macular hole surgery: specifically the importance of deforming the fluid‐air interface at the edges of the macular hole. This will provide a basis for understanding of how vitrectomy effects macular hole closure. Successful macular hole closure occurs when a fluid interface contacts, and is deformed, by the edges of the hole; generating a “surface of tension” (force), which exceeds the “stiffness” of the retina, allowing for reapproximation of the hole edges along the inner retina. Mechanical barriers, such as posterior hyaloid or vitreous, may reduce the interface deformation and transmittal of these forces to the inner retinal surface; peeling ILM or manipulating the hole edge may reduce the “stiffness” of the retina requiring less force to achieve closure. Larger bubbles increase the macular hole interface contact angle creating interface deformation, and force generation, at the hole edge over a greater range of eye position. Conclusion: Macular holes close by a "bridging" along the inner retinal surface with migration assisted by the capillary forces generated by fluid‐air interface deformation at the edges of the macular hole.
Update on ocular surface disorders in aniridia
Authors: BREMOND‐GIGNAC D 
Published: November 2013

AbstractAniridia is a rare bilateral ocular disorder occurring at a frequency of approximately 1 in 80 000. Aniridia is a panophthalmic disease. About one third of these aniridia are sporadic, with many variable expressivities of the features. PAX6 gene anomalies with 11p13 mutations or deletion are involved in aniridia. PAX6 mutations result in alterations in corneal cytokeratin expression, cell adhesion and glycoconjugate expression. Ocular anomalies in aniridia commonly associates cataract, glaucoma, nystagmus, ptosis and ocular surface. Mechanism of limbal stem cell insufficiency will be exposed and often correlated to reduced corneal sensitivity. Therapeutic options will be discussed.
Structure in glaucoma? Yes I can!
Authors: SUNARIC MEGEVAND G 
Published: November 2013

AbstractThis course is designed for young ophthalmologists and will give the opportunity to discuss aspects of the structure and structural changes of the optic nerve head and the retinal nerve fiber layer related to glaucoma and the alteration of the visual function related to this disease. In the last few years there is increasing evidence of the importance of structural measurements particularly early in the disease, and combining information from structure and function can significantly improve detection and assessment of glaucoma progression. Different tools and new technologies for measuring structural changes will be discussed in details such as stereo‐ photographs, HRT, GDx and OCT.
Retinal oximetry methodology
Authors: HARDARSON S 
Published: November 2013

AbstractDisturbances in retinal oxygenation are believed to play an important role in several eye diseases, such as retinal vessel occlusions, diabetic retinopathy and retinopathy of prematurity. Non‐invasive measurements of retinal oxygenation are important for better understanding of disease mechanisms and the technology will hopefully, in the near future, aid in management of the diseases. The technology for retinal oximetry has been developed in the past years and decades and the current oximeters are sensitive to changes in oxygen saturation and give repeatable results. Studies have confirmed differences in retinal vessel oxygen saturation in various eye diseases. Further studies of retinal oxygenation will benefit from development of the methodology. This includes hardware and software development but also standardisation of measurement techniques with the current instruments and better understanding of confounding factors.
Commercial interest
Determination of macular pigment
Authors: BERENDSCHOT T 
Published: November 2013

AbstractIn 1994 ago Seddon et al. observed an inverse association between a diet with a high content of the carotenoids lutein and zeaxanthin, and the prevalence of age‐related macular degeneration. This finding triggered an interest in the macular pigment, since it is solely composed of these two carotenoids. Macular pigment is concentrated in the central area of the retina along the axons of the cone photoreceptors. There are some plausible arguments to assume it exerts a protective effect in the retinal area: It acts as a blue light filter, absorbing between 390 and 540 nm, thereby decreasing chances for photochemical light damage. In addition, macular pigment is capable of scavenging free radicals. In this talk all existing measurement techniques will be discussed to determine the macular pigment optical density and its spatial distribution.
In vivo cell‐scale imaging of the human retina by adaptive optics
Authors: PAQUES M 
Published: November 2013

AbstractDiagnosis and monitoring of retinal diseases, the most important causes of blindness in developed countries, is largely based on accurate imaging of the retina. We have been using a flood imaging, commercially available AO camera (rtx1 from ImagineEye) to examine a variety of retinal diseases. Geographic atrophy can be detected at a very early stage under the form of patches of depigmented RPE filled with numerous clumps of melanin. Time‐lapse imaging show the progression of atrophy at a very small spatial and temporal scale, as well as the motion of melanin clumps within and outside atrophic areas. Diabetic microaneurysms can be distinguished from hemorrages. Epiretinal membranes can be observed under the form of small star‐like hyperreflective spots. Finally, parietal remodelling of small arteries following arterial hypertension can be detected, which may provide a novel quantitative biomarker. To sum up, while AO imaging was originally used for photoreceptor imaging, its scope is now extending. AO fundus imaging will probably establish itself as a reference methodology for early detection and monitoring of a variety of retinal diseases.
Signs and symptoms of uveitis
Authors: NERI P , CAPUANO V , PIRANI V , ARAPI I , MARIOTTI C , GIOVANNINI A 
Published: November 2013

AbstractUveitis is a potentially sight‐threatening disease and can be categorized into: anterior, intermediate, posterior, and panuveitis. The onset of uveitis can be either acute or insidious, involving one or both eyes. The commonest ocular symptoms are: blurred vision, ocular pain, photophobia and floaters, depending on the type of uveitis. Posterior uveitis is usually associated with vitritis. Anterior chamber cells and flare should be graded according to standardized uveitis nomenclature (SUN) working group. Binocular indirect ophthalmoscopy (BIO) score is used to grade vitreous involvement. Vitreous changes may comprehend: vitreous hemorrhage, vitreous strands, and vitreous traction. A further classification of posterior uveitis depends on the primary site of inflammation, which can identify: retinitis, choroiditis, retinochoroiditis, and chorioretinitis. Posterior pole uveal involvement can be: focal, multifocal, and placoid. Retinal vasculitis can be associated with several sub‐types of posterior uveitis. Uveitis can present several complications such as, anterior and posterior synechiae, which can lead to uveitic glaucoma, cystoid macular oedema, retinal and choroidal neovascularizations, and retinal ischemia.
Laboratory work‐up and specialized investigations
Authors: PLEYER U 
Published: November 2013

AbstractBased on the anatomical involvement of the eye intraocular inflammation is classified into anterior, intermediate, posterior and panuveitis. All subtypes of uveitis are potentially related to infectious and noninfectious etiologies. This presentation will assist the participants in accurately diagnosing uveitis in a step latter approach including physical and laboratory investigations. In addition, a tailored approach based on confounding clinical observations with specialized investigations will help to further differentiate clinical entities. In cases of suspected intraocular infections the option of intraocular fluid evaluation for antibody testing and polymerase chain testing against the causative agent will be presented. Taken together, this part of the course will provide a rational decision‐making strategy for diagnosis of patients with uveitis.
Therapeutic management of uveitis
Authors: DICK A 
Published: November 2013

AbstractThis talk will overview the contemporary therapeutic approaches to treatment of non‐infectious non‐infective ocular inflammatory disease. Treatment of non‐infectious uveitis has over past 15 years expanded from the use of traditional therapies including corticosteroids and immunosuppressants to the deployment of targetting the immune response with biologic therapies with monoclonal antibodies and immunoadhesins. Such use will be exemplified with case reports during the talk. Evidence of efficacy of immunosuppressants in the treatment of uveitis, the role of predicting steroid responsiveness, the use of monotherapy with immunosuppression and finally the pathways and evidence of success of biologic therapy will be provided.
The initial consult
Authors: SPILEERS W 
Published: November 2013

AbstractPatients with unvoluntary eye movements frequently consult an ophthalmologist. A correct diagnosis of the type and etiology is important. A clinical approach with selected technical examinations is mandatory for a correct diagnostic approach. Isolated ophthalmological and combined neurological elements can be identified to guide the further approach. Conclusions A practical work‐up of a patient presenting with nystagmus will be presented. Frequently the collaboration with the neurologist is important.
The mechanisms of the action of omega‐3s in the retina
Authors: ACAR N 
Published: November 2013

AbstractAge‐related Macular Degeneration (AMD) is the leading cause of visual loss in Western countries after the age of 50y. Based on large‐scale epidemiologic studies, it appears now as evident that omega‐3 polyunsaturated fatty acids (PUFAs) provide benefits in preventing both, early and late stages of AMD. The aim of this paper is to summarize the knowledge about the biological mechanisms by which omega‐3 PUFAs may be protective for the retina. The content of this presentation will range from biochemical data about the occurrence of omega‐3 PUFAs in retinal cell membranes to results from cellular and animal studies showing that omega‐3 PUFAs can influence processes involved in signal transduction, oxidative stress, apoptosis or inflammation.
New matrix therapy in chronic corneal ulcers resistant to conventional therapies
Authors: HUGNY LARROQUE C , DERRIEN S , COCHENER B 
Published: November 2013

AbstractPurpose To determine the efficacy of a new ophthalmologic solution based on ReGeneraTing Agent technology (RGTA, Cacicol®) in the therapy of chronic corneal ulcers resistant to conventional therapies.Methods This study included 20 patients with chronic corneal ulcers. There were various etiologies:two due to basic chemical burns,two neurotrophic keratitis, one Moreen ulcer, one pseudo‐Mooren, three on IntraCorneal Ring, nine on 9 grafts (one endothelial and 8 penetrating keratoplasties, one post surgery. All patients were previously treated with classical lacrymal substitutes, one with topical ciclosporine, corticoids, and/or A vitamin ocular ointment, and/or one/several amniotic membrane graft. Patients were treated with Cacicol® at a dose regimen of one drop daily every 2 or 3 days for one to three months. The primary outcome measure was healing. The ulcer’s diameter was measured at day 8,then once a month for 3 months.Results Complete healing was observed for 13 patients, i.e. a cure rate of 65 %. For other patients, 6 failures (30%) and one improvement without complete healing (5%) were reported. In the healed group, time of reparation was : 4 in day 8, 4 in one month and 5 in 3 months.Conclusion Cacicol was effective in the treatment of chronic corneal ulcers resistant to conventional therapies. Its efficacy remains to be proven in randomized double‐blind studies.
A RHO kinase inhibitor, AMA0526 improves corneal wound healing after alkali burn injury
Authors: SIJNAVE D , HOLLANDERS K , VAN BERGEN T , VAN DE VELDE S , VANDEWALLE E , MOONS L , STALMANS I 
Published: November 2013

AbstractPurpose The aim of this study was to investigate the efficacy of a locally active ROCK‐inhibitor AMA0526 (Amakem NV) on corneal wound healing induced by alkali burn in an in vivo mouse model.Methods Swiss mice were divided randomly into 3 groups after chemical cauterization of the cornea by alkali. Topical treatment was initiated after the injury and given once daily. All groups received 0.1% of the active ROCK‐inhibitor AMA0526 topical in one eye and vehicle, bevacizumab (2.5%) or dexamethasone (0.1%) in the contralateral eye. A forth group received no treatment and was used as control. Corneal opacity and corneal neovascularization were graded every other day according to a 0‐4 scoring. Blood vessel formation and corneal leukocytes infiltration after injury were assessed by immunohistochemistry.Results Both corneal opacity and neovascularization were reduced after AMA0526 treatment compared to the vehicle treated eye. Infiltration of inflammatory cells and blood vessel formation were significantly inhibited at day 7. AMA0526 treated mice showed significant reduced corneal opacity and inflammation compared to mice treated with bevacizumab. AMA0526 proved to be as efficient as dexamethasone in reducing excessive corneal wound healing.Conclusion Targeting ROCK with a local ROCK inhibitor, AMA0526 is efficacious in improving and preventing corneal opacity and neovascularization after alkali burn. The results presented indicate that ROCK is an appealing target to treat and prevent corneal scarring and neovascularization and illustrate the potential therapeutic benefits of the local ROCK inhibitor, AMA0526.
Experimental evidence of fluid secretion of rabbit lacrimal gland ductal epithelia
Authors: TOTH‐MOLNAR E , KATONA M , FACSKO A , VENGLOVECZ V , NEMETH L , HEGYI P 
Published: November 2013

AbstractPurpose Authors developed a novel lacrimal gland (LG) duct isolation technique earlier (IOVS, 2007; 48:3746‐3755) which makes possible to obtain more information on the function and regulation of LG ductal cells. The role of LG ductal epithelium on fluid secretion is unknown. The aim of the present study was to investigate LG ductal fluid secretion by means of measurement of fluid secretion evoked by different agonists.Methods Experiments were performed on isolated rabbit LG interlobular duct segments maintained in short term culture. The ends of the ducts sealed after overnight incubation forming a closed luminal space. Fluid secretion into closed intraluminal space as swelling response was analyzed using bright field videomicroscopy technique.Results The secretory response to carbachol or to forskolin stimulation was measured in HEPES buffered and in HCO3‐/CO2‐ buffered solutions. Carbachol initiated ductal swelling. This result proves the cholinergic effect‐evoked ductal fluid secretion. Fluid secretion was biphasic consisting of a continuous swelling in the first 5 minutes followed by a plateau phase. Secretory rates did not show a substantial difference measured in HEPES and HCO3‐/CO2 ‐buffered solutions. In contrast to the biphasic effect of carbachol, forskolin stimulation resulted in a rapid, continuous swelling response. The secretory effect of forskolin did not differ in HEPES and HCO3‐/CO2‐buffered solutions.Conclusion Fluid secretion of LG ductal cells induced by carbachol and by forskolin stimulations strongly supports the hypothesis, that LG ductal system is actively involved in lacrimal fluid secretion. Our results provide the first experimental evidence of secretory function of this epithelium.
Pharmacological strategies related to ocular neuroprotection
Authors: GARHOFER G 
Published: November 2013

AbstractOcular neuroprotection is a novel approach in the treatment of eye diseases, aiming to prevent or at least slow down loss of retinal neurons to avoid disease progression. Although ocular neurodegenerative diseases differ in their pathogenetic properties and risk factors from cerebral diseases, mechanisms behind neurodegeneration and cell death show similarities. As such, several new anti‐apoptotic agents, targeting the different mechanisms to induce neuronal cell death have been introduced in the last years. These mechanisms include but are not limited to excitotoxicity, oxidative stress and subclinical inflammation. From a clinical side of view the most commonly used target for neuroprotecive therapy in the past was glutamate excitotoxicity. As glutamate excitotoxicity is among the most important mechanisms to trigger cell death, much emphasis has been put into the development of glutamate antagonists. However, the clinical results of interventions studies fell short of expectations and other strategies came into focus of research. The talk aims to summarize the most promising pharmacological neuroprotective strategies.
Infectious uveitis
Authors: PLEYER U 
Published: November 2013

AbstractThe differential diagnosis of infectious uveitis is broad and an essential step in any initial work‐up. Underlying organisms include all types of infectious agents. The more common infectious causes of uveitis include viral causes, toxoplasmosis, syphilis, tuberculosis and endogenous endophthalmitis that will be covered in this course. Based on clinical features further diagnostic tools will be discussed and critically reviewed. In particular newer evolving techniques in the investigations will be included, e.g. intraocular fluid evaluation for polymerase chain testing for the genome and antibody testing against the causative organisms.
White dot syndromes
Authors: HERBORT C 
Published: November 2013

Abstract"White dot syndromes" (WDS)is a term introduced around 1995 to describe posterior uveitis syndromes that were poorly understood such as MEWDS, APMPPE, multifocal choroiditis (MFC), serpiginous choroiditis (SC), birdshot retinochoroiditis (BRC) and many others depending on the extension with which the term is used. Unfortunatelly the term is of no utility as it is purely based on the the white dots most posterior uveitis exhibit and as it emcompasses entities that look alike but have nothing in common as far as mechanism is concerned. Thanks to indocyanine green angiography (ICGA) it became possible to get away from this pot‐pourri terminology and allowed to sort out choroiditis entities according to the pathophysiological mechanism subdividing choroiditis into diseases of the choriocapillaris (primary choriocapillaritis) including MEWDS, APMPPE, MFC, SC and atypical and overlapping entities on one side and stromal choroiditis on the other side including Vogt‐Koxanangi‐Harada disease (VKH), BRC, sarcoid and tubercular choroiditis. The appraisal of these diseases and the rationale of their new classification will be explained and examples will be given to illustrate this new comprehensive approach that should make WDS obsolete.
Pure neuroretinal dysfunction in diabetic retinopathy occurring prior to endothelial and vascular damage
Authors: REIS A , MATEUS C , MELO P , FIGUEIRA J , CUNHA‐VAZ J , CASTELO‐BRANCO M 
Published: November 2013

AbstractPurpose To search for independent neural damage in type 1 diabetic patients, in the pre‐retinopathy stage of diabetic retinopathy (DR), with preserved blood‐retinal barrier (BRB) permeability.Methods BRB permeability was objectively measured by Vitreous Fluorometry. Neuroretinal function was assessed by standard multifocal electroretinography (mfERG) and by chromatic/achromatic contrast sensitivity (CS) (CCT‐Cambridge Research Systems and Frequency Doubling Perimetry‐FDT, Zeiss), in a sample of 42 patients (age=26.6±5.3years) with preserved visual acuity (VA), divided into two groups:1.With no clinical signs of DR and normal BRB permeability (n=23eyes; VA=1.11±0.15); 2.With BRB breakdown, with no clinical signs of DR or with mild nonproliferative DR (n=61eyes; VA=1.09±0.15). These data were compared with those obtained in 25 age‐matched controls (27.4±5.8years). Non‐parametric statistical analysis was performed at a significance level of p<0.05.Results Amplitude of neurophysiological responses was significantly decreased in all eccentricity rings in both patients groups, when compared with controls (p<0.0001). Changes in implicit time were also found in cases with preserved BRB (p<0.02). Impaired CS along the main chromatic axes was observed (p<0.03) and achromatic thresholds were also different between controls and both clinical groups (p<0.004). No correlation was found between the BRB permeability and the psychophysical and electrophysiological measurements (group with preserved BRB), confirming a lesion mechanism that is independent from endothelial/vascular changes.Conclusion Retinal neuronal changes may occur in type 1 diabetes, independently of the breakdown of the BRB or onset of vasculopathy.
Exudative retinal detachment
Authors: DE SMET MD 
Published: November 2013

AbstractActive and passive retinal water transport mechanisms must be altered to cause an exudative detachment (ED). The retinal pigment epithelium (RPE) plays a critical role. Whenever the RPE pump becomes dysfunctional or its adhesive force is overcome, ED can follow. ED can occur in the presence of reduced pump function with excessive traction as can occur diabetes, retinal detachments (mainly pseudophakic) in the absence of a tear, or certain inflammatory disorders such as pars planitis. Thickened subretinal fluid can compromise the RPE pump as is seen with persistent serous detachments following buckle surgery. However, most cases are due to a generalized depression of the RPE pump coupled with excessive fluid influx ‐ idiopathic and steroid related central serous retinopathy, age related macular degeneration, idiopathic polypoidal vasculopathy, retinal vein occlusion, uveitis (sympathetic and VKH). Treatment will depend on the cause ‐ may include an attempt to stimulate pump function or the elimination of tractional components. In many cases, identifying the presence of an ED leads to a conservative follow‐up with excellent outcomes.
Herpes and Zoster infections update
Authors: LABETOULLE M , ROUSSEAU A 
Published: November 2013

AbstractHerpes Simplex Virus (HSV) and Varicella‐zoster Virus (VZV) are the two leading causes of infectious acquired amblyopia. After a phase a latent infection in the trigeminal ganglia, they may reactivate to eventually infect the cornea. There are several common features of keratitis due to HSV or VZV. The most frequent forms involve the epithelium, with 4 different patterns: punctuate and diffuse, dendritic, geographic, and marginal. Stromal forms of keratitis are mostly non‐necrotic, and usually resolve with a combination of oral antivirals and topical steroids. In contrast, a necrotic stromal keratitis usually requires intravenous antiviral therapy. Endothelial forms of HSV/VZV keratitis are far less frequent. Three different types may be observed: disciform, diffuse or linear, the latter one being the most aggressive. After the acute phase of HSV/VZV keratitis, preventive treatment with oral antivirals may be given according to the clinical history. For VZV, a vaccine is now available. Its effectiveness has been shown for the prevention of herpes zoster ophthalmicus, but its place in patients with recurrent VZV infections of the eye remains to be clarified.