bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phaco it
Authors: Porteous Alastair 
Published: December 2019

AbstractNon‐compliance is a major factor of poor control of glaucoma eye disease. There are many reasons for this, including forgetfulness, difficulty with drop administration and intolerance from side effects. This presentation will focus on how to tackle this chronic problem using cataract surgery to stabilise the disease and lead to a better quality of life for patients. Minimally invasive glaucoma surgery (MIGS) techniques are becoming widely used for mild to moderate glaucoma. These techniques have an improved safety profile compared to more traditional filtration surgery. This presentation will cover how cataract surgery alone and cataract surgery combined with MIGS techniques, using surgical videos, personal experience and evidence from the literature, can be used to reduce drop burden, improve the control of the disease and improve non‐compliance.
Cataract type in mouse exposed to moderate doses of ionizing radiation depends on mouse age at irradiation
Authors: Pawliczek Daniel 
Published: December 2019

AbstractOne noxious agent for cataract formation is ionizing radiation (IR). For doses till or equal 2 Gy it is still unclear, whether opacification occurs and if, how cataract type depends on the animals age at irradiation. Wild‐type and heterozygous Ercc2+/‐ mice were whole‐body irradiated by 0.5 Gy, 1 Gy and 2 Gy of γ‐radiation (dose rate = 0.3 Gy/min), 10 weeks after birth (P70). Another cohort was exposed to 2 Gy, 2 days after birth (P2). All cohorts were investigated by optical coherence tomography (OCT) and eyes were collected for histology after death. OCT revealed frequent lens alteration in the mice irradiated at P2 and P70. These lesions were only subcapsular located in P70 mice and are dose‐dependent in size. Mice irradiated at P2 showed scattering structures within the posterior cortex, 8.5 mth after irradiation. At least 80% of the irradiated animals displayed at least mild posterior cortical cataracts. Histology of irradiated eyes (P70) unravelled the OCT‐detected lesions as cataractous accumulations of enlarged fibre cells, accompanied by subcapsular placed cells with nuclei. Lesions of P2 mice displayed no correlate to the in vivo data. Therefore, we conclude that IR leads to lens opacification in a dose‐dependent manner and its magnitude correlates strongly with age at irradiation. These results help to assess the sensibility of eye lenses to IR in case of exposure. The LDLensRad project received funding from Euratom in the framework of CONCERT, grant No 662287.
Anti‐glaucomatous medication and ocular surface
Authors: Sakellaris Dimitrios 
Published: December 2019

AbstractThe purpose of this talk is to explore the interaction between ocular surface disease (OSD) and anti‐glaucomatous medication, whether a preexisting OSD can affect the success of the anti‐glaucomatous medication in terms of discomfort and non‐compliance and whether the anti‐glaucomatous medication can initiate or worsen OSD.
Objective assessment of progressive macular changes in glaucoma
Authors: Normando Eduardo M. 
Published: December 2019

AbstractThe role of OCT macula scans in glaucoma has been extensively investigated. However, to date, only subjective and qualitative analyses can be performed for macula scans in glaucoma. We propose a novel method to objectively assess glaucoma progression based on the Longitudinal Analysis of the Poster Pole (LaPo). Forty eyes were assessed over 3 years. Conventional Posterior Pole (PPole) and Peripapillary RNFL protocol were acquired using Spectralis OCT. Longitudinal measurements of Total Retina (TR), Retinal Nerve Fiber Layer (RNFL) and Ganglion Cells Layer (GCL) thickness were performed. Thickness gradients and Lineal regression analyses were calculated in each eye over time. All data are expressed as mean ± SD. p < 0.01 was considered as significant. Linear regression analysis of individual super pixel showed that LaPo can detect progression significantly earlier than peripapillary RNFL in 90.4% (TR, p < 0.01), 96% (RNFL, p < 0.01) and 83% (GCL, p < 0.01) of eyes. In this study we have shown a novel method for objectively quantify glaucoma progression using the PPole scanning protocol. We suggest that macular thickness changes are a potential biomarker for glaucoma diagnosis and progression. Our methodology could contribute to the early identification of progressing patients and may also have a role in glaucoma surveillance schemes.
The concept of cataratogenic load to understand ageing and radiation‐induced damage to the lens
Authors: Quinlan Roy , Quinlan Roy 
Published: December 2019

AbstractLens cataract is an iconic age‐related disease. The age of onset is subject to lifestyle, genetic and environmental factors and in this presentation I will review the case for considering the term “cataractogenic load” to explain the variability and nature of age‐related cataract. As we age so there is accumulated biomolecular damage to lens proteins, lipids and DNA. The very nature of lens biology ensures that this damage is accumulated throughout our lifetime and therefore the appearance of cataract could be explained by a threshold that when crossed results in light scatter, the loss of optical function and the appearance of cataract. Ionising radiation is just one of many environmental hazards that could be encountered but especially by those in the airline, space, energy and medical healthcare industries. Ionising radiation generates free radicals causing oxidative stress and indiscriminate damage to all lens biomolecules changing also the biochemical landscape. Ionising radiation therefore can add to the ageing effect and increase the cataractogenic load to accelerate lens aging and the loss of optical function. We will discuss how this affects cataract phenotype and how the timing of the exposure to ionizing radiation might influence the timing of cataract appearance.
In vitro expanded corneal endothelial cell sheets: towards a new therapeutic approach
Authors: Oellerich Silke 
Published: December 2019

AbstractCorneal transplantation is currently the only effective treatment solution to restore corneal clarity in patients with endothelial disorders. Descemet membrane endothelial keratoplasty (DMEK) is the most recent corneal transplantation technique that selectively replaces only Descemet membrane (DM) and endothelium with the same layers of a healthy donor. However, its application is limited by shortage of high‐quality healthy donor tissue. In order to increase the pool of endothelial grafts, new strategies have been developed, which include surgical‐based and tissue‐engineering based approaches.Tissue‐engineered approaches such as endothelial cell sheet transplantation and cell injection rely on the in‐vitro expansion of cultured corneal endothelial cells (CEC). For endothelial cell sheet transplantation suitable cell carriers are required, which could either be natural carriers (e.g. human anterior lens capsules (HALC)) or bioengineered matrices (e.g. 20 µm thick collagen‐based carriers (LK20)).Within the ARREST BLINDNESS project, CEC were cultured on different carriers and the suitability of the cell‐carrier sheets as tissue‐engineered grafts for DMEK‐like procedures was evaluated by performing in‐vitro surgeries. Upon in‐vitro DMEK surgery, CEC‐HALC sheets behaved similarly to a standard DMEK‐graft on all scored aspects such as graft implantation, unfolding and adherence to bare stroma, whereas graft adhesion and surgical handling, respectively, are issues that still need to be addressed for CEC‐LK20 and CEC‐‘denuded DM’ sheets. First results of in‐vivo tests in an animal model will be presented as well as measures to approach legislative issues.
Animal models to study radiation retinopathy
Authors: Matet Alexandre 
Published: December 2019

AbstractRetinal damage following irradiation is a challenge in the current management of eyes treated for intraocular tumors. However, the mechanisms involved in this deleterious process remains non‐elucidated, and therapeutic strategies are limited. To advance in the understanding of this sight‐threatening complication, the development, validation and analysis of reproducible animal models of ocular irradiation is crucial. We will review existing models and discuss their advantages and limitations, in the perspective of reproducing closely radiation‐induced retinal damage as observed in humans.
Advanced in early‐ and adult‐onset glaucoma genetics
Authors: Pasutto Francesca 
Published: December 2019

AbstractGlaucoma is a genetically and clinically heterogeneous disease that can affect individuals at all ages. Rare genetic variants are known to cause early‐onset glaucoma while common variants contribute to adult‐onset open angle glaucoma (POAG). Genome‐wide association studies (GWAS) are an effective approach for discovery genetic risk factors of diseases with complex inheritance such as the adult POAG. The International Glaucoma Genetics Consortium (IGGC) including investigators worldwide has collected over 50,000 POAG samples. The results of recent GWASs of the IGGC leading to the discovery of more than 50 genes will be discussed providing important novel insights into disease pathogenesis. For the early onset‐ and congenital glaucoma currently 9 genes are known and using these genes for genetic testing can inform genetic counseling and risk assessment. However, the diagnostic yield for these genes is less than the half of all early glaucoma implicating the contributions of additional genes. Whole exome sequencing (WES) has been revealed a useful approach for gene discovery particularly in smaller families leading, for example, to the identification of the novel ANGPT1‐TEK signaling pathway in primary congenital glaucoma. Interesting, using WES in our cohort of patients with early onset glaucoma we could identify mutations in different genes involved in others forms of glaucoma and anterior segment anomalies, thus helping not only to identify novel candidate genes but also helping to define the correct diagnosis. Interesting by large patients screening, some genes involved in early onset glaucoma forms, i.e. ANGPT1, contribute also to adult glaucoma.
2000 years under pressure – The history of glaucoma research
Authors: Krogmann Frank 
Published: December 2019

AbstractSince antiquity, glaucoma is known as a rather vaguely defined disease. The Ancient Greeks were the first who described the disorder we call “glaucoma” today already in 400 BC. “Glaykoseis” was first mentioned in Hippocratic writings as a blinding disease occurring most commonly in the elderly. The present talk will describe the very first beginnings of understanding the ophthalmic disease “glaucoma”. The definition of glaucoma has changed drastically since its introduction around the time of Hippocrates. The very first recognition of a disease which might be associated with a rise in intraocular pressure can be found in the Arabian writings, “Book of Hippocratic treatment”, of At‐Tabari (10th century), it took until 1622 to proof this. In Hippocratic writings the term glaucoma was used to describe blindness developing in advancing years associated with a glazed appearance of the pupil. Galen associated the glaucous hue with a large, anterior, or hard crystalline lens. Medieval Arabic authors translated “glaukos” as “zarqaa”, which also commonly described light irides. Ibn Sina (also known as Avicenna) wrote that the zarqaa hue could occur due to anterior prominence of the lens and could occur in an acquired manner. The disease defined by the glaucous pupil in antiquity is ultimately indeterminate. The specific association of elevated intraocular pressure and the eye disease glaucoma was first described by Richard Banister in 1622.
Modeling spinocerebellar ataxia type 7 in the mouse
Authors: Roux Michel 
Published: December 2019

AbstractAutosomal dominant spinocerebellar ataxia 7 (SCA7) is associated with cone‐rod dystrophy. The causative gene codes for ATAXIN‐7, a ubiquitous protein part of the transcriptional complex SAGA. The coding region contains a CAG triplet repeat translated into a poly‐glutamine (Q) stretch. While there are 4 to 36 repeats per allele in the healthy population, higher numbers are found in SCA7 patients. Longer expansions are typically associated with early onset and cause visual loss before cerebellar ataxia. The SCA7 retinal degeneration has previously been modeled using an overexpression of 90‐repeats ATAXIN‐7 only in rods using the rhodopsin promoter (Rho‐90Q) or a knock‐in with 266 repeats in the mouse Ataxin‐7 gene (KI‐266Q). Rho‐90Q may not be a good model for a cone‐rod dystrophy due to the promoter used. KI‐266Q showed reduction of both photopic and scotopic ERG, but the early and severe phenotype compromises animal fertility and causes death at 4‐5 months, thus offering limited possibilities to test therapeutic approaches, especially in the pre‐symptomatic phase. We have thus characterized the retinal phenotype of KI‐140Q mice, in which mouse Ataxin‐7 includes a shorter (140) polyQ stretch. While the photopic ERG and cone opsins expression is comparable in the mutant and control mice at 5 weeks, they progressively decrease and are extinct around 20–25 weeks in KI‐140Q. The retinal structure is preserved at 9 weeks, followed by a moderate thinning of the segments and outer nuclear layer. Overall, the KI‐140Q recapitulates the symptoms of the cone‐rod dystrophy found in patients, and offer a reasonable time‐window to assess treatment efficacy in both the pre‐symptomatic and symptomatic phases of the disease.
The role of the retina in colour vision impairments in ophthalmological and neurological disorders
Authors: Branco Miguel Castelo 
Published: December 2019

AbstractColour vision impairments have been identified in early stages of neurological disorders such as Parkinson′s disease, and the relative contribution of retinal versus cortical mechanisms remains a matter of intense debate. Similar considerations can be raised concerning other neurological disorders such as Multiple Sclerosis (with or without optic neuritis) and Alzheimer's Disease.This may be due to the fact the retina may mirror the brain in terms of pathology, or suffer from retrograde degeneration in the case of multiple sclerosis. Moreover cortical changes secondary to retinal disease, such as glaucoma and diabetic retinopathy may also bias colour perception. Here we review current evidence concerning the relative role of the retina in colour vision deficits in a broad range of neurological and ophthalmological disorders. In particular, we discuss the potential role of colour vision measures as disease related biomarkers that can be used for diagnostic, prognostic and treatment effects assessment.
Trace elements in glaucoma – The impact of analytics
Authors: Michalke Bernhard 
Published: December 2019

AbstractEye diseases, such as glaucoma are leading causes of irreversible vision loss in industrialized countries. Eye diseases have multifactorial pathogenesis, where heavy metal body burden and/or trace element misbalances are accepted causes aside from genetic factors or intraocular pressure in glaucoma. Heavy metals and misbalances in redox‐active trace elements are prone to affect eye‐related health via increased oxidative stress. In this study trace elements and heavy metals were analyzed in aqueous humour samples by Flow‐Injection (FI)‐Inductively Coupled Plasma Mass Spectrometry. The FI‐mode was used to adopt sample introduction to the very low sample volume available. Samples were analyzed in triplicates using standard mode (best sensitivity for Co, Cd, Hg, Pb), dynamic reaction cell (DRC) mode with ammonia as reaction gas (interference elimination best for Mn, Fe Cu, Zn) and DRC with methane as reaction gas for Se. 5‐point calibration curves in the ranges 0‐1000 ng/l for Cd, Hg, Mn, Pb, Se or 0‐100 µg/l for Cu, Fe, Zn showed R2 = 0.989 for Zn and R2 better than 0.999 for the other elements. Analysis of glaucoma patients revealed an unchanged selenium aqueous humor level of POAG patients compared to controls. However, age‐group and sex dependent trends were seen, i.e. a slight increase for the selenium quantiles in POAG and PEXG patients (age 47–60 years), decrease for the first selenium quantile (61–68 years) and an increase of the third tertiles for 70–85 years.
Posterior segment imaging and anomalies in children with Aniridia
Authors: Wowra Bogumil 
Published: December 2019

AbstractCongenital aniridia is a rare, occurring on both sides always malformation of the eye. It occurs at about 1/50 000 births. This feature is inherited. One of ocular manifestation of congenital aniridia is macular hypoplasia which have significant impact for visual aquity and development of vision in early childhood. Fovea and macular structure is changed.
Ocular surface diseases following ocular irradiation
Authors: Horwath‐Winter Jutta 
Published: December 2019

AbstractRadiotherapy is used for many ocular and periocular indications in malignant and benign diseases. In this talk an overview of ocular surface damage secondary to radiotherapy will be provided. Significant side effects on the external eye occur after irradiation including atrophy of the lacrimal and meibomian glands, damage to the conjunctiva and cornea. These may result in the development of ocular surface diseases such as dry eye syndrome, causing severe patient discomfort. The incidence and severity of the side effects varies depending on the type, location and dose of the radiation treatment. The effects can be clinically subtle, but also devastating to the eye. The discussion of characteristic clinical changes and underlying pathophysiologic mechanisms should provide a rational approach to prevention and treatment of irradiation associated side effects. Tear film and ocular surface evaluation should be performed before irradiation and during follow‐up in order to detect acute and chronic complications and to initiate treatment on a timely basis.
The retinal venous pressure ‐ A new measurable parameter in glaucoma risk assessment
Authors: Stodtmeister Richard 
Published: December 2019

AbstractLow ocular perfusion pressure (OPP) is a risk factor for the progression of glaucoma. OPP is calculated as the difference between mean ophthalmic artery pressure and the venous pressure in the eye which is assumed being equal to the intraocular pressure (IOP). Thus lowering IOP lowers the ocular venous pressure and increases the OPP. This view, however, needs a modification because in the past 25 years it has been shown that the retinal venous pressure (RVP) may be considerably higher in approximately one third of glaucoma patients. In an own series of 50 glaucoma patients 16 patients could be identified just because of a lacking spontaneous pulsation of the central retinal vein. These patients had an IOP of 15(4)mmHg (median (interquartile range) and a RVP of 31(12)mmHg. Also other study groups reported on patients with a high RVP despite an inconspicuous IOP. In a long‐term study of 82 months the RVP was strongly predictive for an increased excavation of the optic disc (odds ratio 1.3/mmHg RVP). We hypothesize that the RVP may be a more potent risk factor than the IOP. Until now, the RVP has been measured by the Dynoptor or by contact lens dynamometry. Due to the hesitant acceptance of these measurement techniques a new method has been developed in which the cornea is no longer touched. By including the RVP in glaucoma diagnostics a new parameter may be available for the risk assessment of this disease.
Antisense oligonucleotide‐induced splice modulation for the treatment of Usher syndrome type 2A
Authors: van Wijk Erwin 
Published: December 2019

AbstractMutations in USH2A exon13 are the most frequent cause of both syndromic and non‐syndromic retinitis pigmentosa (RP), for which currently no treatment options exist. It is generally believed that RP due to mutations in this gene is caused by a loss‐of‐function mechanism. In total, over 600 different mutations have been identified in USH2A of which at least three are known to be derived from a common ancestor and are therefore seen more commonly: c.2299delG (p.Glu767fs*21), c.2276G>T (p.Cys759Phe) and c.7595‐2144A>G (p.Lys2532Thrfs*56). The size of the coding sequence (15,606 bp) and the presence of multiple alternatively spliced USH2A transcripts with unknown significance, hamper the development of gene augmentation therapy. Another difficulty in the development of a therapy is the lack of a suitable animal model. The currently available Ush2a mouse model displays only mild retina degeneration with a very late age of onset. Zebrafish ush2a mutant models however, show an early onset retinal dysfunction and are as such provide a unique opportunity to evaluate future therapeutic strategies. Antisense oligonucleotide (AON)‐based splice modulation has been proven to hold great promise as a therapeutic strategy for a number of hereditary conditions, including Usher syndrome. Upon pre‐mRNA binding, AONs will prevent or stimulate binding of the spliceosome thereby modulating splicing events. AONs can be designed and applied for different genes and genetic disorders as the specificity depends on their nucleotide sequence. In this study we explored the therapeutic potential of AON‐induced splice modulation as a therapeutic approach for the future treatment of USH2A‐associated retinal degeneration.