bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of hydration on the ultra‐structural distribution of collagen fibrils and proteoglycans in human corneal stroma
Authors: AKHTAR S , KHAN A , PETROVSKI G , ALBERT R , KIRAT O , ALMUBRAD T 
Published: August 2014

AbstractPurpose We investigated the ultra‐structural changes in the distribution of collagen fibrils (CF) and proteoglycans (PGs) due to hydration in the human corneal stroma.Methods Six fresh human scleral corneal rings were hydrated separately in deionized water for 2hrs and 48hrs. Corneas were divided into two parts. The first part of each cornea was fixed in 2.5% glutaraldehyde containing cuprolinic blue in sodium acetate buffer and processed for electron microscopy to assess proteoglycans. A second part of each cornea was fixed in 2.5% glutaraldehyde in 0.1M phosphate buffer and post fixed in 1% osmium tetroxide to assess collagen fibril diameter.Results In the hydrated corneas the mean diameter of CF in the anterior stroma (23.40±2.61nm), middle stroma (22.48±3.28nm) and posterior stroma (23.58±2.46nm) was less than the CF diameter in the anterior (28.27±4.05nm), middle (28.22±3.09nm) and posterior stroma (29.73±3.72nm) of the normal cornea. Micro‐fibrils within the CF in the hydrated cornea were degenerated. In the hydrated cornea, the mean area of the PGs in the anterior stroma was reduced whereas it increased in the middle stroma compared to those in the normal cornea. The density of the PGs in the hydrated cornea was reduced in the anterior, middle and posterior stroma compared to those in the normal cornea.Conclusion The effect of hydration on the uniform organisation of CF and PGs was higher in the middle and posterior stroma than in the anterior stroma. This could be due to less penetration of water in the interlacing lamellae of the anterior stroma. The reduction in the collagen fibrils diameter could be due to degeneration of microfibrils within the collagen fibrils.
Predegenerated Schwann cells promote neuroprotection and regeneration of retinal ganglion cells in ex vivo rat retinal explants
Authors: SMEDOWSKI A , PIETRUCHA‐DUTCZAK M , KAARNIRANTA K , LEWIN‐KOWALIK J 
Published: August 2014

AbstractPurpose To investigate neuroprotective and pro‐regenerative potential of predegenerated Schwann cells towards RGCs in ex vivo retinal explants.Methods In this study we used two models of rat retinal explants culture ‐ reversed explants from P2 Wistar rats pups and insert explants from 4 weeks old Wistar rats. Both types of explants were cultured in Neurobasal A medium with supplements (B‐27, N2 and GlutaMax). In this way we prepared 32 insert explants (16 were cultured with 2 µl of Schwann cells suspension (104 cells) dropped on the each explants surface, another 16 served as control treated with 2 µl of DPBS) and 30 reversed explants (10 of them were cultured in standard medium, 10 explants were with addition of 5 ng/ml BDNF into medium and 10 were co‐cultured with 104 of Schwann cells). After proper culture time, explants were fixed and processed for immunostainings and stereological analyses.Results In retinal explants cultured in inserts system, there was significantly higher density of RGCs in group treated with Schwann cells in comparison to PBS treated (independent samples t‐test, p<0.05). In reversed retinal explants, there were significant differences between groups expressed in mean and total length and surface of neurites, as well as in number and arboration rate of neurites (U‐Mann Whitney test, p<0.05). Immunofluorescent staining using GAP43 additionally revealed intense neurites outgrowth (also in explants from adult animals).Conclusion Predegenerated Schwann cells exert neuroprotective action and support regeneration of RGCs in neonatal and adult retina in ex vivo conditions.
Cytotoxicity of mesoporous silicon microparticles with different surface modifications on ARPE‐19 cells
Authors: KORHONEN E , RIIKONEN J , XU W , LEHTO VP , KAUPPINEN A 
Published: August 2014

AbstractPurpose Retinal pigment epithelial (RPE) cells play a crucial role in the pathogenesis of age‐related macular degeneration (AMD). However, RPE is a challenging target in a therapeutical sense. In addition to its location, the possible hydrophobicity of drug molecules makes its medication even more challenging. Biodegradable porous silicon (PSi) microparticles could be a promising possibility for delivering hydrophobic drugs to RPE cells. In the present study, we aimed at testing the cytotoxicity of thermally oxidized (ToPSi) and thermally carbonized porous silicon (TCPSi) particles with and without additional surface modification with amino groups on human ARPE‐19 cells. Since the cytotoxicity of PSi particles cannot be tested by the commonly used MTT (3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5‐diphenyltetrazolium bromide) assay due to non‐specific redox reactions, our aim was also to search for alternative assays for working with mesoporous silicon materials.Methods ARPE‐19 cells were treated with microparticles at several concentrations for 24 h. Thereafter, cell viability was measured using a protease viability marker assay (CellTiter‐FluorTM) and a lactate dehydrogenase (LDH) release assay. Cells were also evaluated ocularly under an inverted microscope.Results All tested particles were well tolerated by ARPE‐19 cells. CellTiter‐Fluor assay seemed slightly more reliable than the LDH test.Conclusion Our results show that the tested porous silicon particles did not cause major cytotoxicity on ARPE‐19 cells, and CellTiter‐Fluor assay, especially together with ocular examination, could be suitable for testing cytotoxicity in association with mesoporous silicon particles.
Cellular & molecular origins of the electro‐oculogram
Authors: CONSTABLE P 
Published: August 2014

AbstractThe clinical electro‐oculogram has been used to assess retinal pigment epithelium (RPE) function using the changes in the standing potential of the eye in response to light. However, only a part of this mechanism is fully understood. One important clinical finding is that individuals with Best’s macular dystrophy display a reduced light‐rise and therefore a role for bestrophin in the generation of the light‐rise is necessary. It is now evident that bestrophin acts a regulator of intracellular calcium stores interacting with the L‐type‐Ca2+ channel in the basolateral membrane of the RPE to drive the changes in basolateral chloride conductance. This new role helps to explain the cases of Best’s macular dystrophy in which the light‐rise is normal. However, the initiating events surrounding the rise in intracellular calcium are unknown. One possibility is that light itself is able to elevate intracellular Inositol tri‐phosphate that releases calcium from intracellular stores and initiate the light‐rise. The talk will elaborate on the role of bestrophin in the generation of the light‐rise, and examine light and the onset of phagocytosis as possible triggers for the light‐rise.
Phenotypes of bestrophinopathies
Authors: LEROY BP 
Published: August 2014

AbstractPurpose: To describe the phenotypes of conditions due to mutations in BEST1, the gene encoding bestrophin‐1. Methods: A case presentation format will be used to illustrate the phenotypes and genotypes of the different bestrophinopathies, with special attention to both the clinical and electrophysiological features that distinguish one phenotype from the other, and those they have in common. In addition, the different BEST1 genotypes will be discussed. Results: The phenotypes of Best vitelliform macular dystrophy (BVMD), autosomal dominant vitreoretinochoroidopathy (ADVIRC), and autosomal recessive bestrophinopathy (ARB) are very different. Nevertheless, they share an abnormal electro‐oculography (EOG) as a common feature. Electroretinography is normal in BVMD, whereas a rod‐cone dystrophy is evident in the later stages of ADVIRC and ARB. BVMD is due to a heterozygous missense mutation in BEST1, ADVIRC is due to interaction of several bestrophin protein isoforms, and ARB is probably the null phenotype. Conclusions: The phenotypes of the bestrophinopathies are diverse, although they share an abnormal EOG as the common feature. The specific genotypes are also different, leading to different molecular pathogenetic mechanisms.
RPE Disease beyond BEST1
Authors: MEUNIER I , HAMEL C 
Published: August 2014

AbstractThis presentation will focus on one RPE disease, the vitelliform dystrophies. Vitelliform macular dystrophies include a juvenile form i.e., Best vitelliform macular dystrophy and, an adult form apart from the previous one by Gass. These dystrophies represent the second most common cause of inherited maculopathy, after Stargardt disease. Based on recent human iPS cell studies, impairment in phagocytosis was confirmed, as RPE from BEST1 mutant human iPS‐RPE have disrupted ﬂuid ﬂux and increased accumulation of autoﬂuorescent material after long‐term outer segment feeding when compared with human iPS‐RPE from unaffected siblings. Secondly, the role of the protein in chloride currents activated by intracellular calcium was linked to the regulation and release of endoplasmic reticulum calcium stores. Beyond the major gene BEST1 and a minor gene PRPH2, we will point out the frequencies, the clinical spectrum and mode of inheritance linked to two new causal genes: IMPG1, IMPG2. These new genes introduce a third actor in the causes of vitelliform macular dystrophies; namely, this actor is the interphotoreceptor matrix that joins together the photoreceptors and the RPE.
IgE, anti‐IgE, and allergic keratoconjunctivitis ‐ part 1
Authors: DOAN S 
Published: August 2014

AbstractVernal and atopic keratoconjunctivis (VKC, AKC) are severe types of ocular allergy, characterized by acute and chronic corneoconjunctival inflammation that may lead to visual sequelae. Although topical immunosuppressive drugs such as cyclosporine and tacrolimus are usually effective, some severe may be refractory. Omalizumab is a monoclonal anti IgE antibody, administered systematically and authorized for severe asthma. We will report our clinical experience of omalizumab in AKC and VKC patients, and will also detail a review of the literature.
IgE, anti‐IgE, and allergic keratoconjunctivitis ‐ part 2
Authors: CHIAMBARETTA F 
Published: August 2014

AbstractVernal and atopic keratoconjunctivis (VKC, AKC) are severe types of ocular allergy, characterized by acute and chronic corneoconjunctival inflammation that may lead to visual sequelae. Although topical immunosuppressive drugs such as cyclosporine and tacrolimus are usually effective, some severe may be refractory. Omalizumab is a monoclonal anti IgE antibody, administered systematically and authorized for severe asthma. We will report our clinical experience of omalizumab in AKC and VKC patients, and will also detail a review of the literature.
Food allergy and ocular surface
Authors: FAUQUERT JL 
Published: August 2014

AbstractAllergic diseases of the ocular surface are in most cases associated with allergic triggers. Food allergens are more and more frequently involved in children. We analyzed the incidence of ocular symptoms associated with food allergy. The airway contact with some particular food is known to result in ocular symptoms (fish, peeling of various fruits). Ocular symptoms are frequently associated with food oral syndrome. Moreover, according to allergic patients’ questioning, the intake of food results in ocular symptoms in an important amount of cases, reaching almost 20% of the cases of food allergy (rhino conjunctivitis or conjunctivitis). In patients suspected for food allergy, Oral Food Challenge (OFC) to various allergens revealed ocular involvement in 14% of the patients. Furthermore some authors compared the safety and efficiency of the OFC and the Conjunctival Provocation Test to assess food allergy in children. They justify this practice on the frequency of instillation of cow’s milk on the ocular surface and its absence of side effect on one hand and on the difficulties to practice oral food challenges in young children on the other hand. Thus the eye should be considered as an interesting target for food allergy investigation
Molecular allergens and tear investigation
Authors: CHABANE H 
Published: August 2014

AbstractTears immunological investigations are limited in routine practice because of the small volume of fluid collected. Only few tests can be performed in tears: Total IgE, screening test or specific IgE to aeroallergen to confirm allergic sensitization. Inflammatory mediators in lachrymal fluid are only measured for a research purpose. During the last decade, an increasing number of specific IgE to molecular allergens became available for routine use. Molecular allergens largely contributed to an improvement of allergy diagnosis by distinguishing between true sensitization and cross‐reactivity and a better indication of allergen immunotherapy in polysensitized patients. However, each of these single tests needs 50‐100 µl of serum. More recently, allergen arrayed biochip technology became routinely available (ImmunoCAP ISAC) enabling the quantification of specific IgE against 112 allergens, using only 30 µl of serum. The allergen biochip technology seems to be a promising tool to assess local synthesis of IgE in tears in case of suspicion of allergy and the negativity of both skin prick tests and serum specific IgE. Large‐scale studies are needed to confirm the usefulness of this tool for tears testing in allergic conjunctivitis.
New therapeutic approaches and challenges for the treatment of dry eye disease
Authors: SULLIVAN DA 
Published: August 2014

AbstractInnumerable individuals suffer from tear film dysfunctions, which are collectively diagnosed as dry eye disease (DED). In the United States alone DED afflicts tens of millions of people, especially women, and is one of the most frequent causes of patient visits to eye care practitioners. DED is characterized by a vicious cycle of tear film hyperosmolarity and instability and ocular surface stress, leading to increased friction, inflammation and damage to the eye. DED is caused primarily by meibomian gland dysfunction, and is associated with significant pain, decreased vitality and poorer general health. Because of diminished worker productivity, the burden of DED for the United States is estimated to be over $55.4 billion. There is no safe and effective global treatment for DED, and its therapy remains a profound unmet need throughout the world. A virtual kaleidoscope of new therapeutic approaches have been proposed to treat the mucin, aqueous and/or lipid tear film deficiencies, as well as the ocular surface damage, associated with DED. My presentation will highlight these approaches, and also address the significant clinical endpoint challenges that serve as barriers to the successful development of potential treatments for DED.
Commercial interest
Eye and genes: the new ophthalmology
Authors: SCHORDERET D 
Published: August 2014

AbstractFor many years, ophthalmology has based its practice on observing, trying, deducing and remembering. For many pioneers, this approach was not sufficient and tools were designed to improve the diagnostic and intervention capacities for these ocular diseases. Although inheritable eye disorders have been identified many years ago–Dalton described color blindness in 1798 – it is only in the second part of the 20th century that genetics flourished. Franceschetti and Klein from Geneva published numerous reports on dysmorphology, and were part of a great effort to categorize all syndromes so that nature’s experiments were not lost. Although both were ophthalmologists, they founded the first Institute of Medical Genetics in Switzerland and made significant contributions to the field. I was blessed to discover genetics through David Klein and to further do my doctoral thesis with Eric Engel, his successor, in Geneva. Fifteen years later, the identification of the genes responsible for inherited diseases was done either by karyotyping or by linkage analysis followed by physical mapping. The former was based on luck, and often, we didn’t have any. For the latter, we needed large families and new technologies, like autoradiograms or automated
Visual acuity loss in open‐angle glaucoma patients: causes and risk factor
Authors: AYCHOUA N , JANSONIUS NM 
Published: August 2014

AbstractPurpose To identify causes of visual acuity loss in open angle‐glaucoma (OAG) patients and to determine associated risk factors.Methods From the visual field database of the University Medical Center Groningen, 400 patients with at least 3 reliable visual fields were randomly selected. Of these, 233 had OAG. OAG patients with a visual acuity of 0.5 or less in at least one eye were considered as cases; controls had to have a visual acuity above 0.5 in both eyes. Causes of visual acuity loss were determined from the medical records. Potential risk factors for visual acuity loss in OAG (age, gender, myopia, baseline IOP, corneal thickness, and visual field mean deviation [MD]) were assessed by comparing cases with acuity loss due to OAG with the controls, using logistic regression.Results Of the 233 patients with OAG, 134 (57%) were cases and 99 (43%) controls. Concerning the cases, visual acuity loss was caused by OAG in 40%, cataract 17%, AMD 14%, vitreo‐retinal surgery 10%, corneal pathology 4.5%, acquired retinal disorders 10%, and neuro‐ophthalmological disorders 4.5%. Among the assessed risk factors, cases had a lower MD (OR=0.90; P<0.001) and a higher age (OR=1.05; P=0.015).Conclusion Visual acuity loss in OAG is common but mostly due to other eye co‐morbidities. A lower MD and an older age were highly significant risk factors.
Intraocular pressure modulation by neuropeptides ‐ the effect of vasopressin
Authors: BOGNER B , RUNGE C , STROHMAIER C , TROST A , KASER‐EICHBERGER A , KREFFT K , GRABNER G , KIEL JW , SCHROEDL F , REITSAMER HA 
Published: August 2014

AbstractElevated intraocular pressure (IOP) is a major risk factor for glaucoma. Currently, the primary strategy to slow down glaucoma progression is IOP reduction. Numerous studies investigated the IOP lowering effects of neuropeptides, but the complex physiological mechanisms involved are difficult to interpret. Therefore, we investigated the effect of arginine‐vasopressin (AVP) on IOP in a multiparameter approach. In a rabbit model the effect of i.v.‐applied AVP on IOP, ciliary blood flow (CilBF) and aqueous flow (AqF) was measured simultaneously by manometry, laser‐Doppler flowmetry and fluorophotometry. AVP caused a dose‐dependent decrease of IOP, CilBF and AqF. Based on the Goldmann equation the decrease of AqF at 0.08 ng/kg/min AVP (low dose) accounted for 77.1% of the IOP reduction (9.56±2.35%), while AqF at 1.33 ng/kg/min AVP (high dose) accounted for 28.4% of the IOP decline (41.02±3.19%). The results indicate that AqF reduction by low dose AVP is mainly caused by inhibition of ciliary epithelium secretion. At high dose AVP AqF reduction is caused by decreased CilBF or more likely by a combination of CilBF decline and secretory inhibition. This conclusion is only possible with the multiparameter measurement approach presented.
Reconstitution of a corneal endothelium by intracameral injection of cultured endothelial cells
Authors: BRUNETTE I , BOSTAN C , THERIAULT M , FORGET K , PROULX S 
Published: August 2014

AbstractThe only currently available treatment for irreversible corneal endothelial failure is allo‐transplantation, which is overshadowed by optical distortion of the posterior surface, postoperative donor corneal endothelial cells attrition and risk of rejection. Assessment of the in vivo functionality of a corneal endothelium reconstituted by the injection of corneal endothelial cells in the anterior chamber of an endothelial deficiency model allows to consider cell‐injection as a possible therapy for corneal endotheliopathies.
Function follows morphology? New aspects of macula OCT analysis
Authors: GUTHOFF R 
Published: August 2014

AbstractFactors that are predictive for the outcome of medical or surgical therapy to anatomic success are desirable. Clinical tools such as optical coherence tomography and autofluorescence provide to demonstrate early morphological alterations. The value in identifying subclinical pathologies that affects the macula may help to understand better the natural course. The examination results of these tools may be useful for the correlation with post‐treatment visual acuity to better predict the eventual visual function.
Diabetic macular edema ‐ back to laser therapy?
Authors: JOUSSEN A 
Published: August 2014

AbstractTreatment of diabetic macular edema has changed considerably since approval of several intravitreal drugs. Several studies demonstrated superiority of intravitreal injections over laser therapy. Nevertheless laser approaches are currently reconsidered with adapted protocols. This overview critically discusses the effectiveness of the treatment approaches on the background of the pathophysiology of diabetic macular edema.
Healthcare resource use and costs in persistent non‐anterior non‐infectious uveitis
Authors: THORNE J , TUNDIA N , SKUP M , MACAULAY D , REVOL C , CHAO J , BAO Y , DICK A 
Published: August 2014

AbstractPurpose To assess direct and indirect economic burden for privately insured US employees with persistent non‐anterior non‐infectious uveitis (NIU) compared with matched controls without uveitis.Methods Persistent cases were 18–64 years old with ≥2 ICD‐9 diagnoses for intermediate‐, posterior‐ or pan‐NIU (OptumHealth, 01/1998–03/2012) with ≥90 days of corticosteroid, immunosuppressant, and/or biologic use. Cases were matched 1:1 by sex, age, region and index date to controls. Direct (medical services and prescription drugs) and indirect (disability and medically‐related absenteeism) healthcare resource use (HRU) and costs (2012 USD) were compared using Wilcoxon/McNemar tests and multivariate regression (adjusting for baseline characteristics).Results Annual unadjusted mean direct HRU and costs, including inpatient (0.3 vs. 0.1 stays; $3,628 vs $586), outpatient (26.3 vs 9.6 visits; $12,038 vs $3,065), ophthalmology/optometry (6.6 vs 0.5 visits; $3,486 vs $83), emergency (0.6 vs 0.1 visits; $267 vs $31), and prescription drugs (13.3 vs 4.5; $10,345 vs $1,499) were significantly higher for cases vs controls (all P<.05). Indirect HRU and costs (35.5 vs 11.5 days; $6,624 vs $1,816), specifically absenteeism (14.3 vs 4.0 days; $3,818 vs $862), also were higher for cases vs controls (all P<.05). Adjusted total direct costs ($35,739 vs $7,670) and indirect costs ($6,902 vs $1,612) were significantly higher for cases vs controls (all P<.05).Conclusion Persistent non‐anterior NIU is associated with substantial direct and indirect costs.
Commercial interest