bluuebunny/crossref_metadata_2025_split huggingface dataset:
Corneal bacterial diseases
Authors: CREUZOT CP , BRON AM 
Published: September 2008

Abstract Purpose To present the main causes of corneal bacterial diseases and suggest an appropriate management. Bacterial keratitis is the most common cause of infected corneal ulceration. Methods The epidemiology of corneal bacterial diseases and their link with different risk factors will be studied. The initial presentation is important to determine the potential stain responsible for the infection and to assess the overall severity of the disease. Local and general criteria evaluations lead to a proper management. Bacterial identification plays a key‐role in the etiological diagnosis. Results Contact lens wear, trauma, preexisting ocular disease and corneal surgery are the main risk factors for corneal bacterial disease. Specific signs to identify bacteria remain rare but the circumstances (contact lens wear, aspect of the infiltrate) can help to determine the first line treatment. However laboratory methods remain the only way to diagnose a corneal bacterial disease with certainty. The aspect of the infiltrate, the intraocular involvement and an immunosuppressed patient may influence the outcome. The treatment is based on an initial broad‐spectrum antibacterial therapy with secondary adaptation to the identified bacteria. Conclusion Multiple microorganisms are involved in corneal diseases. The local and systemic risk factors have to be identified to treat these diseases in emergency still considered as a leading cause of visual loss.
Ghrelin’s MRNA levels in the developing rat’s eye
Authors: ROCHA DE SOUSA A , RAMOS‐TAVARES M , TELES A , LEITE‐MOREIRA AF 
Published: September 2008

Abstract Purpose The aim of the present study was to investigate the expression of ghrelin the late phase of development of the rat eye. Methods Wistar rats (n=16) were euthanized 22 days post‐conception (n=8) or 15 days after delivery (n=8). The eye globes were enucleated and dissected, and the cornea, iris, lens, retina and sclera were microdissected. A portion of the gastric fundus was also collected. The lens could only be isolated 15 days after birth.To evaluate the levels of ghrelin mRNA in the distinct eye tissues and the stomach an equal amount of total mRNA of each sample (50ng) underwent two‐step real‐time RT‐PCR with specific primers. Glyceraldehyde 3‐phosphate dehydrogenase (GAPDH) and β actin were used as internal controls. Data is presented as mean±SE in relative expression units. Comparisons were performed with two way ANOVA. Results GAPDH and β actin mRNA levels differed between tissues, precluding their usage as internal control genes, nevertheless, β‐actin levels were similar in the iris and retina and the expression of ghrelin normalized for β‐actin did not differ at birth or 15 days after between iris (1.0±0.3 and 0.4±0.3, respectively) and retina (1.2±0.3 and 0.5±0.3, respectively). Absolute ghrelin mRNA levels were also not different at birth or 15 days after in each of the tissues evaluated but were higher in the retina (1.0±0.2) than in the cornea (0.4±0.1), sclera (0.5±0.1) and gastric fundus (0.3±0.1). The lens showed the lowest value of expression (0.1±0.0). Conclusion Ghrelin is more expressed in the newborn retina than in the stomach, lens, cornea and sclera. The expression in the iris and retina is similar. The high expression of ghrelin in some tissues of the eye at these stages suggests it may have a role in the eye's development.
History of amblyopia
Authors: GRZYBOWSKI A 
Published: September 2008

Abstract Purpose Review the history of amblyopia. Methods Analysis of original and secondary contributions in the history of amblyopia. Results Traditionally amblyopia has been classified into different subgroups according to the major disorder which is responsible for its occurrence; accordingly, we distinguish among strabismic amblyopia, anisometropic amblyopia, isoametropic amblyopia and deprivation amblyopia. Since strabismus is the most visible disorder leading to amblyopia, the history of strabismus diagnosis can be roughly included in the history of amblyopia in the clinical context. It is known that Hippocrates described strabismus and differentiated it into comitant and non‐comitant. Later Paulus of Aegina and Ambroise Pare not only diagnosed the disorder, but also attempted to treat it. One of the first explanations of the amblyopia mechanisms was given by de la Hire who suggested that in strabismus the most sensitive part of the retina is eccentrically displaced to an abnormal position. This idea was later supported by Johannes Muller. The first treatment of amblyopia was attempted in 1743 by George L. de Buffon, who covered the better eye and suggested the use of glasses for the weaker eye. In the 1930s orthoptic programs were introduced and in the 1950s pleoptic techniques began to be used. Finally, the experiments carried out in the 1960s and 1970s by Hubel and Weisel suggested that the neural basis for amblyopia was related to a massive reduction in the binocular neurons and a shift in the ocular dominance of neural activity towards the unaffected eye. Conclusion Although our present understanding of the underlying mechanisms of amblyopia is much greater, our treatment methods are still rooted in history.
A role for canonical WNT signaling in lens development
Authors: DELONGH R 
Published: September 2008

Abstract Purpose To investigate Wnt signalling in lens development we conditionally deleted β‐catenin (CatnβEx3‐6) or mutated exon3 of β‐catenin (CatnβEx3) or truncated adenomatous polyposis coli (Apc580S) to inactivate or activate the pathway in different cellular compartments of the murine lens. Methods Cre deletor lines that express Cre in fibers only (MLR39) or in fibers and epithelium (MLR10), were used to conditionally mutate floxed CatnβEx3‐6, CatnβEx3 and Apc580S alleles in developing mouse lens from E13. Lenses from mutant and wild‐type mice were analyzed by histology, immunofluorescence and PCR arrays. Results MLR10 intercrosses result in microphthalmia; MLR39 intercrosses show no ocular abnormalities at weaning. Mice with loss of β‐catenin in fibres (MLR39Cre/CatnβEx3‐6) develop cataract in later life. Analyses of MLR10‐derived mutant mice at E13.5 show that loss of β‐catenin inactivates Wnt signals and results in loss of lens cell progenitors, with decreased E‐cadherin, cyclinD1 and cMyc expression, reduced BrdU and phosphohistone3 (pH3) labeling and premature cell cycle exit (p57Kip2). As well as Wnt signal effects, loss of β‐catenin deregulates adherens junctions resulting in loss of hexagonal fibre structure. By contrast, activating mutations of Wnt pathway (CatnβEx3, Apc580S) result in increased epithelial proliferation (BrdU, cyclinD1, PH3), apoptosis (TUNEL) and inhibition of fibre differentiation (β‐crystallin, p57Kip2). Pathway specific PCR arrays confirmed modulation of Wnt signaling in each lens mutant and show altered expression of Notch pathway, indicating these pathways operate as part of a network. Conclusion These data show Wnt signals play key roles in regulating proliferation and differentiation of lens epithelial cells and that the pathway is tightly regulated.
Monitoring retinal ganglion cells in vivo
Authors: PAQUES M , SAHEL JA 
Published: September 2008

AbstractProgress in imaging techniques will considerably increase our knowledge on retinal cell pathophysiology and death during optic nerve disesases as a whole. Experimentally, current in vivo imaging using the green laser reflectance mode of the SLO allows noninvasive microscopic‐scale definition of the nerve fibers. However, loss of the axons is a late and irreversible event, thus imaging the retinal ganglion cells themselves would be preferable in order to detect diseased states at an earlier stage. Retrogradelly‐labelled RGCs can be conveniently seen in vivo, but such imaging require invasive procedures, the effect of which on RGC physiology remains uncertain. The recent development of molecular imaging of apoptotic ganglion cells is promising. The cSLO also allows in vivo imaging of other cellular compartments that are relevant for glaucoma, for instance microglial cells. In humans, current techniques allow imaging of the nerve fiber layer with a relatively low resolution. The GDx evaluates the nerve fiber layer thickness through light polarisation, and high resolution OCT through mapping of its thickness around the optic nerve. Yet, it is likely that these systems lack sensitivity for detection of the early loss of the NFL, and even more for early dysfunction of RGCs. Presently, adaptive optics does not appear to be a technique of choice for the NFL, but technological progress may prove this assertion to be wrong. In the future, techniques allowing increased contrast of fibrillar structures such as en face OCT may prove of interest.
Evaluation of the retinal nerve fiber layer in patients with multiple sclerosis
Authors: GARCIA MARTIN E , PUEYO V , FERNANDEZ TIRADO J , MARTIN J , ARA JR , HONRUBIA FM , PINILLA I 
Published: September 2008

Abstract Purpose To evaluate the changes in one year in the retinal nerve fiber layer (RNFL) in patients with Multiple Sclerosis (MS) by means of ocular imaging technologies. Methods Forty‐two patients with MS (84 eyes) were enrolled in this study. None of the patients had an optic neuritis episode in at least 6 months prior to the inclusion, nor during the follow‐up. All patients underwent a complete ophthalmic examination that included visual acuity (logMAR), colour vision (Ishihara pseudoisochromatic plates), refractive evaluation, visual field examination, optical coherence tomography (OCT) and scanning laser polarimetry (GDx). All the patients were re‐evaluated in a period of 12 months in order to quantify the changes in the retinal nerve fiber layer (RNFL). Results All the parameters showed a decrease in the RNFL thickness during the 12‐month follow‐up greater than the decrease due to the age in healthy patients, although these changes were not detected by the standard automated perimetry. Differences were statistically significant (P<0,05, t test) in the mean and inferior RNFL thickness and macular volume provided by OCT and in the TSNIT SD provided by GDx. The greater differences were obtained in the mean RNFL thickness (87,86 µm vs 90,13 µm). Conclusion Progressive axonal loss can be detected in the optic nerve of MS patients. Ocular imaging technologies are useful tools to evaluate structural abnormalities in the RNFL and changes in time.
Wernicke encephalopathy
Authors: BORRUAT FX 
Published: September 2008

AbstractWernicke’s encephalopathy is an acute neurological disorder caused by thiamine (Vitamin B1) deficiency and characterized by the clinical triad of ophthalmoplegia, ataxia and mental confusion. Ophthalmoplegia commonly takes the form of horizontal and/or vertical gaze palsy often accompanied by bilateral abduction deficits. Upbeat nystagmus is characteristic. Mental status changes may be mild therefore unappreciated. MRI abnormalities (periaqueductal area, midbrain tegmentum, mamillary bodies and dorsomedial thalamus) can be found in up to 60% of patients who are imaged within 2 weeks of symptom onset. The condition is life‐threatening but early therapy with intraveinous or intramuscular 100mg thiamine with glucose supplementation can reverse symptoms and signs within hours.
Existence of limbal epithelial crypt within the infant limbus
Authors: YEUNG AM , TINT NL , HOPKINSON A , DUA HS 
Published: September 2008

Abstract Purpose The Limbal Epithelial Crypt (LEC) has been suggested to be the limbal epithelial stem cell niche and the limbus has been shown to demonstrate regional variations in association with the LEC. Our aims were to 1) to determine the existence of LEC in the infant age group and 2) compare and contrast the corneo‐scleral tissue between infant and the adult by use of immunofluorescent imaging. Methods Donor eyes were processed and snap frozen in liquid nitrogen. Using a Leica cryostat machine, corneo‐scleral sections were prepared and examined under microscopy for presence of LEC structures. Limbal sections were fixed, and stained with a range of current postulated markers of stem cells and cell differentiation by standard immunofluorescent imaging techniques. Results Immunostaining in the infant group demonstrates that both limbal and corneal epithelium consist of cells that are characteristic of cells with less differentiated nature. No classical adult LEC was discernable in corneo‐scleral rims of a 2 year old or a 4‐month old infant. However, adult LEC immunofluorescence, demonstrate similar characteristics to the infant limbus. Conclusion We hypothesize that the absence of classical adult LEC in infants suggests that LEC may arise during the natural human growth, and may act as a repository for limbal epithelial stem cells in the human adult.
The effect of spongy layer (sl) isolated from amniotic membrane on ocular cells growth
Authors: LAZUTINA E , SULEMAN H , DUA HS , TINT NL , JAMES DK , HOPKINSON A 
Published: September 2008

Abstract Purpose The extraembryonic coelom or spongy layer (SL) is the gelatinous, biochemically complex layer, which functions as a physical boundary between the vascular chorion and avascular amnion membrane (AM). SL often remains associated with the AM and is partially but variably removed during preparation for transplantation. We have shown that SL contains a similar profile of potentially beneficial factors as AM, but at considerably higher levels, which may explain in part the observed clinical variation. However, the effects of SL on ocular cell growth have yet to be established Methods Soluble proteins were extracted from freeze‐dried SL to generate a soluble (sSL) and an insoluble structural SL fraction (iSL). Cultured corneal epithelial cells (CEC), keratocyte derived fibroblasts (KDF) and lymphocytes were stimulated with sSL and iSL fractions at varying dilutions, and the effects on cell proliferation (WST‐1) and cytotoxicity were measured. Results At physiological concentration (16mg/ml) iSL killed all cell types within a few hours. Serial dilution of iSL (16mg/ml,8mg/ml,3.2mg/ml,0.32mg/ml) reduced rate of death, but death still occurred. Stimulation with sSL killed CEC at all concentrations, whilst the most dilute sSL fraction promoted KDF growth. Conclusion SL exerts a powerful cytotoxic effect on ocular and immune cells. However, the depot of factors contained within the SL may over time be released over time to promote cell growth. Therefore in the current situation where SL is typically ignored during AM preparation for transplantation, may have significant implications for the clinical efficacy of AM.
SUMOylation during nuclear degradation in lens fibre cells
Authors: PRESCOTT AR 
Published: September 2008

Abstract Purpose To investigate the role of SUMO (small ubiquitin‐related modifier) in organelle elimination and nuclear reorganisation during lens fibre cell differentiation. Methods Antibodies raised against the small protein modifiers SUMO were localised by indirect immunofluorescence and laser scanning confocal microscopy in cryo‐sections of bovine lenses. The localisation of these antibodies was correlated with other antibodies targeted to several nuclear compartments previously shown to be rearranged during nuclear elimination in the lens (Gribbon et al. EJCB 81:557‐66). Results In the lens epithelium and most recently differentiated fibre cells SUMO is present in a single small bright (as yet undefined) compartment in the nucleus and as a diffuse, fine punctate nucleoplasmic distribution. In the nuclei of deeper fibres the SUMO becomes associated with nucleolar caps, these caps are distinct from those containing proteins from other nuclear bodies; eg. coilin from Cajal bodies. Finally in the very last intact nuclei SUMO becomes associated with the nuclear membrane, and or the lamina, and or nuclear pores. Conclusion The post‐translational modification of proteins by SUMO can have many consequences including the regulation of protein‐protein interactions, inhibition of transcription and regulation of enzyme activity. SUMOylation can occur on many, both cytoplasmic and nuclear proteins but little is known about its role in cell differentiation. Interestingly in the context of lens development SUMO has been implicated in the cellular responses to hypoxia ‐ a metabolic stress that has been suggested to be involved in lens fibre cell differentiation.
f‐Visual evoked potentials (f VEPs), nystagmus vs. motor & neurological disorders in quadriplegia
Authors: TIGANITA S , KOZEIS N , TYRADELIS E , GATZIOUFAS Z , ZAFEIRIOU D 
Published: September 2008

Abstract Purpose To correlate flash VEPs and nystagmus with the severity of the motor and brain disorder in spastic quadriplegic children. Methods 52 quadriplegic children (2‐9 years of age) participated in this study. Flash VEPs (ICEVE), and brain MRI were performed, also nystagmus (clinical evaluation) and gross motor function (GMFCS) were evaluated. Results 29 children were premature and 23 were full terms. 15 out of 52 (28.84%) had normal f VEPs and 37(71.15%) had abnormal. epilepsy, 13 (25%) had nystagmus (horizontal). 73.07% of the children had moderate to very severe motor disorders. 32 children (61.53%) had periventricular leukomalacia and 20 (38.47%) had various brain damages. Conclusion Affected flash VEPs and nystagmus are common in quadriplegic children. There is a statistically significant relationship between VEPs, nystagmus and neurological and brain damage.
Regulators of angiogenesis in the vitreous
Authors: BISHOP PN , LE GOFF MM , TAKANOSU M , HENRY SP , MAYNE R 
Published: September 2008

Abstract Purpose Preretinal neovascularisation is a form of angiogenesis i.e. growth of new blood vessels (into the vitreous) from the pre‐existing vessels (the retinal vasculature). The vitreous contains pro‐ and anti‐angiogenic molecules and normally the balance favours an anti‐angiogenic state. However in diseases such as proliferative diabetic retinopathy, excess pro‐angiogenic molecules, e.g. VEGF, stimulate preretinal neovascularisation. Anti‐angiogenic molecules identified in the vitreous to date include PEDF, thrombospondin‐1 and endostatin, but their relative importance in inhibiting preretinal neovascularisation remains unclear. Here we show that an endogenous glycoprotein of the vitreous called opticin has potent anti‐angiogenic properties, and provide evidence that it has a pre‐eminent role in inhibiting pre‐retinal neovascularisation. Methods Opticin null mice were generated and bred onto a C57/BL6 background. The opticin null mice and wild‐type mice +/‐ intravitreal injection with recombinant opticin (at P14) were investigated using the oxygen‐induced retinopathy model (75% oxygen from P7‐12, and analysis at P17 by serial histological sectioning). Results The opticin null mice demonstrated increased preretinal neovascular nuclei per cross section (109 +/‐ 6 S.E) compared to wild‐type controls (73 +/‐ 3) (P < 0.0001). The opticin injected wild‐type eyes showed a decrease in preretinal neovascular nuclei per cross‐section (38 +/‐ 3) compared to eyes injected with PBS alone (76 +/‐ 4) (P < 0.0001). Conclusion Opticin inhibits preretinal neovascularisation in a dose‐dependent manner. This is the first time that a knockout mouse has demonstated increased neovascularisation using this model. Opticin, or molecules derived from opticin, represent potential therapeutics.
Visual development in premature infants without serious events in their pre – and perinatal period.
Authors: AGGELIDOY E , KOZEIS N , FELEKIDIS A , KAPSOS A , PAPPAS K , HRISOGLOU M 
Published: September 2008

Abstract Purpose To follow the visual development of premature neonates without serious health problems. Methods 49 premies (GA 26 < β < 35 & βW 890 < β < 2240gr), with no neurological and ophthalmological lesions, participated in this study. Brain ultrasound, fundoscopy, cycloplegic refraction and assessment of the visual function (VFA‐K test) were performed in 10th and 16th adjusted month of age. All the babies had a psychokinetic assessment (twice) (DENVER test). Results 41 out of 49 neonates had GA <32 weeks .and 30 out of 49 had βW <1500 gr. 26 neonates had normal brain echo and 23 appeared with mild enlargement of brain ventricles. During the 1st examination, 3 neonates appeared with refractive error >1.00 D, 4 had strabismus, 4 had mildly abnormal VFA‐K test score and 10 had reduced DENVER score. During the 2nd examination, the results were the same apart from an improvement in VFA‐K and DENVER score. Conclusion In the vast majority of the premature infants with no serious health problems, the visual function develops normally.
Is diabetic retinopathy an inflammatory, oxidative stress, genetic, mediated process ?
Authors: DE SOUZA RAMALHO P , PEREIRA DA SILVA A , PEGO P , BICHO MP 
Published: September 2008

Abstract Purpose Diabetic Retinopathy (DR)neurovascular degenerative process of systemic disease is one of the main causes of blindness in adults(20‐70 years).Multifactor machanisms with growing evidence of hyperglycaemia induced inflammation and oxidative stress with genetic influence can lead to retinal cell apoptosis in early STZ diabetic rats. Expression of inflammation and oxidative stress markers and their genetic phenotypes in diabetics under treatment and in controls were studied. Methods Transmembrane Reductase (TMR), Erythropoeitin (EPO) activity and Haptoglobin (Hp) genotypes were determined in 60 type 2 diabetics, 26 with and 34 without retinopathy (mean age 64.2 ±11.64 years) of both sexes and in 44 non diabetic controls. TMR (mmol/l cell/h) was determined by spectophotometry, EPO(mIu/ml) by ELISA and Hp genetic phenotypes using polyachrilamide gel electrophoresis. Student t test, ANOVA,χ2 and Pearson correlation was used. Results TMR activity was high in retinopathy subjects (5.29 ± 2.11 vs 4.11 ± 1.51 in controls p=0.016). EPO serum levels were high in retinopathy patients (15.15 ± 11.14 vs 9.47 ± 6.57 in controls p=0.043). Hp 2.2 allele genotype predominance in diabetics with retinopathy (40.9%).Hp 2.1 genotype higher incidence in diabetics without retinopathy (70.6%) p=0.028). Conclusion High inflammatory/oxidative activity expressed by TMR,EPO,Hp and other markers in diabetic retinopathy,supports our hypothesis. EPO has also antiapoptotic, cell regenerative angiogenic properties. Its up‐regulation in retinopathy could be endogenous auto‐protective mechanism.