Ocular Structures (ocular + structure)

Distribution by Scientific Domains


Selected Abstracts


Fishing Down Under: case report and review of management of a fishhook injury of the eyelid

CLINICAL AND EXPERIMENTAL OPTOMETRY, Issue 5 2008
AJ Kreis
A 21-year-old man presented to the emergency department of the Royal Victorian Eye and Ear Hospital with a fishhook embedded in his unprotected left upper eyelid. The fishhook was removed after exploration of the left eye by vertical eyelid incision. Subsequent eyelid reconstruction by lid margin adaptation was performed. Management of these injuries depends on type of hook, the involved ocular structure and location of the hook. This is an update on management options, where triage and surgical approaches are discussed. This case illustrates the risk to the eyes while fishing. Persons with an interest in fishing should be advised to wear eye protection. [source]


Coordinated regulation of dorsal bone morphogenetic protein 4 and ventral Sonic hedgehog signaling specifies the dorso-ventral polarity in the optic vesicle and governs ocular morphogenesis through fibroblast growth factor 8 upregulation

DEVELOPMENT GROWTH & DIFFERENTIATION, Issue 4 2010
Takuma Kobayashi
Dorsal and ventral specification in the early optic vesicle plays a crucial role in vertebrate ocular morphogenesis, and proper dorsal-ventral polarity in the optic vesicle ensures that distinct structures develop in separate domains within the eye primordium. The polarity is determined progressively during development by coordinated regulation of extraocular dorsal and ventral factors. In the present study, we cultured discrete portions of embryonic chick brains by preparing anterior cephalon, anterior dorsal cephalon and anterior ventral cephalon, and clearly demonstrate that bone morphogenetic protein 4 (BMP4) and Sonic hedgehog (Shh) constitute a dorsal-ventral signaling system together with fibroblast growth factor 8 (FGF8). BMP4 and Shh upregulate Tbx5 and Pax2, as reported previously, and at the same time Shh downregulates Tbx5, while BMP4 affects Pax2 expression to downregulate similarly. Shh induces Fgf8 expression in the ventral optic vesicle. This, in turn, determines the distinct boundary of the retinal pigmented epithelium and the neural retina by suppressing Mitf expression. The lens develops only when signals from both the dorsal and ventral regions come across together. Inverted deposition of Shh and BMP4 signals in organ-cultured optic vesicle completely re-organized ocular structures to be inverted. Based on these observations we propose a novel model in which the two signals govern the whole of ocular development when they encounter each other in the ocular morphogenic domain. [source]


7 Tesla MR imaging of the human eye in vivo

JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 5 2009
Kathryn Richdale OD
Abstract Purpose: To develop a protocol which optimizes contrast, resolution and scan time for three-dimensional (3D) imaging of the human eye in vivo using a 7 Tesla (T) scanner and custom radio frequency (RF) coil. Materials and Methods: Initial testing was conducted to reduce motion and susceptibility artifacts. Three-dimensional FFE and IR-TFE images were obtained with variable flip angles and TI times. T1 measurements were made and numerical simulations were performed to determine the ideal contrast of certain ocular structures. Studies were performed to optimize resolution and signal-to-noise ratio (SNR) with scan times from 20 s to 5 min. Results: Motion and susceptibility artifacts were reduced through careful subject preparation. T1 values of the ocular structures are in line with previous work at 1.5T. A voxel size of 0.15 × 0.25 × 1.0 mm3 was obtained with a scan time of approximately 35 s for both 3D FFE and IR-TFE sequences. Multiple images were registered in 3D to produce final SNRs over 40. Conclusion: Optimization of pulse sequences and avoidance of susceptibility and motion artifacts led to high quality images with spatial resolution and SNR exceeding prior work. Ocular imaging at 7T with a dedicated coil improves the ability to make measurements of the fine structures of the eye. J. Magn. Reson. Imaging 2009;30:924,932. © 2009 Wiley-Liss, Inc. [source]


Do multipurpose contact lens disinfecting solutions work effectively against non-FDA/ISO recommended strains of bacteria and fungi?

OPHTHALMIC AND PHYSIOLOGICAL OPTICS, Issue 1 2010
Maureen Boost
Abstract Purpose:, Recent outbreaks of microbial keratitis have increased concerns about the efficacy of multipurpose solutions (MPS) against ,real-world' organisms. This study determined, in accordance with FDA/ISO standard methods, the effects of five MPS against clinical isolates and type strains of bacteria, and isolates of fungi from subjects' ocular structures; and of three MPS against environmental fungal isolates. Method:, MPS were challenged with bacteria (type strains (ATCC) and clinical isolates of bacterial pathogens obtained from a district hospital laboratory) and with fungal isolates from both the periocular and conjunctival structures and from environmental air. Results:, All MPS demonstrated at least a 3-log reduction of challenged cell viability of all bacterial species tested, with the exception of MPS D against a canine infection Staphylococcus aureus isolate. Whilst all MPS tested were able to effect a 1.0-log reduction of viability of Fusarium solani (ATCC 36031), only two MPS had 90% viability reduction against all fungi of human origin and only one of these against all environmental fungal isolates. Effectiveness of these two solutions against fungal isolates compared to the remaining three MPS was found to be statistically significant (p = 0.003). Conclusions:, All MPS demonstrated a 99.9% viability reduction against a wide range of bacteria including major ocular pathogens not currently included in the FDA panel. The inability of three MPS to achieve a 90% reduction against fungal isolates is of concern as there has been a recent upsurge in reports of fungal keratitis. We would recommend extension of the current FDA testing panel for MPS to include more fungal isolates. [source]


4143: The German Mouse Clinic: recent findings from the Eye Screen

ACTA OPHTHALMOLOGICA, Issue 2010
O PUK
Purpose The purpose of this study was the large-scale screening of different mouse mutant lines in order to detect novel models for eye disorders. Methods The eyes of the mouse mutants were analyzed by slit lamp biomicroscopy, funduscopy, laser interference biometry, optokinetic drum, and histology. Results In the past 12 months, 46 mouse mutant lines were investigated in the primary Eye Screen of the German Mouse Clinic (GMC). These included Csemp1 and Aey69 that exhibited irregular eye development. All tested mice of the mutant line Csemp1 unexpectedly showed white fundus flecks and significantly reduced axial eye lengths. Moreover, we additionally found strong opacities in a least a portion of the Csemp1 mutant lenses. Aey69 mice are severely microphthalmic due to a yet undefined ENU-induced mutation. The rudimentary eyes completely lack ocular structures as iris or lens. Further significant irregularities in fat metabolism, immunology, and behaviour were detected in the GMC-wide primary screen. Linkage studies mapped the mutated site on chromosome 3 within a 0.78 Mb spanning region between the flanking microsatellite markers D3Mit188 and D3Mit76. Among the 34 positional candidate genes, Tnrc4 (elav-like family member 3) and Selenbp1 (selenium binding protein 1) are expressed in the eye. Sequencing studies in order to detect the causative mutation of Aey69 are in process. Conclusion Two novel mouse models for microphthalmia were detected in the primary Eye Screen of the GMC. These mutant lines will provide further insights into molecular mechanisms behind this kind of eye disease. [source]


Corneal hysteresis measured with the Ocular Response Analyzer® in normal and glaucomatous eyes

ACTA OPHTHALMOLOGICA, Issue 1 2010
Olivia Abitbol
Abstract. Purpose:, To identify differences in corneal hysteresis (CH) and central corneal thickness (CCT) between healthy and glaucomatous patients. Methods:, Retrospective observational study. One hundred and thirty-three eyes of 75 healthy and 58 glaucomatous patients were included. CH was measured in each patient using Ocular Response Analyzer. CCT was determined by ultrasonic pachymetry. For each patient, one eye was randomly selected. We used a Student t -test to search for significant differences between the different groups (p<0.05). Results:, In healthy and glaucomatous eyes, mean CH values were 10.46 ± 1.6 and 8.77 ± 1.4 mm Hg, respectively. Mean CCT values were 560.2 ± 36.3 and 535.3 ± 42.7 ,m, respectively. CH and CCT were significantly lower in glaucomatous eyes than in normal eyes, (p<0.05). Discussion:, In our series, CH was lower in glaucomatous than in normal eyes. The relationship between glaucoma, IOP, and ocular structures may not be confined to the consideration of CCT. A low CH value could be responsible for under-estimation of IOP. CH could also be a risk factor for glaucoma, independent of IOP. Further studies are needed to support these hypotheses. Conclusion:, In our investigation, CCT and CH were significantly lower in glaucomatous eyes than in healthy eyes. [source]


In vivo confocal microscopic evaluation of inflammatory changes in the ocular surface

ACTA OPHTHALMOLOGICA, Issue 2009
A LABBE
Purpose The ocular surface constitutes a complex physiopathological and anatomical entity assuring the barrier between the outside world and the fragile ocular structures. Ophthalmic instruments such as the slit lamp, which magnifies approximately 40 times, cannot provide details of the corneal structures at the cellular level. Methods In vivo confocal microscopy using the HRT Rostock Cornea module® (HRT / RCM) provides better resolution and therefore outlines distinctively in vivo inflammatory changes occurring in the ocular surface. Results In vivo confocal microscopy is capable of providing corneal, conjunctival and limbal cellular details in different ocular surface diseases such as dry eye, infectious keratitis, toxic keratitis, corneal intraepithelial neoplasia or vernal keratoconjunctivitis. Conclusion In correlation with ex vivo impression cytology analysis, in vivo confocal microscopy constitutes an interesting aid in the diagnosis and management of complex ocular surface conditions. [source]


Ocular rigidity in living human eyes in health and disease

ACTA OPHTHALMOLOGICA, Issue 2009
IG PALLIKARIS
Purpose It is known that the balance between aqueous humor secretion and outflow rate controls the steady - state average intraocular pressure (IOP). It has been also early identified that blood circulation results to IOP fluctuations practically synchronous to cardiac function. IOP is the primary mechanical load to several ocular structures including the optical nerve head. Methods In-vivo intraoperative measurement of these quantities as well as secretion/outflow coefficients in humans allowed us to quantify ocular rigidity, IOP and its fluctuations (and pulsatile blood flow) in a series of physiological and pathological eyes. Ocular rigidity, outflow facility and pulsatile ocular blood flow were measured intraoperatively in a cohort of 63 patients undergoing cataract surgery. Measurements were also performed in a series of age related macular degeneration (AMD) patients. Results The eye, is a living structure under a continuously varying mechanical load that is strongly related to ocular haemodynamics. Ocular rigidity ranged from 0.0122 to 0.0343 (mean 0.0208),l-1. Outflow facility coefficient (derived from pressure decay curves) was 0.33 (sd 0.15),l/min/mmHg. Pulsatile ocular blood flow exhibited a strong negative correlation to IOP in all subjects. The ocular rigidity coefficient was higher in wet AMD patients compared to patients with dry AMD and healthy controls. Conclusion There are indications that this mechanical load, associated also to ocular rigidity, can not only inter-modulate blood flow but also have a long-term effect on other structures in the eye. Understanding the role of these parameters may contribute to the understanding of ocular disease. [source]


Measurement of time-resolved autofluorescence

ACTA OPHTHALMOLOGICA, Issue 2008
D SCHWEITZER
Purpose Functional alterations are first signs of reversible pathologic processes. Whereas microcirculation studies metabolism globally, autofluorescence of endogenous fluorophores has the potential for description of cellular basic processes. Therefore, a discrimination of fluorophores is required in the tissue. Methods Besides excitation and emission spectra, the fluorescence lifetime after short-time excitation is a promising substance-specific mark. Using the opto-mechanical system of a HRA II (Heidelberg Engineering), a fluorescence lifetime mapper was developed. Picosecond pulse-lasers (448nm, 468nm, 100ps FWHM, 80MHz) can be used for excitation and the emission will be detected in 2 spectral ranges (490-560nm, 560-700nm). The dynamic fluorescence will be detected in time-correlated single photon counting (SPC 150, Becker/Hickl, Berlin). An on line image registration is realised by simultaneously detected infrared images during measuring time. Approximating the fluorescence decay by 3-exponential model function, images (lifetime and amplitudes), histograms, and cluster diagrams can be calculated for interpretation. Results Examples are given for healthy subjects, AMD patients (non-exudative, exudative, geographic atrophy), diabetic retinopathy, and oedema. Measurements of excitation and emission spectra as well as lifetimes are performed of expected substances and of anatomical ocular structures for comparison. Conclusion Fluorescence lifetime measurement at the eye is a new method for evaluation of functional metabolic state. [source]


The eye in focus: accommodation and presbyopia

CLINICAL AND EXPERIMENTAL OPTOMETRY, Issue 3 2008
W Neil Charman DSc PhD
Current understanding of the anatomy, function and performance of the accommodative system of the young, adult human eye is outlined. Most major current models of the accommodative mechanism are based on Helmholtz's original ideas but, despite of a growing volume of related research, uncertainty continues over the relative contributions made to the overall mechanism by different ocular structures. The changes with age are then discussed. Although the amplitude of accommodation decreases steadily from later childhood, the speed and accuracy of the system within the available amplitude are little impaired until the age of about 40, when the amplitude falls below that needed for normal near work. A review of the available evidence on age-related change in the lens, capsule, ciliary body and other relevant ocular structures confirms that geometric and viscoelastic lenticular changes play major roles in the progressive loss of accommodation. Other factors may also contribute in an, as yet, unquantified way and a full understanding of the origins of presbyopic change remains elusive. [source]


Clinical and molecular aspects of aniridia

CLINICAL GENETICS, Issue 5 2010
H Kokotas
Kokotas H, Petersen MB. Clinical and molecular aspects of aniridia. Aniridia is a severe, congenital ocular malformation inherited in an autosomal-dominant fashion with high penetrance and variable expression. Eye morphogenesis in humans involves a molecular genetic cascade in which a number of developmental genes interact in a highly organized process during the embryonic period to produce functional ocular structures. Among these genes, paired box gene 6 (PAX6) has an essential role as it encodes a phylogenetically conserved transcription factor almost universally employed for eye formation in animals with bilateral symmetry, despite widely different embryological origins. To direct eye development, PAX6 regulates the tissue-specific expression of diverse molecules, hormones, and structural proteins. In humans, PAX6 is located in chromosome 11p13, and its mutations lead to a variety of hereditary ocular malformations of the anterior and posterior segment, among which aniridia and most probably foveal hypoplasia are the major signs. Aniridia occurs due to decreased dosage of the PAX6 gene and exists in both sporadic and familial forms. The mutations are scattered throughout the gene and the vast majority of those reported so far are nonsense mutations, frameshift mutations, or splicing errors that are predicted to cause pre-mature truncation of the PAX6 protein, causing haploinsufficiency. Here we review the data regarding the mechanisms and the mutations that relate to aniridia. [source]