Latrunculin-A causes mydriasis and cycloplegia in the cynomolgus monkey.
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PURPOSE: To determine the effect of latrunculin (LAT)-A, which binds to G-actin and disassembles actin filaments, on the pupil, accommodation, and isolated ciliary muscle (CM) contraction in monkeys. METHODS: Pupil diameter (vernier calipers) and refraction (coincidence refractometry) were measured every 15 minutes from 0.75 to 3.5 hours after topical LAT-A 42 microg (approximately 10 microM in the anterior chamber [AC]). Refraction was measured every 5 minutes from 0.5 to 1.5 hours after intracameral injection of 10 microl of 50 microM LAT-A (approximately 5 microM in AC), with intramuscular infusion of 1.5 mg/kg pilocarpine HCl (PILO) during the first 15 minutes of measurements. Pupil diameter was measured at 1 and 2 hours, and refraction was measured every 5 minutes from 1 to 2 hours, after intravitreal injection of 20 microl of 1.25 mM LAT-A (approximately 10 microM in vitreous), with intramuscular infusion of 1.5 mg/kg PILO during the first 15 minutes of measurements (all after topical 2.5% phenylephrine), and contractile response of isolated CM strips, obtained <1 hour postmortem and mounted in a perfusion apparatus, to 10 microM PILO +/- LAT-A was measured at various concentrations. RESULTS: Topical LAT-A of 42 microg dilated the pupil without affecting refraction. Intracameral LAT-A of 5 microM inhibited miotic and accommodative responses to intramuscular PILO. Intravitreal LAT-A of 10 microM had no effect on accommodative or miotic responses to intramuscular PILO. LAT-A dose-dependently relaxed the PILO-contracted CM by up to 50% at 3 microM in both the longitudinal and circular vectors. CONCLUSIONS: In monkeys, LAT-A causes mydriasis and cycloplegia, perhaps related to its known ability to disrupt the actin microfilament network and consequently to affect cell contractility and adhesion. Effects of LAT-A on the iris and CM may have significant physiological and clinical implications. (+info)
VEGF deprivation-induced apoptosis is a component of programmed capillary regression.
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The pupillary membrane (PM) is a transient ocular capillary network, which can serve as a model system in which to study the mechanism of capillary regression. Previous work has shown that there is a tight correlation between the cessation of blood flow in a capillary segment and the appearance of apoptotic capillary cells throughout the segment. This pattern of cell death is referred to as synchronous apoptosis (Lang, R. A., Lustig, M., Francois, F., Sellinger, M. and Plesken, H. (1994) Development 120, 3395-3404; Meeson, A., Palmer, M., Calfon, M. and Lang, R. A. (1996) Development 122, 3929-3938). In the present study, we have investigated whether the cause of synchronous apoptosis might be a segmental deficiency of either oxygen or a survival factor. Labeling with the compound EF5 in a normal PM indicated no segmental hypoxia; this argued that oxygen deprivation was unlikely to be the cause of synchronous apoptosis. When rat plasma was used as a source of survival factors in an in vitro PM explant assay, inhibition of vascular endothelial growth factor (VEGF) all but eliminated the activity of plasma in suppressing apoptosis. This argued that VEGF was an important plasma survival factor. Furthermore, inhibition of VEGF in vivo using fusion proteins of the human Flk-1/KDR receptor resulted in a significantly increased number of capillaries showing synchronous apoptosis. This provides evidence that VEGF is necessary for endothelial cell survival in this system and in addition, that VEGF deprivation mediated by flow cessation is a component of synchronous apoptosis. (+info)
Adenosine stimulates Cl- channels of the nonpigmented (NPE) cells of the ciliary epithelium. We sought to identify the specific adenosine receptors mediating this action. Cl- channel activity in immortalized human (HCE) NPE cells was determined by monitoring cell volume in isotonic suspensions with the cationic ionophore gramicidin present. The A3-selective agonist N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (IB-MECA) triggered shrinkage (apparent Kd = 55 +/- 10 nM). A3-selective antagonists blocked IB-MECA-triggered shrinkage, and A3-antagonists (MRS-1097, MRS-1191, and MRS-1523) also abolished shrinkage produced by 10 microM adenosine when all four known receptor subtypes are occupied. The A1-selective agonist N6-cyclopentyladenosine exerted a small effect at 100 nM but not at higher or lower concentrations. The A2A agonist CGS-21680 triggered shrinkage only at high concentration (3 microM), an effect blocked by MRS-1191. IB-MECA increased intracellular Ca2+ in HCE cells and also stimulated short-circuit current across rabbit ciliary epithelium. A3 message was detected in both HCE cells and rabbit ciliary processes using RT-PCR. We conclude that human HCE cells and rabbit ciliary processes possess A3 receptors and that adenosine can activate Cl- channels in NPE cells by stimulating these A3 receptors. (+info)
Congenital duplication of the lens.
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A case of reduplication of the lens with uveal coloboma is described. This is a rare condition and, unlike the two previously reported cases, the other ocular structures and adnexae appeared normal. (+info)
A prospective study of xenon arc photocoagulation for central retinal vein occlusion.
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Twenty patients with central retinal vein occlusion were randomly divided into two groups in a prospective study to evaluate the effects of xenon are photocoagulation in central retinal vein occlusion. The patients in one group were treated with 360 degrees scatter xenon photocoagulation and the others received no treatment. The average follow-up was 18 months. There were no cases of rubeosis or neovascular glaucoma in the treated group. Two patients in the untreated group developed rubeosis with subsequent neovascular glaucoma. There was no significant difference in the visual prognosis or in fundus neovascularization between the groups. (+info)
Pilocarpine induces an increase in the anterior chamber angular width in eyes with narrow angles.
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AIM: To determine the mechanical effects of pilocarpine on the trabecular-iris angle opening in eyes with narrow angles, compared with its effects on healthy control subjects with wide angles. METHODS: A narrow angle was defined as 25 degrees or less of trabecular-iris angle on ultrasound biomicroscopic examination. The change in anterior chamber depth (ACD), trabecular-iris angle (TIA), angle opening distance (AOD, distance between trabecular meshwork and iris) measured at 250 microm and 500 microm from the scleral spur (AOD250 and AOD500), and iris thickness was determined in 30 eyes of 30 patients (13 men and 17 women, between 63 and 82 years (mean 70.4 years)) with narrow angles and in 30 sex and age matched control subjects with wide angles before and 1 hour after the instillation of 2% pilocarpine hydrochloride by ultrasound biomicroscopy. RESULTS: In all eyes with narrow angles, pilocarpine increased the TIA, AOD250, and AOD500; these changes increased significantly and linearly as the corresponding pretreatment values decreased (r = 0.807, p = 0.0001; r = 0.787, p = 0.0001; r = 0.852, p = 0.0001). Of 30 eyes with wide angles, 23 eyes whose ACD was 2670 microm and more showed a decrease in the TIA, AOD250, and AOD500; the changes in TIA, AOD250, and AOD500 also significantly correlated with the corresponding pretreatment values (r = 0.913, p = 0.0001; r = 0.882, p = 0.0001; r = 0.895, p = 0.0001). Pilocarpine induced a smaller decrease in ACD in eyes with narrow angles than in those with wide angles (p = 0.0001). There was a linear correlation between the increase in ACD change and the decrease in pretreatment ACD in eyes with narrow angles and those with wide angles (r = 0.781, p = 0.0003; r = 0.798, p = 0.0001). CONCLUSIONS: The finding that pilocarpine increases angular width in patients with narrow angles indicates that this agent is useful for treating patients with narrow angles and angle closure glaucoma. The prediction of the pilocarpine induced change in the angle may assist ophthalmologists in treating such patients. (+info)
Ultrasound biomicroscopic measurement of development of anterior chamber angle.
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AIM: To establish normative values for the anterior segment in normal infants and children in relation to age. METHODS: Anterior segments were measured in 46 normal infants and children (21 males and 25 females, aged from 1 to 60 months (mean 17.09 (SD 16.99) months)), by use of ultrasound biomicroscopy. RESULTS: Anterior chamber depth, trabecular-iris angle, angle opening (trabecular-iris) distances at 250 and 500 microm from the scleral spur, and the thickness of the thickest part of the iris were 1724-3473 microm (2505 (SD 480) microm), 15.35-44.79 degrees (28.74 (7.46) degrees ), 116-367 microm (247.4 (65.9) microm), 166-509 microm (349.5 (87.1) microm), and 249-579 microm (434.6 (74.6) microm), respectively. All factors in this study showed a significant correlation with logarithm of age (r = 0.937, p = 0. 0001; r = 0.867, p = 0.0001; r = 0.929, p = 0.0001; r = 0.917, p = 0. 0001; r = 0.748, p = 0.0001), and significantly correlated with each other. CONCLUSIONS: Ultrasound biomicroscopy is a powerful tool for obtaining precise images and measurement of the development of the anterior segment in infants and children. Normative values were established for anterior segment dimensions in relation to age. Anterior chamber depth, trabecular-iris angle, angle opening distances at 250 and 500 microm from the scleral spur, and iris thickness showed linear increases in relation to logarithm of age. (+info)
Dendritic cells and macrophages in the uveal tract of the normal mouse eye.
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BACKGROUND/AIMS: Dendritic cells (DC) and macrophages are components of the immune cell populations in the uveal tract whose density, distribution, turnover, and function may play a role in the maintenance of immunological homeostasis in the eye. Little is known of these cells in the mouse eye despite this being the predominant experimental model in many studies of ocular immune responses and immunoinflammatory mediated eye diseases. The aim of the present study was to obtain further immunophenotypic data on resident tissue macrophages and DC populations in the mouse uveal tract. METHODS: Pieces of iris, ciliary body, and choroid dissected from perfusion fixed BALB/c mice were incubated whole in a variety of anti-macrophage and DC monoclonal antibodies (mAbs). Labelled cells were visualised using either single or double immunoperoxidase techniques. RESULTS: Quantitative analysis and double immunolabelling revealed that 80% of F4/80(+) cells (a mAb that recognises both DC and macrophages) in the iris are macrophages (SER4(+)). The iris contained a network of Ia+ cells (412 (SD 130) cells/mm2) of which two thirds appear to be DC. A similar pattern was observed in the ciliary body and choroid. Only a few DC in the uveal tract were very weakly reactive for mAbs which recognise B7-1 (CD80), B7-2 (CD86), beta2 integrin (mAb N418), and multivesicular bodies associated with antigen presentation (mAb M342). CONCLUSIONS: The present study reveals that the mouse uveal tract, like the rat, contains rich networks of DC and resident tissue macrophages. The networks of resident tissue macrophages in the mouse uveal tract closely resemble similar networks in non-ocular tissues. The phenotype of uveal tract DC suggests they are in the "immature" phase of their life cycle, similar to Langerhans cells of the skin, thus implying their role in situ within the eye is antigen capture and not antigen presentation. (+info)