| 11. |
- Jakobsson, Gunnar, et al.
(author)
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Capsule complication during cataract surgery: Retinal detachment after cataract surgery with capsule complication: Swedish Capsule Rupture Study Group report 4.
- 2009
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In: Journal of cataract and refractive surgery. - : Ovid Technologies (Wolters Kluwer Health). - 1873-4502 .- 0886-3350. ; 35:10, s. 1699-705
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Journal article (peer-reviewed)abstract
- PURPOSE: To study the incidence, characteristics, and results of retinal detachment (RD) after cataract surgery with a capsule complication. SETTING: Ten ophthalmic surgery departments in Sweden. METHODS: In this case-control study, data on cataract surgery cases with a capsule complication (study group) or with no complication (control group) in 2003 were extracted from the Swedish National Cataract Register. Patients with RD during a 3-year follow-up were identified. RESULTS: The study group comprised 324 patients and the control group, 331 patients. Retinal detachment occurred in 13 study group patients, for a 3-year incidence of 4.0%. In the control group, 1 patient (0.3%) had RD. Multivariate analysis showed an adjusted odds ratio (OR) of 14.8 for RD after capsule complication (95% confidence interval [CI], 1.9-114; P = .01). Subgroup analysis of the study group using a binary logistic regression model showed that male sex (OR, 8.5; 95% CI, 1.7-43.8; P = .001) and lens remnants in the vitreous (OR, 14.4; 95% CI 2.6-78.8; P = .002) were additional risk factors. Axial myopia was significantly associated with an increased risk as a single factor but not as a multiple factor. In general, the final visual outcome for RD after a capsule complication was poor; 3 eyes had a visual acuity of 0.50 or better. Eight eyes (62%) had a final visual acuity worse than 0.10 and 6 eyes, 0.02 or worse. CONCLUSIONS: The risk for RD after cataract surgery increased significantly when a capsule complication occurred, leading to poor final visual acuity in most cases.
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| 12. |
- Karlsson, Jan-Olof, 1944, et al.
(author)
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Acute Effects of the Sigma-2 Receptor Agonist Siramesine on Lens Epithelial Cells
- 2007
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In: Invest. Ophthalmol. Vis. Sci.. ; 48:5, s. 2432-
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Conference paper (peer-reviewed)abstract
- PurposeExperiments were carried out to study the effects of siramesine on markers for apoptosis, oxidative damage and mitochondrial function in primary cultures of human lens epithelial cells (HLEC). MethodsHLEC were incubated with 25 {micro}M siramesine for 1, 2, 3, 4, 6 and 8 hours. Caspase-3 was assayed in cell extracts with DEVD-AMC. Mitochondrial depolarization was assayed with JC-1. Peroxide production was studied with DCF-DA and superoxide levels with hydroethidium. Glutathione levels were assayed with monochlorobimane. ResultsSiramesine induced a significant increase of caspase-3 activity after 6h exposure to 25 {micro}M siramesine. Nuclear morphology examined with Hoechst 33342 showed signs of apoptosis after the same time intervals. A significant increase in the production of peroxide and superoxide were found up to 4 -8 hours after administration of siramesine. ConclusionsSiramesine, a piperidine analogue, was developed for the treatment of psychiatic disorders and is considered to be relatively nontoxic. This study, and others, indicate effects on cell growth, apoptosis and production of ROS. The sigma-2 receptor may be a regulator of HLEC growth and apoptosis.
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| 13. |
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| 14. |
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| 15. |
- Petersen, Anne, 1962, et al.
(author)
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Effects Of Dexamethasone In The Lens
- 2006
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In: Invest. Ophthalmol. Vis. Sci.. ; 47:5, s. 4110-
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Conference paper (peer-reviewed)abstract
- Purpose: The aim of the study was to investigate effects of glucocorticoids in the lens. Methods: Lens epithelial cells (HLEC) were exposed to dexamethasone for 24 hours. Cells were assayed for changes in superoxide production using dihydroethidium (HET), for alterations in peroxide production using DCFH-DA or for GSH variations using monochlorobimane (MCB). Apoptosis was determined by Caspase-3 assay and by nuclear morphology of Hoechst stained cells. Mitochondria depolarisation was measured using the potential-sensitive colour JC-1. Morphology was examined by transmission electron microscopy (TEM). Results: Apoptosis were increased in HLEC exposed to 1, 10, 100 and 1000 {micro}M dexamethasone as revealed by nuclear morphology studies. Caspase-3 activity was increased at 100 and 1000 {micro}M dexamethasone. No effect on GSH, superoxide or peroxide production by dexamethasone was present. High concentrations of dexamethasone (1000 {micro}M) depolarised the mitochondria. TEM showed multilayering of cells, mitochondrial changes and accumulation of membrane delimited electron dense material. Conclusions: The mechanism underlying dexamethasone induced apoptosis and morphological changes in HLEC are probably not due to oxidative effects.
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| 16. |
- Petersen, Anne, 1962, et al.
(author)
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Effects of dexamethasone on human lens epithelial cells in culture
- 2008
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In: Mol Vis. - 1090-0535. ; 14, s. 1344-52
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Journal article (peer-reviewed)abstract
- PURPOSE: Treatment with glucocorticoids is a well known risk factor for cataract development, although the pathogenic mechanism has not been elucidated. The aim of the study was to investigate the effects of glucocorticoids in cultured human lens epithelial cells. METHODS: Human lens epithelial cells (HLECs) were exposed to dexamethasone for 24 h. The number of viable cells was determined using the 3-[4, 5-dimethylthiazolyl-2]-2, 5-diphenyltetrazolium bromide (MTT) assay, and proliferation was quantified using Ki-67. Apoptosis was investigated by measuring caspase-3 activity and by evaluating nuclear morphology of cells stained with Hoechst 33342. Mitochondria depolarization was measured using the potential-sensitive color, JC-1. Cells were assayed for changes in superoxide production using dihydroethidium (HET), for alterations in peroxide production using dichlorofluorescein diacetate (DCFH-DA), and for glutathione (GSH) variations using monochlorobimane (MCB). Caspase-3 activity was also measured in HLECs simultaneously exposed to dexamethasone and the glucocorticoid antagonist, RU486. RESULTS: Low doses of dexamethasone (0.1 microM) resulted in increased proliferation of HLECs. Apoptosis was increased in HLECs exposed to 1 microM, 10 microM, and 100 microM of dexamethasone as revealed by nuclear morphology studies. Apoptosis was also confirmed by measuring caspase-3 activation. No effect on superoxide production by dexamethasone was seen. There were no effects on GSH levels or mitochondrial depolarization either. Only the highest concentration of dexamethasone (100 microM) caused an increase in peroxide production. In HLECs incubated with the glucocorticoid antagonist, RU486, apoptosis was induced at a lower concentration of dexamethasone (0.1 microM) than with dexamethasone alone. CONCLUSIONS: Low doses of dexamethasone cause a moderate increase in proliferation of cultured HLECs. Slightly higher but still physiologically relevant concentrations of dexamethasone result in a dose-dependent increase in apoptosis. Dexamethasone-induced apoptosis in HLECs does not seem to involve oxidative mechanisms. The proapoptotic effect of dexamethasone does not appear to act through the glucocorticoid receptor. Effects on proliferation and/or dysregulation of apoptosis in lens epithelial cells may be an important factor in human steroid-induced posterior subcapsular cataract.
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| 17. |
- Petersen, Anne, 1962, et al.
(author)
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Intracellular effects of NSAIDs/ASA in oxidatively stressed human lens epithelial cells in culture.
- 2008
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In: Ophthalmic research. - : S. Karger AG. - 1423-0259 .- 0030-3747. ; 40:2, s. 77-85
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Journal article (peer-reviewed)abstract
- The aim of the study was to examine the effects of nonsteroidal anti-inflammatory drugs (NSAIDs)/acetylsalicylic acid (ASA) on human lens epithelial cells (HLECs) during oxidative stress. HLECs were exposed to H2O2 in the absence or presence of indomethacin, diclofenac, celecoxib (NSAIDs) or ASA for 24 h. HLECs were assayed for changes in superoxide and peroxide production and for variations in glutathione. Mitochondrial depolarization was measured using the membrane potential-sensitive dye JC-1. The results of the study include reduction in superoxide and peroxide production as well as reduction in glutathione depletion in oxidatively stressed HLECs incubated with low concentrations of NSAIDs/ASA. However, no protection against H2O2-induced mitochondrial depolarization by NSAIDs/ASA could be seen. In conclusion, NSAIDs/ASA display reactive oxygen species-scavenging properties in H2O2-exposed HLECs in culture.
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| 18. |
- Petersen, Anne, 1962, et al.
(author)
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Potential Protective Effects of NSAIDs/ASA in Oxidatively Stressed Human Lens Epithelial Cells and Intact Mouse Lenses in Culture
- 2005
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In: Ophthalmic Res. - : S. Karger AG. - 0030-3747. ; 37:6, s. 318-327
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Journal article (peer-reviewed)abstract
- Purpose: To study possible toxic effects of indomethacin, diclofenac, and celecoxib (NSAIDs) and acetylsalicylic acid (ASA) as well as potentially protective effects of these substances in oxidatively stressed human lens epithelial cells (HLEC) and in intact mouse lenses in culture. Methods: HLEC and mouse lenses were incubated with NSAIDs or ASA alone or in the presence of H(2)O(2). To study apoptosis the cells were then either stained with Hoechst 33342 or assayed for caspase-3 activity. Mouse lenses were studied with respect to lens transparency. Results: Low concentrations of NSAIDs/ASA caused a significant protection against H(2)O(2)-induced apoptosis in HLEC whereas higher concentrations were toxic. Conclusion: The protective effects of NSAIDs/ASA against oxidative damage are confined to a relatively small therapeutic window. Copyright (c) 2005 S. Karger AG, Basel.
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