36 results on '"Theodoropoulou S"'
Search Results
2. Democracy with foresight: the key to a socially sustainable transition in Europe (and beyond)
- Author
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Countouris, N., Piasna, A., Theodoropoulou, S., Azmanova, Albena, Nicolaidis, Kalypso, Countouris, N., Piasna, A., Theodoropoulou, S., Azmanova, Albena, and Nicolaidis, Kalypso
- Abstract
How can the European Union steer a course towards long-term social and ecological well-being in a context of incessant emergencies? Two decades of perpetual crisis management have greatly eroded Europe’s capacity to pursue a sustainable future, as considerations of short-term expediency continue to hamper the four transitions that are necessary – green, digital, geopolitical and socio-economic. At the same time, however, few polities in the world are better suited to the design and promotion of long-term policies. This editorial draws on its authors’ respective research into progressive social transformation and sustainable European integration to identify a path for the socially sustainable transition which we now need and which the rest of this issue of Benchmarking Working Europe further explores.
- Published
- 2023
3. Study of Xbal and Pvull polymorphisms of estrogen receptor alpha (ERα) gene in girls with precocious/early puberty
- Author
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Theodoropoulou, S. Papadopoulou, A. Karapanou, O. Priftis, K. Papaevangelou, V. Papadimitriou, A.
- Abstract
Purpose: Studies examining association of estrogen receptor alpha (ERα) polymorphisms with early puberty are scarce and results are controversial; data in Caucasian girls are lacking. Main objective was to determine association of Xbal and Pvull polymorphisms of ERα gene in Greek girls with precocious/early puberty Methods: We studied 107 girls with idiopathic precocious/early puberty and 81 young women with pubertal maturation within normal age (controls). Pubertal stage, height SDS (HSDS), and BMI z-score were determined in patients. In controls, height was measured and menarcheal age was self-reported. All participants in the study were genotyped for XbaI and PvuII polymorphisms of the ERα gene. Results: There was no significant difference in XbaI and PvuII polymorphisms between patients and controls. Homozygous, xx and pp, girls had an earlier onset of puberty, although non-significant, than heterozygous or with no polymorphisms p = 0.9; in girls with pubertal onset
- Published
- 2021
4. Structural and optical characterization of pyrolytic carbon derived from novolac resin
- Author
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Theodoropoulou, S., Papadimitriou, D., Zoumpoulakis, L., and Simitzis, J.
- Published
- 2004
- Full Text
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5. Serous macular detachment due to nasally located optic disc pit-coloboma
- Author
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Theodoropoulou, S. Theodossiadis, G. Sallam, A. Theodossiadis, P.
- Published
- 2018
6. Spontaneous resolution of vitreomacular traction demonstrated by spectral-domain optical coherence tomography
- Author
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Theodossiadis, G.P. Grigoropoulos, V.G. Theodoropoulou, S. Datseris, I. Theodossiadis, P.G.
- Subjects
genetic structures ,sense organs ,eye diseases - Abstract
Purpose To evaluate the natural course of idiopathic vitreomacular traction (VMT) with spectral-domain optical coherence tomography (SDOCT) from the vitreomacular adhesion (VMA) stage to the spontaneous resolution of VMT. Design Prospective observational case series. Methods We studied the natural course of idiopathic VMT in 46 eyes (46 patients), divided into those that proceeded to spontaneous VMT resolution (12 cases) and those that remained at the VMT stage (34 cases). All patients were examined with SDOCT at regular 3-month intervals. We recorded the vitreomacular angle of VMA nasally and temporally, the horizontal diameter of VMA, macular thickness, visual acuity, photoreceptor layer, and external limiting membrane. Results In the 12 eyes that proceeded to spontaneous resolution, the vitreous adhesion angle had a mean increase of 38 degrees at VMT, compared to the angle at the VMA stage. In the 34 eyes that remained at the VMT stage, the mean angle of traction increased by only 1 degree throughout follow-up. In all 46 patients, the angle at the VMT stage was significantly associated with traction resolution (nasally P =.001, temporally P 400 μm compared with that of eyes with a VMT diameter
- Published
- 2014
7. Photoreceptor layer changes overlying drusen in eyes with age-related macular degeneration associated with vitreomacular traction
- Author
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Theodossiadis, P.G. Theodoropoulou, S. Stamatiou, P. Datseris, I. Theodossiadis, G.P.
- Subjects
genetic structures ,sense organs ,eye diseases - Abstract
Purpose: To investigate by spectral-domain optical coherence tomography (SD-OCT) changes of photoreceptor layers over drusen in cases of dry type age-related macular degeneration associated with vitreomacular traction (VMT). Methods: Clinical examination, fluorescein angiography, fundus photography, and SD-OCT data were retrospectively studied for a consecutive series of 27 patients with drusen, pseudodrusen, and VMT. Control groups of 32 patients with VMT without drusen and 34 patients with drusen and pseudodrusen without VMT were also studied. Results: The examination revealed disruption of the line corresponding to the inner segment ellipsoid (ISel), previously called inner segment/outer segment junction, of photoreceptor layer, and development of cystoid edema in significantly higher incidence in VMT associated with drusen group. 22 out of 32 eyes with VMT and drusen (68.75%) had disrupted ISel, compared to 8 out of 37 (21.6%) control eyes with drusen only and to 12 out of 37 (32.4%) control eyes with VMT only. Chi-square analysis showed significant association between drusen and pseudodrusen on fovea, VMT, and localization of ISel disruption. The changes of the ISel were mainly found in the area that corresponded to VMT. The SD-OCT revealed drusen throughout the macula and discontinuation of ISel only in the fovea in 4 of 32 (12.5%) eyes with VMT, whereas none of 37 control eyes with drusen only had similar appearance. Conclusions: The drusen in association with the cystoid macular edema induced by vitreous traction contribute to the photoreceptor layer defect overlying drusen in the fovea. In addition, the number of drusen and pseudodrusen was increased in the area of the vitreous traction compared to the peripheral retina. © 2013 Wichtig Editore.
- Published
- 2013
8. Dry eye in Graves' ophthalmopathy: Correlation with corneal hypoesthesia
- Author
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Achtsidis, V. Tentolouris, N. Theodoropoulou, S. Panagiotidis, D. Vaikoussis, E. Saldana, M. Gouws, P. Theodossiadis, P.G.
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genetic structures ,sense organs ,eye diseases - Abstract
Purpose: To evaluate dry eye disease and corneal sensitivity in patients with early and active Graves' ophthalmopathy (GO). Methods: A total of 52 eyes of 26 patients with early GO and 74 eyes of 37 age- and sex-matched controls were included in our study. Dry eye disease was assessed based on the criteria of theInternational Dry Eye Workshop. Diagnosis of early GO was based on the European Group on Graves' Orbitopathy consensus statement. Clinical Activity Score (CAS) and Werner-NOSPECS Score were determined. Corneal sensitivity was assessed using a Cochet-Bonnet aesthesiometer. Results: A total of 67.8% of patients with early GO and 13.5% of healthy controls had ocular surface dryness (p
- Published
- 2013
9. The effect of alpha antagonists on pupil dynamics: Implications for the diagnosis of intraoperative floppy iris syndrome
- Author
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Theodossiadis, P.G. Achtsidis, V. Theodoropoulou, S. Tentolouris, N. Komninos, C. Fountas, K.N.
- Abstract
Purpose: To assess pupil dynamics quantitatively in relation to the use of α 1-adrenoceptor antagonists, which contribute to the features of intraoperative floppy iris syndrome, using a new, hand-held, digital pupillometer. Design: Prospective case-control study. Methods: We studied 15 and 25 patients administered tamsulosin and alfuzosin, respectively, as well as 25 control patients. Resting pupil diameter and subsequent contraction, latency, constriction velocity, and dilation velocity were recorded using an electronic pupillometer. All pupil measurements were performed before and after pharmacologic dilation. Results: In predilation pupillary measurements, we detected a significant decrease in maximum pupillary diameter by 0.50 ± 0.19 mm (P =.011) and in the mean percentage of diameter reduction after stimulation (5.23 ± 2.42%, P =.035) in the tamsulosin group. Alfuzosin also induced a significant decrease in maximum pupillary diameter (0.49 ± 0.17 mm, P =.005). Constriction velocity was significantly reduced by 0.70 ± 0.20 m/s (P =.001) in the tamsulosin group and by 0.54 ± 0.18 m/s (P =.004) in the alfuzosin group. In terms of postdilation measurements, maximum and minimum pupil diameters were reduced significantly only in the tamsulosin group (by 1.09 ± 0.31 mm [P =.001] and by 0.89 ± 0.36 mm [P =.016], respectively). Conclusions: We describe a reliable, accurate, and rapid method to acquire quantitative pupil measurements and identify the tendency for intraoperative floppy iris syndrome before cataract surgery after the use of alfuzosin and tamsulosin. This investigation also analyzed the similarities and differences induced by the 2 drugs in predilation and postdilation pupil dynamics, demonstrating that tamsulosin is more potent than alfuzosin in inducing intraoperative floppy iris syndrome. © 2012 Elsevier Inc.
- Published
- 2012
10. Hemodialysis-induced alterations in macular thickness measured by optical coherence tomography in diabetic patients with end-stage renal disease
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Theodossiadis, P.G. Theodoropoulou, S. Neamonitou, G. Grigoropoulos, V. Liarakos, V. Triantou, E. Theodossiadis, G.P. Vlahakos, D.V.
- Subjects
genetic structures ,sense organs ,eye diseases - Abstract
Background/Aims: To evaluate changes in macular thickness measured by optical coherence tomography (OCT) during a hemodialysis (HD) session in diabetic patients with end-stage renal disease. Methods: 72 eyes of 36 diabetic patients with and without macular edema were evaluated before and immediately after an HD session. Average and maximum macular thicknesses in the central disk (6 mm in diameter) and total macular volume were measured. Results: In the eyes with diabetic macular edema, maximum macular thickness within the central disk of 6 mm, and mainly in its peripheral parts, was significantly reduced by 31.18 ± 4.18 μm after HD (p < 0.001). Average macular thickness and total macular volume were also significantly reduced (p = 0.003 and 0.015, respectively). In diabetic eyes without edema, maximum macular thickness decreased significantly by 11.21 ± 1.98 μm after HD (p < 0.001), while average macular thickness and total macular volume decreased slightly (p = 0.034, p = 0.043). Best-corrected visual acuity failed to change. We found a significant association of macular thickness changes with osmolality reduction and the presence of macular edema. Conclusion: HD decreases macular thickness in diabetic patients with macular edema, while there exists a less-pronounced effect in diabetic eyes without edema. Copyright © 2011 S. Karger AG, Basel.
- Published
- 2012
11. The epidemiology of cataract: A study in Greece
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Theodoropoulou, S. Theodossiadis, P. Samoli, E. Vergados, I. Lagiou, P. Tzonou, A.
- Subjects
eye diseases - Abstract
Purpose: We conducted a case-control study to identify risk factors for cataract in the Mediterranean Greek population. Three hundred and fourteen cases and 314 frequency-matched controls of both genders, aged 45-85, attending the ophthalmology department of a major teaching hospital in Athens, Greece, were included in the study. Methods: Cases were medically diagnosed and classified. Controls were healthy visitors without cataract. A detailed questionnaire, covering demographic, socioeconomic, somatometric, lifestyle and medical history variables, provided data on possible risk factors for cataract. Analyses were conducted through multiple logistic regression. Main outcome measures: Cataract overall and by type: nuclear, cortical and posterior subcapsular (PSC). Results: Statistically significant increased risk for cataract overall was found for current (OR = 1.99, 95%CI: 1.23-3.23) and ex-smokers (OR = 1.64, 95%CI: 1.02-2.70), history of coronary heart disease (OR = 2.25, 95%CI: 1.43-3.55), family history of ophthalmologic diseases (OR = 1.51, 95%CI: 1.03-2.20) and higher sunlight exposure at the beach (OR = 2.26, 95%CI: 1.37-3.72) as well as at work (OR = 2.03, 95%CI: 1.32-3.12). Use of measures protecting against sunlight at the beach, i.e. hat (OR = 0.58, 95%CI: 0.39-0.85) and vision repair spectacles (OR = 0.44, 95%CI: 0.30-0.65), were associated with reduced risk. Results for cataract overall were also evident for the nuclear type and in most circumstances for PSC type, but were only suggestive for the cortical type of cataract. Conclusion: We identified certain possible risk factors for age-related cataract. In a Mediterranean Greek population, we found that smoking, use of cortisone drops, cardiovascular heart disease and sunlight exposure increase the risk for cataract, while use of hat and vision repair spectacles act protectively. © 2010 The Authors Journal compilation © 2010 Acta Ophthalmol.
- Published
- 2011
12. Interleukin 33/ST2 signaling regulates inflammatory response in choroidal stroma and ocular angiogenesis: implications for age-related macular degeneration
- Author
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Theodoropoulou, S., primary, Doyle, S., additional, Copland, D., additional, Liu, J., additional, Wu, J., additional, Campbell, M., additional, and Dick, A., additional
- Published
- 2015
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13. Chronic coffee consumption has an unfavorable effect on aortic stiffness and wave reflections
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Vlachopoulos, C Ioakeimidis, N Dima, I Panagiotakos, D and Theodoropoulou, S Velitzelou, K Stefanadis, C
- Published
- 2005
14. Attentional facilitation of response is impaired for antisaccades but not for saccades in patients with schizophrenia: Implications for cortical dysfunction
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Smyrnis, N. Malogiannis, I.A. Evdokimidis, I. Stefanis, N.C. Theleritis, C. Vaidakis, A. Theodoropoulou, S. Stefanis, C.N.
- Abstract
The facilitation of response known as the "gap effect" (a decrease of response latency), observed for saccades and antisaccades when attention is modulated prior to such eye movements, was studied in patients with schizophrenia and in controls. The hypothesis tested was whether patients would show a deficient attentional facilitation in response latency. Fifteen patients with schizophrenia and 17 healthy controls performed blocks of saccades and antisaccades in a "gap" condition and an "overlap" condition. Saccade and antisaccade response latencies as well as the error rate for antisaccades were measured for each subject. A similar gap effect (decrease in latency for the gap compared to the overlap condition) was present in the saccade task for patients and controls. In contrast the gap effect in the antisaccade task was absent in 50% of patients compared to none of the controls. This finding was interpreted as indicative of deficient pre-processing in antisaccade-specific cortical areas in schizophrenia (such as the prefrontal cortex), while visually guided saccade processing remained intact. Our results, in addition to many other recent findings, could lead to specific hypotheses on cortical dysfunction in schizophrenia. © Springer-Verlag 2004.
- Published
- 2004
15. Cytokine serum levels, autologous mixed lymphocyte reaction and surface marker analysis in never medicated and chronically medicated schizophrenic patients
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Theodoropoulou, S Spanakos, G Baxevanis, CN Economou, M and Gritzapis, AD Papamichail, MP Stefanis, CN
- Abstract
A number of immunological parameters were studied in 82 DSM-III-R diagnosed schizophrenic patients (53 first drug-naive and 29 medicated chronic patients) as well as 67 healthy blood donors. The serum levels of interleukin-2 (IL-2), interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) were measured and correlated with cellular immunity, as assessed by the autologous mixed lymphocyte reaction (AMLR). T lymphocyte subsets were also examined. The above immune parameters were reassessed in a subgroup of ii first-episode, drug-naive patients 1 month after neuroleptic medication. IL-2 serum levels were significantly lower, and IL-1 beta and TNF-alpha were significantly higher in schizophrenic patients compared with healthy donors (P
- Published
- 2001
16. Ultra-wide field imaging of retinopathy of prematurity (ROP) using Optomap-200TX
- Author
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Theodoropoulou, S., primary, Ainsworth, S., additional, and Blaikie, A., additional
- Published
- 2013
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17. Atypical toxoplasmic retinochoroiditis
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Theodoropoulou, S., primary, Schmoll, C., additional, Templeton, K., additional, and Dhillon, B., additional
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- 2012
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18. Optical properties of carbon materials formed by pyrolysis of novolac-resin/biomass composites
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Theodoropoulou, S., primary, Papadimitriou, D., additional, Zoumpoulakis, L., additional, and Simitzis, J., additional
- Published
- 2004
- Full Text
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19. Interleukin 33/ ST2 signaling regulates inflammatory response in choroidal stroma and ocular angiogenesis: implications for age-related macular degeneration.
- Author
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Theodoropoulou, S., Doyle, S., Copland, D., Liu, J., Wu, J., Campbell, M., and Dick, A.
- Subjects
- *
RETINAL degeneration , *BLINDNESS , *INTERLEUKIN-33 - Abstract
Purpose Age-related macular degeneration (AMD) is a leading cause of irreversible blindness. We wished to elaborate mechanisms that regulate RPE-choroidal microenvironment in AMD. We hypothesize that retinal pigment epithelial cells (RPE) produce interleukin 33 (IL-33) and regulate choroidal stromal fibroblasts and mast cell activation and angiogenesis in an ST2-dependent manner. Through such mechanisms, change in choroidal architecture may contribute to AMD phenotypes observed clinically. Methods Upon treatment, RPE cells, human choroidal fibroblasts and bone-marrow-derived mast cells (BMMC) were assayed by RT- PCR, Western Blot and ELISA. Choroidal sprouting assay and laser-induced choroidal neovascularization (CNV) were used as models of ocular angiogenesis. Results TLR-stimulation of RPE significantly up-regulated IL-33 expression. ST2+ BMMC generated a spectrum of inflammatory cytokines when cultured with IL-33 rich RPE supernatant. Pretreatment with IL-33 antagonist markedly inhibited the ability of BMMC to produce inflammatory mediators. Importantly, activation of inflammatory cascade upon RPE supernatant treatment was abrogated in ST2-/- BMMC. In a wound-healing assay, recombinant IL-33 treatment of human choroidal fibroblasts impaired their ability to migrate and contract collagen gel. Furthermore, IL-33 treatment promoted vascular choroidal sprouting in WT and IL33-/- explants. CNV was also regulated by exogenous and endogenous IL-33 in WT and IL33-/- mice respectively. Conclusions Our data illuminate an endogenous IL-33/ ST2 pathway between RPE function and choroidal stroma, influencing tissue remodeling and regulating angiogenesis. Our findings support IL-33/ ST2 axis as a therapeutic target in AMD. [ABSTRACT FROM AUTHOR]
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- 2015
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20. Anti-VEGF Therapy to Treat Corneal Neovascularization.
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Papathanassiou, M., Theodoropoulou, S., Analitis, S., and Tzonou, A.
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- *
VASCULAR endothelial growth factors , *NEOVASCULARIZATION - Abstract
The article discusses the role of anti-vascular endothelial growth factor (VEGF) therapy in treatment of corneal neovascularization.
- Published
- 2013
21. Hybrid Nanoparticles from Random Polyelectrolytes and Carbon Dots.
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Theodoropoulou S, Vardaxi A, Kagkoura A, Tagmatarchis N, and Pispas S
- Abstract
The present study concerns the preparation of hybrid nanostructures composed of carbon dots (CDs) synthesized in our lab and a double-hydrophilic poly(2-dimethylaminoethyl methacrylate- co -oligo(ethylene glycol) methyl ether methacrylate) (P(DMAEMA- co -OEGMA)) random co polymer through electrostatic interactions between the negatively charged CDs and the positively charged DMAEMA segments of the co polymer. The synthesis of P(DMAEMA- co -OEGMA) co polymer was conducted through RAFT polymerization. Furthermore, the co polymer was converted into a strong cationic random polyelectrolyte through quaternization of the amine groups of DMAEMA segments with methyl iodide (CH
3 I), and it was subsequently utilized for the complexation with the carbon dots. The molecular, physicochemical, and photophysical characterization of the aqueous solution of the co polymers and their hybrid nanoparticles was conducted using dynamic and electrophoretic light scattering (DLS, ELS) and spectroscopic techniques, such as UV-Vis, fluorescence (FS), and FT-IR spectroscopy. In addition, studies of their aqueous solution using DLS and ELS showed their responsiveness to external stimuli (pH, temperature, ionic strength). Finally, the interaction of selected hybrid nanoparticles with iron (III) ions was confirmed through FS spectroscopy, demonstrating their potential application for heavy metal ions sensing.- Published
- 2024
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22. Unravelling the therapeutic potential of IL-33 for atrophic AMD.
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Clare AJ, Liu J, Copland DA, Theodoropoulou S, and Dick AD
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- Aged, Angiogenesis Inhibitors, Cytokines metabolism, Humans, Interleukin-33 metabolism, Retinal Pigment Epithelium pathology, Vascular Endothelial Growth Factor A metabolism, Visual Acuity, Geographic Atrophy pathology, Wet Macular Degeneration drug therapy, Wet Macular Degeneration metabolism
- Abstract
Age-related macular degeneration (AMD), a degenerative disease affecting the retinal pigment epithelium (RPE) and photoreceptors in the macula, is the leading cause of central blindness in the elderly. AMD progresses to advanced stages of the disease, atrophic AMD (aAMD), or in 15% of cases "wet" or neovascular AMD (nAMD), associated with substantial vision loss. Whilst there has been advancement in therapies treating nAMD, to date, there are no licenced effective treatments for the 85% affected by aAMD, with disease managed by changes to diet, vitamin supplements, and regular monitoring. AMD has a complex pathogenesis, involving highly integrated and common age-related disease pathways, including dysregulated complement/inflammation, impaired autophagy, and oxidative stress. The intricacy of AMD pathogenesis makes therapeutic development challenging and identifying a target that combats the converging disease pathways is essential to provide a globally effective treatment. Interleukin-33 is a cytokine, classically known for the proinflammatory role it plays in allergic disease. Recent evidence across degenerative and inflammatory disease conditions reveals a diverse immune-modulatory role for IL-33, with promising therapeutic potential. Here, we will review IL-33 function in disease and discuss the future potential for this homeostatic cytokine in treating AMD., (© 2021. The Author(s).)
- Published
- 2022
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23. Interleukin-33 regulates metabolic reprogramming of the retinal pigment epithelium in response to immune stressors.
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Scott LM, Vincent EE, Hudson N, Neal C, Jones N, Lavelle EC, Campbell M, Halestrap AP, Dick AD, and Theodoropoulou S
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- Animals, Cell Line, Cell Proliferation, Cell Survival, Energy Metabolism, Gene Knockdown Techniques, Glycolysis drug effects, Humans, Hydrogen Peroxide pharmacology, Interferon Inducers pharmacology, Interleukin-33 drug effects, Interleukin-33 genetics, Lipopolysaccharides pharmacology, Mice, Mice, Knockout, Mitochondria drug effects, Oxidants pharmacology, Oxidation-Reduction drug effects, Oxidative Stress, Poly I-C pharmacology, Primary Cell Culture, Pyruvic Acid metabolism, Cell Respiration physiology, Glycolysis physiology, Interleukin-33 metabolism, Mitochondria metabolism, Retinal Pigment Epithelium metabolism
- Abstract
It remains unresolved how retinal pigment epithelial cell metabolism is regulated following immune activation to maintain retinal homeostasis and retinal function. We exposed retinal pigment epithelium (RPE) to several stress signals, particularly Toll-like receptor stimulation, and uncovered an ability of RPE to adapt their metabolic preference on aerobic glycolysis or oxidative glucose metabolism in response to different immune stimuli. We have identified interleukin-33 (IL-33) as a key metabolic checkpoint that antagonizes the Warburg effect to ensure the functional stability of the RPE. The identification of IL-33 as a key regulator of mitochondrial metabolism suggests roles for the cytokine that go beyond its extracellular "alarmin" activities. IL-33 exerts control over mitochondrial respiration in RPE by facilitating oxidative pyruvate catabolism. We have also revealed that in the absence of IL-33, mitochondrial function declined and resultant bioenergetic switching was aligned with altered mitochondrial morphology. Our data not only shed new light on the molecular pathway of activation of mitochondrial respiration in RPE in response to immune stressors but also uncover a potentially novel role of nuclear intrinsic IL-33 as a metabolic checkpoint regulator.
- Published
- 2021
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24. Treatment with interleukin-33 is non-toxic and protects retinal pigment epithelium in an ageing model of outer retinal degeneration.
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Clare AJ, Copland DA, Nicholson LB, Liu J, Neal CR, Moss S, Dick AD, and Theodoropoulou S
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- Animals, Disease Models, Animal, Humans, Immunohistochemistry, Macular Degeneration etiology, Macular Degeneration metabolism, Macular Degeneration pathology, Mice, Mice, Knockout, Retinal Degeneration drug therapy, Retinal Degeneration pathology, Retinal Pigment Epithelium pathology, Retinal Pigment Epithelium ultrastructure, Treatment Outcome, Aging genetics, Aging metabolism, Interleukin-33 pharmacology, Retinal Degeneration etiology, Retinal Degeneration metabolism, Retinal Pigment Epithelium drug effects, Retinal Pigment Epithelium metabolism
- Abstract
The leading cause of central vision loss, age-related macular degeneration (AMD), is a degenerative disorder characterized by atrophy of retinal pigment epithelium (RPE) and photoreceptors. For 15% of cases, neovascularization occurs, leading to acute vision loss if left untreated. For the remaining patients, there are currently no treatment options and preventing progressive RPE atrophy remains the main therapeutic goal. Previously, we have shown treatment with interleukin-33 can reduce choroidal neovascularization and attenuate tissue remodelling. Here, we investigate IL-33 delivery in aged, high-fat diet (HFD) fed mice on a wildtype and complement factor H heterozygous knockout background. We characterize the non-toxic effect following intravitreal injection of IL-33 and further demonstrate protective effects against RPE cell death with evidence of maintaining metabolic retinal homeostasis of Cfh+/-~HFD mice. Our results further support the potential utility of IL-33 to prevent AMD progression., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)
- Published
- 2020
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25. Treatment of diabetic retinopathy through neuropeptide Y-mediated enhancement of neurovascular microenvironment.
- Author
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Ou K, Copland DA, Theodoropoulou S, Mertsch S, Li Y, Liu J, Schrader S, Liu L, and Dick AD
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- Animals, Apoptosis drug effects, Cellular Microenvironment drug effects, Diabetes Mellitus, Experimental drug therapy, Diabetes Mellitus, Experimental genetics, Diabetes Mellitus, Experimental pathology, Diabetic Retinopathy genetics, Diabetic Retinopathy pathology, Endothelial Cells drug effects, Humans, Mice, N-Methylaspartate pharmacology, Neuropeptide Y genetics, Rats, Retina drug effects, Retina pathology, Retinal Ganglion Cells drug effects, Retinal Ganglion Cells pathology, Retinal Neovascularization genetics, Retinal Neovascularization pathology, Vascular Endothelial Growth Factor A pharmacology, Diabetic Retinopathy drug therapy, N-Methylaspartate genetics, Neuropeptide Y pharmacology, Retinal Neovascularization drug therapy, Vascular Endothelial Growth Factor A genetics
- Abstract
Diabetic retinopathy (DR) is one of the most severe clinical manifestations of diabetes mellitus and a major cause of blindness. DR is principally a microvascular disease, although the pathogenesis also involves metabolic reactive intermediates which induce neuronal and glial activation resulting in disruption of the neurovascular unit and regulation of the microvasculature. However, the impact of neural/glial activation in DR remains controversial, notwithstanding our understanding as to when neural/glial activation occurs in the course of disease. The objective of this study was to determine a potential protective role of neuropeptide Y (NPY) using an established model of DR permissive to N-methyl-D-aspartate (NMDA)-induced excitotoxic apoptosis of retinal ganglion cells (RGC) and vascular endothelial growth factor (VEGF)-induced vascular leakage. In vitro evaluation using primary retinal endothelial cells demonstrates that NPY promotes vascular integrity, demonstrated by maintained tight junction protein expression and reduced permeability in response to VEGF treatment. Furthermore, ex vivo assessment of retinal tissue explants shows that NPY can protect RGC from excitotoxic-induced apoptosis. In vivo clinical imaging and ex vivo tissue analysis in the diabetic model permitted assessment of NPY treatment in relation to neural and endothelial changes. The neuroprotective effects of NPY were confirmed by attenuating NMDA-induced retinal neural apoptosis and able to maintain inner retinal vascular integrity. These findings could have important clinical implications and offer novel therapeutic approaches for the treatment in the early stages of DR., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)
- Published
- 2020
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26. Dysregulated claudin-5 cycling in the inner retina causes retinal pigment epithelial cell atrophy.
- Author
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Hudson N, Celkova L, Hopkins A, Greene C, Storti F, Ozaki E, Fahey E, Theodoropoulou S, Kenna PF, Humphries MM, Curtis AM, Demmons E, Browne A, Liddie S, Lawrence MS, Grimm C, Cahill MT, Humphries P, Doyle SL, and Campbell M
- Subjects
- Animals, Blood-Retinal Barrier diagnostic imaging, Blood-Retinal Barrier drug effects, Capillary Permeability drug effects, Capillary Permeability physiology, Chlorocebus aethiops, Claudin-5 genetics, Diet, High-Fat adverse effects, Disease Models, Animal, Fluorescein Angiography, Fundus Oculi, Gene Knockdown Techniques, Geographic Atrophy drug therapy, Geographic Atrophy etiology, Geographic Atrophy prevention & control, Healthy Volunteers, Humans, Magnetic Resonance Imaging, Mice, Mice, Transgenic, Photoperiod, RNA, Small Interfering metabolism, Retinal Pigment Epithelium drug effects, Retinal Pigment Epithelium pathology, ARNTL Transcription Factors metabolism, Blood-Retinal Barrier pathology, Circadian Clocks physiology, Claudin-5 metabolism, Geographic Atrophy pathology
- Abstract
Age-related macular degeneration (AMD) is the leading cause of central retinal vision loss worldwide, with an estimated 1 in 10 people over the age of 55 showing early signs of the condition. There are currently no forms of therapy available for the end stage of dry AMD, geographic atrophy (GA). Here, we show that the inner blood-retina barrier (iBRB) is highly dynamic and may play a contributory role in GA development. We have discovered that the gene CLDN5, which encodes claudin-5, a tight junction protein abundantly expressed at the iBRB, is regulated by BMAL1 and the circadian clock. Persistent suppression of claudin-5 expression in mice exposed to a cholesterol-enriched diet induced striking retinal pigment epithelium (RPE) cell atrophy, and persistent targeted suppression of claudin-5 in the macular region of nonhuman primates induced RPE cell atrophy. Moreover, fundus fluorescein angiography in human and nonhuman primate subjects showed increased retinal vascular permeability in the evening compared with the morning. These findings implicate an inner retina-derived component in the early pathophysiological changes observed in AMD, and we suggest that restoring the integrity of the iBRB may represent a novel therapeutic target for the prevention and treatment of GA secondary to dry AMD.
- Published
- 2019
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27. Clinical pathophysiology of thyroid eye disease: The Cone Model.
- Author
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Meyer P, Das T, Ghadiri N, Murthy R, and Theodoropoulou S
- Subjects
- Adipose Tissue pathology, Eye Movements physiology, Graves Ophthalmopathy diagnostic imaging, Humans, Magnetic Resonance Imaging, Ocular Motility Disorders physiopathology, Oculomotor Muscles diagnostic imaging, Orbit pathology, Tomography, X-Ray Computed, Graves Ophthalmopathy physiopathology, Models, Biological, Oculomotor Muscles pathology
- Abstract
The clinical features of thyroid eye disease are dictated by the orbit's compartmentalisation; particularly, the muscle cone, which is delimited by the rectus muscles, their inter-muscular septa and the posterior sclera. The cone is anchored to the orbit apex and contains the posterior globe, the muscle bellies, a fat pad, and the blood circulation, optic nerve, and CSF sheath. It is surrounded by mobile extraconal fat, retained by the orbital septum.Thyroid eye disease is caused by expansion of muscle bellies and fat within the cone. Mechanical properties of the cone determine that the disease partitions into three phases: circumferential expansion, with forward displacement of extraconal fat; axial elongation, with increasing cone pressure; impedance of posterior venous outflow, with cone oedema and venous flow reversal.Venous flow reversal can be observed in the conjunctival circulation. It is initially transient, accompanying rises in cone pressure caused by eye movements, but later becomes permanent. It is a useful clinical sign that locates diseased muscles and anticipates venous compressive crises.Strabismus arises when inflamed rectus muscles, swollen by hydrated glycosaminoglycans, lose contractility and compliance. The incomitance is moderated by increasing stiffness affecting all the rectus muscles, as they are stretched during cone expansion.Immunomodulation, which rapidly reduces cone volume, relieving muscle elongation and stiffness, may paradoxically unmask strabismus. However, ciclosporin A suppresses late post-inflammatory fibrosis and only 4 of 71 patients so-treated required strabismus surgery.The cone model also accounts for the variety of clinical presentations of thyroid eye disease.
- Published
- 2019
- Full Text
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28. Müller Cells Stabilize Microvasculature through Hypoxic Preconditioning.
- Author
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Ou K, Mertsch S, Theodoropoulou S, Wu J, Liu J, Copland DA, Scott LM, Dick AD, Schrader S, and Liu L
- Subjects
- Angiopoietin-Like Protein 4 analysis, Cell Line, Cell Proliferation drug effects, Cell Survival drug effects, Culture Media, Conditioned pharmacology, Ependymoglial Cells cytology, Ependymoglial Cells metabolism, Glycolysis drug effects, Humans, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Microvessels metabolism, Mitochondria drug effects, Mitochondria metabolism, Neovascularization, Physiologic drug effects, TOR Serine-Threonine Kinases metabolism, Vascular Endothelial Growth Factor A analysis, Cell Hypoxia
- Abstract
Background/aims: Hypoxia of the retina is a common pathogenic drive leading to vision loss as a result of tissue ischemia, increased vascular permeability and ultimately retinal neovascularisation. Here we tested the hypothesis that Müller cells stabilize the neurovascular unit, microvasculature by suppression of HIF-1α activation as a result of hypoxic preconditioning., Methods: Tube Formation Assay and In vitro Vascular Permeability Image Assay were used to analyze angiogenesis and vascular integrity. Seahorse XF Cell Mito Stress Test was used to measure mitochondrial respiration. Gene and protein expression were examined by qRTPCR, ELISA and western blot., Results: Hypoxic insult induces a significant induction of proangiogenic factors including vascular endothelial growth factor (VEGF) and angiopoietinlike 4 (ANGPTL-4) resulting in angiogenesis and increased vascular permeability of vascular endothelial cells. Hypoxic preconditioning of a human retinal Müller glia cell line significantly attenuates HIF-1α activation through the inhibition of mTOR and concomitant induction of aerobic glycolysis, stabilizing endothelial cells., Conclusion: Hypoxic preconditioning of Müller cells confers a robust protection to endothelial cells, through the suppression of HIF1α activation and its downstream regulation of VEGF and ANGPTL-4., Competing Interests: The authors declare that there is no conflict of interest regarding the publication of this paper., (© Copyright by the Author(s). Published by Cell Physiol Biochem Press.)
- Published
- 2019
- Full Text
- View/download PDF
29. Serous macular detachment due to nasally located optic disc pit-coloboma.
- Author
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Theodoropoulou S, Theodossiadis G, Sallam A, and Theodossiadis P
- Published
- 2018
- Full Text
- View/download PDF
30. A Perspective of AMD Through the Eyes of Immunology.
- Author
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Copland DA, Theodoropoulou S, Liu J, and Dick AD
- Subjects
- Animals, Complement Factor H genetics, Humans, Inflammasomes immunology, Immunity, Cellular physiology, Immunity, Innate physiology, Inflammation immunology, Macular Degeneration immunology
- Abstract
Despite strong genetic associations, compelling human histological data and numerous hypotheses generated with supportive animal data, the mechanisms of inflammation or inflammatory control of cell health during progression of age-related macular degeneration arguably remain elusive. This perspective delivers a view that maintaining tissue health requires active immune cellular and tissue pathways, but when responses are perturbed or exaggerated, chronic inflammation is destructive. There are potential pathways and processes to enable understanding and determine how potential causative factors including altered cellular metabolism, senescence, oxidative stress disrupt tissue homeostasis are engaged. Establishing differences in the immune phenotype between normal aging and AMD, and how the inter-relatedness of these triggers contribute to pathobiology is integral for future therapeutic success.
- Published
- 2018
- Full Text
- View/download PDF
31. Impairing autophagy in retinal pigment epithelium leads to inflammasome activation and enhanced macrophage-mediated angiogenesis.
- Author
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Liu J, Copland DA, Theodoropoulou S, Chiu HA, Barba MD, Mak KW, Mack M, Nicholson LB, and Dick AD
- Subjects
- Animals, Autophagy, Caspase 3 metabolism, Cells, Cultured, Coculture Techniques, Macular Degeneration pathology, Mice, Retinal Pigment Epithelium immunology, Rotenone pharmacology, Choroidal Neovascularization immunology, Inflammasomes metabolism, Macrophages cytology, Macular Degeneration immunology, Retinal Pigment Epithelium cytology
- Abstract
Age-related decreases in autophagy contribute to the progression of age-related macular degeneration (AMD). We have now studied the interaction between autophagy impaired in retinal pigment epithelium (RPE) and the responses of macrophages. We find that dying RPE cells can activate the macrophage inflammasome and promote angiogenesis. In vitro, inhibiting rotenone-induced autophagy in RPE cells elicits caspase-3 mediated cell death. Co-culture of damaged RPE with macrophages leads to the secretion of IL-1β, IL-6 and nitrite oxide. Exogenous IL-6 protects the dysfunctional RPE but IL-1β causes enhanced cell death. Furthermore, IL-1β toxicity is more pronounced in dysfunctional RPE cells showing reduced IRAK3 gene expression. Co-culture of macrophages with damaged RPE also elicits elevated levels of pro-angiogenic proteins that promote ex vivo choroidal vessel sprouting. In vivo, impaired autophagy in the eye promotes photoreceptor and RPE degeneration and recruitment of inflammasome-activated macrophages. The degenerative tissue environment drives an enhanced pro-angiogenic response, demonstrated by increased size of laser-induced choroidal neovascularization (CNV) lesions. The contribution of macrophages was confirmed by depletion of CCR2(+) monocytes, which attenuates CNV in the presence of RPE degeneration. Our results suggest that the interplay between perturbed RPE homeostasis and activated macrophages influences key features of AMD development.
- Published
- 2016
- Full Text
- View/download PDF
32. Ultra-wide field imaging of retinopathy of prematurity (ROP) using Optomap-200TX.
- Author
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Theodoropoulou S, Ainsworth S, and Blaikie A
- Subjects
- Bronchopulmonary Dysplasia complications, Female, Humans, Infant, Newborn, Ranibizumab, Retinopathy of Prematurity complications, Antibodies, Monoclonal, Humanized therapeutic use, Ophthalmoscopy methods, Retinopathy of Prematurity drug therapy, Retinopathy of Prematurity pathology
- Published
- 2013
- Full Text
- View/download PDF
33. Aminoimidazole carboxamide ribonucleotide (AICAR) inhibits the growth of retinoblastoma in vivo by decreasing angiogenesis and inducing apoptosis.
- Author
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Theodoropoulou S, Brodowska K, Kayama M, Morizane Y, Miller JW, Gragoudas ES, and Vavvas DG
- Subjects
- Aminoimidazole Carboxamide metabolism, Aminoimidazole Carboxamide pharmacology, Animals, Cell Cycle, Cell Line, Tumor, Cell Proliferation, Cyclins metabolism, Mice, Mice, Nude, Neoplasm Transplantation, Ribonucleotides metabolism, S Phase, Aminoimidazole Carboxamide analogs & derivatives, Antineoplastic Agents pharmacology, Apoptosis, Neovascularization, Pathologic drug therapy, Retinoblastoma drug therapy, Ribonucleotides pharmacology
- Abstract
5-Aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR), an analog of AMP is widely used as an activator of AMP-kinase (AMPK), a protein that regulates the responses of the cell to energy change. Recently, we showed that AICAR-induced AMPK activation inhibits the growth of retinoblastoma cells in vitro by decreasing cyclins and by inducing apoptosis and S-phase arrest. In this study, we investigated the effects of AMPK activator AICAR on the growth of retinoblastoma in vivo. Intraperitoneal injection of AICAR resulted in 48% growth inhibition of Y79 retinoblastoma cell tumors in mice. Tumors isolated from mice treated with AICAR had decreased expression of Ki67 and increased apoptotic cells (TUNEL positive) compared with the control. In addition, AICAR treatment suppressed significantly tumor vessel density and macrophage infiltration. We also showed that AICAR administration resulted in AMPK activation and mTOR pathway inhibition. Paradoxically observed down-regulation of p21, which indicates that p21 may have a novel function of an oncogene in retinoblastoma tumor. Our results indicate that AICAR treatment inhibited the growth of retinoblastoma tumor in vivo via AMPK/mTORC1 pathway and by apoptogenic, anti-proliferative, anti-angiogenesis mechanism. AICAR is a promising novel non-chemotherapeutic drug that may be effective as an adjuvant in treating Retinoblastoma.
- Published
- 2013
- Full Text
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34. Atypical toxoplasmic retinochoroiditis.
- Author
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Theodoropoulou S, Schmoll C, Templeton K, and Dhillon B
- Subjects
- Adult, Anti-Bacterial Agents administration & dosage, Antimalarials administration & dosage, Aqueous Humor microbiology, Chorioretinitis drug therapy, Chorioretinitis microbiology, DNA, Bacterial analysis, Diagnosis, Differential, Drug Therapy, Combination, Humans, Intravitreal Injections, Male, Polymerase Chain Reaction, Toxoplasma genetics, Toxoplasmosis, Ocular drug therapy, Toxoplasmosis, Ocular microbiology, Chorioretinitis diagnosis, Clindamycin administration & dosage, Pyrimethamine administration & dosage, Toxoplasma isolation & purification, Toxoplasmosis, Ocular diagnosis
- Abstract
We report a case of re-activation of Toxoplasma gondii as a cause of atypical retinal necrosis in an immunocompetent individual. The rapid development of necrotising confluent retinochoroiditis and vitreous inflammation necessitated urgent aqueous humor PCR analysis, which was positive for T gondii. The patient was treated with two intravitreal injections of clindamycin, along with oral sulphadiazine, pyrimethamine, folinic acid and prednisolone. He developed central retinal arterial occlusion, as a complication of toxoplasmic retinochoroiditis, and immediate anterior chamber paracentesis was performed with visual recovery. The injection of intravitreal clindamycin with concomitant oral therapy was associated with control of toxoplasmic retinochoroiditis and resolution of vitreous inflammation.
- Published
- 2012
- Full Text
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35. Heat shock protein 70 (HSP70) is critical for the photoreceptor stress response after retinal detachment via modulating anti-apoptotic Akt kinase.
- Author
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Kayama M, Nakazawa T, Thanos A, Morizane Y, Murakami Y, Theodoropoulou S, Abe T, Vavvas D, and Miller JW
- Subjects
- Animals, Caspases metabolism, Diterpenes administration & dosage, Diterpenes pharmacology, Enzyme Activation drug effects, Gene Expression Profiling, Gene Expression Regulation drug effects, HSP70 Heat-Shock Proteins genetics, Male, Mice, Models, Biological, Phosphorylation drug effects, Photoreceptor Cells, Vertebrate drug effects, Photoreceptor Cells, Vertebrate metabolism, Protein Binding drug effects, Quercetin administration & dosage, Quercetin pharmacology, Rats, Retinal Detachment genetics, Apoptosis drug effects, HSP70 Heat-Shock Proteins metabolism, Photoreceptor Cells, Vertebrate pathology, Proto-Oncogene Proteins c-akt metabolism, Retinal Detachment enzymology, Retinal Detachment pathology, Stress, Physiological drug effects
- Abstract
Photoreceptor apoptosis is a major cause of vision loss in many ocular diseases. Significant progress has been made to elucidate the molecular pathways involved in this process, yet little is known about proteins counteracting these apoptotic pathways. It is established that heat shock proteins (HSPs) function as molecular helper proteins (chaperones) by preventing protein aggregation and facilitating refolding of dysfunctional proteins, critical to the survival of all organisms. Here, we investigated the role of HSP70 on photoreceptor survival after experimental retinal detachment (RD) in mice and rats. We found that HSP70 was up-regulated after RD and associated with phosphorylated Akt, thereby preventing its dephosphorylation and further activation of cell death pathways. Administration of quercetin, which inhibits HSP70 and suppresses Akt phosphorylation significantly increased photoreceptor apoptosis. Similarly, RD-induced photoreceptor apoptosis was augmented in mice carrying hypomorphic mutations of the genes encoding HSP70. On the other hand, administration of geranylgeranylacetone, which induces an increase in HSP70 significantly decreased photoreceptor apoptosis after RD through prolonged activation of Akt pathway. Thus, HSP70 may be a favorable potential target to increase photoreceptor cell survival after RD., (Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
36. The epidemiology of cataract: a study in Greece.
- Author
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Theodoropoulou S, Theodossiadis P, Samoli E, Vergados I, Lagiou P, and Tzonou A
- Subjects
- Age Distribution, Aged, Aged, 80 and over, Case-Control Studies, Cataract classification, Female, Greece epidemiology, Humans, Male, Middle Aged, Risk Factors, Sex Distribution, Surveys and Questionnaires, Visual Acuity physiology, Cataract epidemiology
- Abstract
Purpose: We conducted a case-control study to identify risk factors for cataract in the Mediterranean Greek population. Three hundred and fourteen cases and 314 frequency-matched controls of both genders, aged 45-85, attending the ophthalmology department of a major teaching hospital in Athens, Greece, were included in the study., Methods: Cases were medically diagnosed and classified. Controls were healthy visitors without cataract. A detailed questionnaire, covering demographic, socioeconomic, somatometric, lifestyle and medical history variables, provided data on possible risk factors for cataract. Analyses were conducted through multiple logistic regression., Main Outcome Measures: Cataract overall and by type: nuclear, cortical and posterior subcapsular (PSC)., Results: Statistically significant increased risk for cataract overall was found for current (OR = 1.99, 95%CI: 1.23-3.23) and ex-smokers (OR = 1.64, 95%CI: 1.02-2.70), history of coronary heart disease (OR = 2.25, 95%CI: 1.43-3.55), family history of ophthalmologic diseases (OR = 1.51, 95%CI: 1.03-2.20) and higher sunlight exposure at the beach (OR = 2.26, 95%CI: 1.37-3.72) as well as at work (OR = 2.03, 95%CI: 1.32-3.12). Use of measures protecting against sunlight at the beach, i.e. hat (OR = 0.58, 95%CI: 0.39-0.85) and vision repair spectacles (OR = 0.44, 95% CI: 0.30-0.65), were associated with reduced risk. RESULTS for cataract overall were also evident for the nuclear type and in most circumstances for PSC type, but were only suggestive for the cortical type of cataract., Conclusion: We identified certain possible risk factors for age-related cataract. In a Mediterranean Greek population, we found that smoking, use of cortisone drops, cardiovascular heart disease and sunlight exposure increase the risk for cataract, while use of hat and vision repair spectacles act protectively., (© 2010 The Authors. Journal compilation © 2010 Acta Ophthalmol.)
- Published
- 2011
- Full Text
- View/download PDF
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