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2.
Am J Ophthalmol ; 260: 132-139, 2024 04.
Article in English | MEDLINE | ID: mdl-38151196

ABSTRACT

PURPOSE: Myopia is the most prevalent refractive error, imposing a substantial economic burden. Physical indicators constitute significant influencing factors for myopia. The National Health and Nutrition Examination Survey (NHANES) investigates the health and nutritional status of both children and adults in the United States. This study leveraged NHANES to explore the association between physical indicators and myopia among American adolescents. DESIGN: Retrospective case-control study. METHODS: The final study cohort consisted of 9008 adolescents. Demographic data, physical indicators, and vision data were extracted. The association between myopia and demographic factors, as well as physical indicators, employed weighted methods. Regression models were utilized to identify the associations between physical indicators and myopia. Cumulative odds logistic regression analysis was employed to investigate the association between physical indicators and the degree of myopia. Restricted cubic spline analysis was employed to examine the potential nonlinear relationship between physical indicators and the risk of myopia. RESULTS: The occurrence of myopia was significantly correlated with age (P < .001) and race (P = .019). Adolescents in the fourth percentile for weight (odds ratio [OR] 1.38, 95% confidence interval [CI] 1.13-1.70) and body mass index (BMI) (OR 1.26, 95% CI 1.05-1.51) exhibited an increased possibility of myopia. The highest risk of myopia was observed when the BMI approached 30. Height emerged as a risk factor for the degree of myopia (OR 1.02, 95% CI 1.01-1.03). CONCLUSIONS: A certain association existed between physical indicators and myopia. Weight and BMI were related to the occurrence of myopia, while height and race were associated with the degree of myopia.


Subject(s)
Myopia , Adult , Child , Humans , Adolescent , United States/epidemiology , Nutrition Surveys , Retrospective Studies , Case-Control Studies , Myopia/epidemiology , Risk Factors , Prevalence
3.
Arch Biochem Biophys ; 669: 1-10, 2019 07 15.
Article in English | MEDLINE | ID: mdl-31112708

ABSTRACT

Glaucoma is a major cause of irreversible blindness in the world and filtering surgery is commonly carried out to control intraocular pressure. Failure of filtering surgery is usually due to postoperative scarring, and fibroblast proliferation, collagen production and subconjunctival fibrosis play a prominent role in obstructing aqueous humor from the anterior chamber to the subconjunctival space. Zinc oxide (ZnO) nanoparticles have been widely applied in biomedical fields. However, the influence of ZnO nanoparticles on human tenon fibroblasts (HTFs) is still unclear. In the present study, we first explored the effects of various concentrations of ZnO nanoparticles on HTFs proliferation, reactive oxygen species (ROS) generation, cell cycle arrest, and apoptosis. Further, we determined the changes of transforming growth factor-ß (TGF-ß1), fibronectin (FN) extra domain A (ED-A), and procollagen I carboxyterminal propeptide (PICP) at mRNA and protein levels, explored the effect of ZnO nanoparticles on the collagen lattice contraction in HTFs. The results indicated that ZnO nanoparticles can efficiently inhibit HTFs proliferation, elevate ROS production level, and induce cell cycle arrest at G2/M phase, leading to HTFs apoptosis. ZnO nanoparticles can also decrease the expressions of TGF-ß1, ED-A, and PICP at mRNA and protein levels; significantly prevent fibroblast-mediated collagen lattice contraction. Taken together, ZnO nanoparticles can efficiently ameliorate collagen lattice contraction in HTFs, and may be a promising antifibrotic agent in glaucoma filtration surgery. Our findings provide a new insight on anti-scar formation after glaucoma filtration surgery by using ZnO nanoparticles.


Subject(s)
Collagen/metabolism , Fibroblasts/drug effects , Metal Nanoparticles/chemistry , Tenon Capsule/cytology , Zinc Oxide/pharmacology , Apoptosis/drug effects , Cell Proliferation/drug effects , Fibronectins/metabolism , G2 Phase Cell Cycle Checkpoints/drug effects , Humans , Peptide Fragments/metabolism , Procollagen/metabolism , Transforming Growth Factor beta1/metabolism , Zinc Oxide/chemistry
4.
Eur J Pharmacol ; 777: 33-40, 2016 Apr 15.
Article in English | MEDLINE | ID: mdl-26930229

ABSTRACT

As an anti-microtubule agent, paclitaxel has been widely applied clinically. However, the effects of paclitaxel on human tenon's fibroblast (HTF) proliferation and migration in vitro was still unclear. In the present study, we explored the influences of paclitaxel on HTF cell proliferation, cell viability, cell cycle phase distribution under various concentrations of paclitaxel (i.e., 0, 10(-8), 10(-7), 10(-6)mol/l) via real-time cell electronic system and flow cytometry, further determined the expression of TGF-ß1 and connective tissue growth factor (CTGF) after treatment with different concentrations of paclitaxel. Moreover, extra cellular matrix production and collagen lattice contraction assay were also explored. The results indicate that paclitaxel could apparently inhibit the cell viability, induces the elevation of S and G2/M phases of HTFs, and downregulates the expression of both TGF-ß1 and CTGF. Meanwhile, the levels of fibronectin extra domain A (EDA), collagen and collagen lattice contraction were apparently reduced after treatment with paclitaxel. Overall, paclitaxel could apparently inhibit the proliferation of HTFs and leads to cell cycle arrest at both S and G2/M phases, attenuates the generation of collagen and collagen lattice contraction, decreases the expressions of TGF-ß1, CTGF and fibronectin EDA. The inhibitory mechanism of paclitaxel on HTFs is involved in TGF-ß1 signaling pathway.


Subject(s)
Collagen/metabolism , Fibroblasts/cytology , Fibroblasts/drug effects , Paclitaxel/pharmacology , Signal Transduction/drug effects , Tenon Capsule/cytology , Transforming Growth Factor beta1/metabolism , Cell Cycle/drug effects , Cell Proliferation/drug effects , Connective Tissue Growth Factor/genetics , Fibroblasts/metabolism , Fibronectins/biosynthesis , Gene Expression Regulation/drug effects , Humans , RNA, Messenger/genetics , RNA, Messenger/metabolism
5.
Neurosci Lett ; 526(1): 24-8, 2012 Sep 20.
Article in English | MEDLINE | ID: mdl-22917607

ABSTRACT

BACKGROUND: Recently, alpha-lipoic acid (ALA) has been reported to afford protection against neurodegenerative disorders in humans and experimental animals, yet little study elucidates whether it works in glaucomatous optic neuropathy. OBJECTIVE: This study aims to investigate whether ALA possesses neuroprotection against hydrostatic pressure-induced damage and explore its possible protective mechanism in cultured retinal ganglion cells (RGCs) in vitro. METHODS: RGC-5 cells were differentiated using staurosporine and pre-treated with different concentrations of ALA, then subjected to 50mm Hg hydrostatic pressure for 6h. After elevated hydrostatic pressure, cell viability was measured using MTT assay and apoptosis was evaluated using flow cytometry with Annexin V/PI staining. Intracellular reactive oxygen species (ROS) changes were determined by flow cytometry based on 2',7'-dichlorofluorescein diacetate (DCFH-DA). The expression of manganese superoxide dismutase (MnSOD) was measured via quantitative real-time PCR and Western blotting analysis. RESULTS: Increases of apoptotic rate and ROS production were observed in pressure-treated RGC-5 cells compared to normal control cells. In contrast, pretreatment of ALA significantly reduced the production of ROS, increased the expression of MnSOD and prevented apoptosis in pressure-treated RGC-5 cells. CONCLUSIONS: These findings suggest that there are protective effects of ALA against elevated hydrostatic pressure-induced damage in RGC-5 cells, indicating ALA might be a potential therapeutic agent for glaucomatous optic neuropathy.


Subject(s)
Neuroprotective Agents/pharmacology , Retinal Ganglion Cells/drug effects , Thioctic Acid/pharmacology , Animals , Apoptosis , Cell Line , Hydrostatic Pressure/adverse effects , Rats , Reactive Oxygen Species/metabolism , Retinal Ganglion Cells/cytology , Superoxide Dismutase/metabolism
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