Effectiveness and safety of overnight orthokeratology with Boston XO2 high-permeability lens material: A 24 week follow-up study.

OBJECTIVE: To examine the effectiveness of overnight orthokeratology lenses made with Boston XO2, highly gas-permeable lens material for the temporary correction of myopia. METHODS: Myopic individuals from 9 to 62 years of age were eligible. Participants ≤ 12 years of age were required to have myopia ≤-4.00 D and astigmatism ≤ 1.50 D, and for those 13-62 years of age myopia ≤-5.00 D and astigmatism ≤ 3.00 D. All participants were required to have normal healthy eyes and not be receiving any ocular medications or systemic medications likely to affect the results of visual acuity. Participants wore the lenses for a minimum of 7h during sleep, and were evaluated on day 1 and weeks 1, 2, 4, 12, and 24. Success was defined as LogMAR ≤ 0.1. RESULTS: A total of 126 participants (63.5% females) with a mean age of 20.4 ± 11.5 years were recruited. Baseline LogMAR, and vertical and horizontal corneal curvature were 0.8, 7.7 mm, and 7.9 mm, respectively, in both eyes. A consistent decrease in LogMAR was noted from day 1 to week 12. The success rate increased with length of time (from 33.9% to 100% for the right eye and from 35.5% to 100% for the left eye from day 1 to week 24). No severe complications were noted. CONCLUSION: Overnight orthokeratology with lenses made of Boston XO2 material are effective and safe for the temporary reduction of myopia.

Silibinin inhibits ICAM-1 expression via regulation of N-linked and O-linked glycosylation in ARPE-19 cells.

To evaluate the effects of silibinin on intercellular adhesion molecule-1 (ICAM-1) expression, we used ARPE-19 cells as a model in which tumor necrosis factor (TNF-α) and interferon (IFN-γ) enhanced ICAM-1 expression. This upregulation was inhibited by silibinin. In an adherence assay using ARPE-19 and THP-1 cells, silibinin inhibited the cell adhesion function of ICAM-1. The inhibitory effects of silibinin on ICAM-1 expression were mediated via the blockage of nuclear translocation of p65 proteins in TNF-α and phosphorylation of STAT1 in IFN-γ-stimulated cells. In addition, silibinin altered the degree of N-linked glycosylation posttranslationally in ARPE-19 cells by significantly enhancing MGAT3 gene expression. Silibinin can increase the O-GlcNAc levels of glycoproteins in ARPE-19 cells. In a reporter gene assay, PUGNAc, which can also increase O-GlcNAc levels, inhibited NF-κB reporter activity in TNF-α-induced ARPE-19 cells and this process was augmented by silibinin treatment. Overexpression of OGT gene was associated with reduced TNF-α-induced ICAM-1 levels, which is consistent with that induced by silibinin treatment. Taken together, silibinin inhibits ICAM-1 expression and its function through altered O-linked glycosylation in NF-κB and STAT1 signaling pathways and decreases the N-linked glycosylation of ICAM-1 transmembrane protein in proinflammatory cytokine-stimulated ARPE-19 cells.

Glucosamine sulfate inhibits TNF-alpha and IFN-gamma-induced production of ICAM-1 in human retinal pigment epithelial cells in vitro.

PURPOSE: Glucosamine sulfate (GS) is a naturally occurring sugar that possesses some immunosuppressive effects in vitro and in vivo, but its mechanism is unknown. We investigated whether GS could modulate the proinflammatory cytokine-induced expression of the gene for intercellular adhesion molecule (ICAM)-1, an inflammatory protein in human retinal pigment epithelial (RPE) cells. METHODS: ARPE-19 cells were used as a model to determine the effects of GS on the expression of the ICAM-1 gene upregulated by TNF-alpha or IFN-gamma, by Western blot analysis and semiquantitative reverse transcription polymerase chain reaction (RT-PCR). The activation and nuclear translocation of the nuclear factors NF-kappaB and STAT1 were evaluated by immunocytochemistry, Western blot analysis, and electrophoretic mobility shift assay (EMSA). RESULTS: Both TNF-alpha and IFN-gamma increased the expression of ICAM-1 at the mRNA and protein levels in a time- and dose-dependent manner in ARPE-19 cells. GS effectively downregulated the TNF-alpha- or IFN-gamma-induced expression of ICAM-1 in the protein and mRNA level in a dose-dependent manner. GS further inhibited the nuclear translocation of p65 proteins in TNF-alpha and phosphorylated STAT1 in IFN-gamma-stimulated ARPE-19 cells. CONCLUSIONS: GS inhibits the expression of the ICAM-1 gene in ARPE-19 cell stimulated with TNF-alpha or IFN-gamma through blockade of NF-kappaB subunit p65 and nuclear translocation of STAT1. This study has demonstrated a potentially important property of GS in reducing ICAM-1 mediated inflammatory mechanisms in the eye.

Glucosamine sulfate inhibits proinflammatory cytokine-induced icam-1 production in human conjunctival cells in vitro.

PURPOSE: We investigated whether glucosamine sulfate modulates the production of ICAM-1 induced by proinflammatory cytokines and whether glucosamine sulfate inhibits leukocyte adhesion to a monolayer of human conjunctival epithelial cells stimulated with proinflammatory cytokines. METHODS: We used flow cytometry and either primary cultured human conjunctival cells or the Chang conjunctival cell model to determine the effects of glucosamine sulfate on the production of ICAM-1 in response to tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1beta, IL-6, TNF-alpha plus IFN-gamma, or TNF-alpha plus IL-1beta. The effects of glucosamine sulfate on the expression of the ICAM-1 gene, upregulated by various cytokines, were determined by semiquantitative reverse transcription-polymerase chain reaction. The activation and nuclear translocation of the nuclear factors NF-kappaB and STAT1 were evaluated by the transient transfection of reporter gene systems and immunocytochemistry. The influence of glucosamine-sulfate-modulated ICAM-1 on neutrophil adhesion was demonstrated in a model that measures the adherence of conjunctival cells and neutrophils. RESULTS: TNF-alpha, IFN-gamma, and IL-1beta significantly increased the production of ICAM-1 by both primary cultured human conjunctival cells and Chang conjunctival cells. Glucosamine sulfate effectively downregulated the production of ICAM-1 induced by TNF-alpha, IFN-gamma, IL-1beta, TNF-alpha plus IFN-gamma, or TNF-alpha plus IL-1beta. This downregulation occurred through the interferon-stimulated response element, IFN-gamma activation sequence, and binding sequence of NF-kappaB at the mRNA and protein levels. Glucosamine sulfate further inhibited the nuclear translocation of p65 protein in TNF-alpha- and IL-1beta-stimulated Chang conjunctival cells and phosphorylated STAT1 in IFN-gamma-stimulated Chang conjunctival cells. Glucosamine sulfate also significantly reduced the number of neutrophils adhering to a conjunctival monolayer in response to TNF-alpha, IFN-gamma, or IL-1beta. CONCLUSIONS: Our results suggest that glucosamine sulfate inhibits ICAM-1 production in conjunctival epithelial cells in vitro. Therefore, glucosamine sulfate might be valuable in the treatment of inflammatory ocular-surface conditions.

Retinoic acid induces VEGF gene expression in human retinal pigment epithelial cells (ARPE-19).

PURPOSE: The aim of this study was to evaluate the expression of vascular endothelial growth factor (VEGF) in response to retinoic acid (RA) in human retinal pigment epithelial cells. METHODS: Expression of VEGF in human ARPE-19 cells was determined by a semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). mRNA stability was assessed after the administration of actinomycin D. The induction of the VEGF gene by various RAs was also determined by semiquantitative RT-PCR. RESULTS: All-trans retinoic acid (atRA) time-dependently increased VEGF mRNA levels. The effect of atRA was dose-dependent in a range between 10(-7) M and 10(-6) M. Treatment with actinomycin D revealed that atRA induces the VEGF gene at the transcriptional level. Of the various RAs tested, atRA was the most potent inducer of the VEGF gene. CONCLUSIONS: We demonstrated that atRA stimulates the induction of the VEGF gene in ARPE-19 cells, suggesting a novel pathway for the development of age-related macular degeneration.

Corneal iron ring associated with orthokeratology.

Two teenaged girls had orthokeratology to correct myopia. The postoperative development of corneal iron rings in both eyes was disclosed by a biomicroscopic examination at 3 months in 1 patient and 5 months in the other. The location of the corneal iron rings coincided with the fitting curve of the reverse-geometry rigid contact lens, suggesting that the rings might have developed from tear pooling.

Pre-Descemet's corneal dystrophy associated with ichthyosis.

Pre-Descemet's dystrophy is a symmetrical bilateral comeal dystrophy consisting of multiple small discrete opacities of lipid-like material in the deep stroma just anterior to the pre-Descemet's membrane. We presented a case of a 46-year-old male who visited our hospital on account of acute conjunctivitis. On routine examination, we found multiple fine gray dots in the pre-Descemet's area and large, dark, scaly skin lesions over extensor surfaces of the extremities. After consultation with a dermatologist, X-linked recessive ichthyosis was diagnosed.