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The Effect of Multifocal Contact Lenses on Accomodation and Phoria in a Pediatric PopulationThe increasing prevalence of the use of distance-centered multifocal (MF) contact lenses as a method of myopia control in the pediatric population calls for a better understanding of binocularity and accommodation in children wearing these lenses. This was a prospective, randomized, crossover, single visit study that enrolled myopic children with normal accommodation and binocular vision and no history of myopia control treatment. All subjects were fitted with Coopervision Biofinity single vision (SV) and MF (+2.50D center distance add) contact lenses. Accommodative responses (photorefraction) and phorias (Modified Thorington) were measured at 4 distances (>3m, 100cm, 40cm, 25cm). Secondary measures included high and low contrast logMAR acuity, accommodative amplitude, and accommodative facility. Differences between MF and SV contact lenses were analyzed using repeated measures regression and paired t-tests. A total of 16 subjects, aged 10-15 years, completed the study. There was a small decrease in high (SV: -0.08, MF: +0.01) and low illumination (SV:-0.03, MF: +0.08) (both p<0.01) visual acuity, and contrast sensitivity (SV: 2.0 log units, MF: 1.9, p=0.015) with MFs. Subjects were more exophoric at 40cm (SV: -0.41 Δ, MF: -2.06 Δ) and 25cm (SV: -0.83 Δ, MF: -4.30 Δ) (both p<0.01). With MFs, subjects had decreased accommodative responses at distance (SV: -0.04 D; MF: -0.37 D, p=0.02), 100 cm (SV: +0.37 D; MF: -0.35 D, p<0.01), 40 cm (SV: +1.82 D; MF: +0.62 D, p<0.01), and 25 cm (SV: +3.38 D; MF: +1.75 D, p<0.01). There were no significant differences in accommodative amplitude (p=0.66) or accommodative facility (p=0.54). Children wearing MF contact lenses exhibited reduced accommodative responses and more exophoria at increasingly higher accommodative demands than with SV contact lenses. This suggests that children may be relaxing their accommodation and using the positive addition or increased depth of focus from added spherical aberration of the MF lenses. Further studies are needed to evaluate other lens designs, different amounts of positive addition and aberrations, and long-term adaptation to lenses.
Triptolide Induces Increases in Migration via Mitogen-activated Protein Kinase Phosphatase-1 control of P38 and JNK MAPK ActivationPurpose Triptolide is a Chinese herbal extract known for its anti-inflammatory and immunosuppressive effects in treating chronic inflammatory diseases and tumors. As these attributes promote wound healing, we determined if triptolide enhances corneal wound healing by stimulating human corneal epithelial cell (HCEC) migration through changes in negative feedback regulation by a dual specificity protein Phosphatase (DUSP1) of MAPK signaling mediated effect. Methods SV40-adenovirus-immortalized HCEC were maintained in DMEM/F12. Specific shRNA for MKP-1(DUSP1) and c-jun NH2- terminal kinase JNK-1 were transduced to establish stable cell lines deficient in their respective gene expression. Scratch wound assay was employed to assess cell migration rates by taking time-dependent serial photographs of cells following wound creation. Hydroxyurea (2.5 mM) was also added to the medium to inhibit cell proliferation during the experiment. Cell Titer-Glo® luminescent cell viability assay was used to evaluate cell viability by measuring ATP production by HCEC. Results Triptolide did not affect cell viability up to 10nM and stimulated wound closure through increases in migration. Maximal responses occurred at 1nM. These increases in migration were suppressed below that in the untreated control when p38 or JNK MAPK activation was inhibited. In the MKP-1 knockdown cells, migration was stimulated relative to the control and triptolide failed to augment this response. In JNK-1 knockdown cells, migration is comparable to SV40 wild type cells. In JNK-1 knockdown cells, triptolide mediated increases are diminished completely in the presence of p38 inhibition. Conclusions Triptolide at concentrations up to 10 nM promotes cell migration without compromising cell survival. Such promotion is mediated by loss of MKP-1 negative feedback control of p38 and JNK activation. Therefore, triptolide stimulates cell migration through inhibition of MKP-1 (DUSP1) stabilization induced by kinase mediated phosphorylation.