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Although 1% atropine effectively slows myopia progression, it is associated with adverse effects, including photophobia, blurred near vision, and poor compliance. We investigated whether lower doses of atropine would control myopia progression. One hundred and eighty-six children, from 6 to 13 years of age, were treated each night with different concentrations of atropine eye drops or a control treatment for up to 2 years. The mean myopic progression in each of the groups was 0.04 +/-0.63 diopter per year (D/Y) in the 0.5% atropine group, 0.45+/-0.55 D/Y in the 0.25% atropine group, and 0.47+/-0.91 D/Y in the 0.1% atropine group. All atropine groups showed significantly less myopic progression than the control group (1.06+/-0.61 D/Y) (p<0.01). Our study also showed that 61% of students in the 0.5% atropine group, 49% in the 0.25% atropine group and 42% in the 0.1% atropine group had no myopic progression. However, 4% of children in the 0.5% atropine group, 17% in the 0.25% atropine group, and 33% in the 0.1% atropine group still had fast myopic progression (>-1.0 D/Y). In contrast, only 8% of the control group showed no myopic progression and 44% had fast myopic progression. These results suggest that all three concentrations of atropine had significant effects on controlling myopia; however, treatment with 0.5% atropine was the most effective.

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ABSTRACT.Purpose: This randomized clinical trial assessed the treatment effects of atropine and/or multi-focal lenses in decreasing the progression rate of myopia in children. Methods: Two hundred and twenty-seven schoolchildren with myopia, aged from 6 to 13 years, who were stratified based on gender, age and the initial amount of myopia were randomly assigned to three treatment groups: 0.5% atropine with multi-focal glasses, multi-focal glasses, and single vision spectacles. Each subject was followed for at least eighteen months. These results report on the 188 patients available for the follow-up.

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Expression of the granulocyte-macrophage colony-stimulating factor (GM-CSF) gene in T cells is activated by the combination of phorbol ester (phorbol myristate acetate) and calcium ionophore (A23187), which mimic antigen stimulation through the T-cell receptor. We have previously shown that a fragment containing bp -95 to +27 of the mouse GM-CSF promoter can confer inducibility to reporter genes in the human Jurkat T-cell line. Here we use an in vitro transcription system to demonstrate that a cis-acting element (positions -54 to -40), referred to as CLEO, is a target for the induction signals. We observed induction with templates containing intact CLEO but not with templates with deleted or mutated CLEO. We also observed that two distinct signals were required for the stimulation through CLEO, since only extracts from cells treated with both phorbol myristate acetate and A23187 supported optimal induction. Stimulation probably was mediated by CLEO-binding proteins because depletion of these proteins specifically reduced GM-CSF transcription. One of the binding factors possessed biochemical and immunological features identical to those of the transcription factor APi. Another factor resembled the T-cell-specific factor NFAT. The characteristics of these two factors are consistent with their involvement in GM-CSF induction. The presence of CLEO-like elements in the promoters of interleukin-3 (IL-3), IL-4, IL.5, GM-CSF, and NFAT sites in the IL-2 promoter suggests that the factors we detected, or related factors that recognize these sites, may account for the coordinate induction of these genes during T-cell activation.

Most schoolchildren had little or no astigmatism. In Taiwan, most astigmatism is <1 D and is myopic with-the-rule astigmatism. There was more myopic astigmatism and with-the-rule astigmatism in 2000 than in 1995.