The prevalence of myopia has markedly increased in East and Southeast Asia, and pathologic consequences of myopia, including myopic maculopathy and high myopia-associated optic neuropathy, are now some of the most common causes of irreversible blindness. Hence, strategies are warranted to reduce the prevalence of myopia and the progression to high myopia because this is the main modifiable risk factor for pathologic myopia. On the basis of published population-based and interventional studies, an important strategy to reduce the development of myopia is encouraging schoolchildren to spend more time outdoors. As compared with other measures, spending more time outdoors is the safest strategy and aligns with other existing health initiatives, such as obesity prevention, by promoting a healthier lifestyle for children and adolescents. Useful clinical measures to reduce or slow the progression of myopia include the daily application of low-dose atropine eye drops, in concentrations ranging between 0.01% and 0.05%, despite the side effects of a slightly reduced amplitude of accommodation, slight mydriasis, and risk of an allergic reaction; multifocal spectacle design; contact lenses that have power profiles that produce peripheral myopic defocus; and orthokeratology using corneal gas-permeable contact lenses that are designed to flatten the central cornea, leading to midperipheral steeping and peripheral myopic defocus, during overnight wear to eliminate daytime myopia. The risk-to-benefit ratio needs to be weighed up for the individual on the basis of their age, health, and lifestyle. The measures listed above are not mutually exclusive and are beginning to be examined in combination.

The eyes of chicks require only a brief period of lens wear to initiate compensation in the appropriate direction. Because the refractive status changes little during the period of lens wear, the authors conclude that eyes can rapidly determine the sign of the imposed blur without resorting to a trial-and-error method.

BackgroundSarcopenia and sarcopenic obesity (SO) have a greater impact on the elderly. This study aimed to explore whether there were sex differences in the prevalence and adverse outcomes of sarcopenia and SO in community-dwelling elderly individuals in East China.MethodsThis was a cross-sectional study that enrolled 213 males and 418 females aged > 65 years. Demographic characteristics, body composition, hand grip, gait speed, and indices of glucose and lipid metabolism were collected. Sarcopenia and SO were diagnosed using the Asian Working Group for Sarcopenia criteria.Results(1) The prevalence of sarcopenia was 19.2% in males and 8.6% in females. The prevalence of SO was 7.0% in males and 2.4% in females. (2) In males, the odds ratios (ORs) of osteoporosis and dyslipidemia in the SO group were 4.21-fold and 4.15-fold higher than those in the normal group, respectively. In females, the ORs of osteoporosis and hyperglycemia in the SO group were 1.12-fold and 4.21-fold higher than those in the normal group.ConclusionsMales were more likely to be sarcopenic and to have SO than females using the AWGS criteria. Females with SO were more likely to have higher blood glucose, whereas males with SO were more likely to have osteoporosis and dyslipidemia.

Purpose In chicks, ocular growth inhibition is associated with choroidal thickening and growth stimulation with choroidal thinning, suggesting a mechanistic link between the two responses. Because muscarinic antagonists inhibit the development of myopia in animal models by a non-accommodative mechanism, we tested the hypothesis that agonists would stimulate eye growth and thin the choroid. We also hypothesized that the effective growth-inhibiting antagonists would thicken the choroid. Methods Chicks, age 12–16 days, were used. In vivo: Agonists: Single intravitreal injections (20 µL) of oxotremorine (oxo), pilocarpine (pilo), carbachol (carb), or arecaidine (arec) were given to otherwise untreated eyes. A-scan ultrasonography was done prior to injections, and at 3, 24, 48 and 72 h. Antagonists: — 10D lenses were worn on one eye for 4 days. Atropine (atro), pirenzepine (pirz), oxyphenonium (oxy) or dicyclomine (dicy) were injected (20 µL) daily into lens-wearing eyes; saline injections were done as controls. Ultrasonography was done on d1 and on d4; on d4 measurements were done before and 3 h after injections. In vitro Paired eyecups of retinal pigment epithelium (RPE), choroid and sclera were made from 1-week old chicks. All drugs except atropine were tested on one eyecup, its pair in plain medium. Choroidal thickness was measured at various times over 48 h. Results Agonists: In vivo, oxotremorine caused an increase in the rate of axial elongation (drug vs saline: 24–72 h: 338 µm vs 250 µrn; p < 0.001). All except pilocarpine caused choroidal thinning by 24 h (oxo, carb and arec vs saline: −25, −35 and −46 µm vs 3 µm). In vitro, all agonists thinned choroids by 24 h (oxo: −6 vs 111 µm; pilo: 45 vs 212 µm; carb: −58 vs 65 µm; arec: 47 vs 139 µm; p < 0.05). Antagonists: Atropine, pirenzepine and oxyphenonium inhibited the development of myopia in negative lens-wearing eyes, and also caused choroidal thickening (drug vs saline: 42, 80, 88 vs 10 µm per 3 h). In vitro, pirenzepine thickened choroids by 3 h (77 vs 2 µm, p < 0.01). Conclusions Muscarinic agonists caused choroidal thinning in intact eyes and eyecups, supporting a role for acetylcholine in the choroidal response to hyperopic defocus or form deprivation. Only oxotremorine stimulated eye growth, which is inconsistent with a muscarinic receptor mechanism for antagonist-induced eye growth inhibition. The dissociation between choroidal thinning and ocular growth stimulation for the other agonists in vivo suggest separate pathways for the two.