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INTRODUCTION:Smoking is hazardous to health and places a heavy economic burden on individuals and their families. Clearly, smoking in China is prevalent since China is the largest consumer of tobacco in the world. Chinese smoking and nonsmoking households were compared in terms of the incidence and intensity of Catastrophic Health Expenditures (CHEs). The factors associated with catastrophic health expenditures were analyzed. METHODS:Data for this study were collected from two waves of panel data in 2011 and 2013 from the national China Health and Retirement Longitudinal Study (CHARLS). A total of 8073 households with at least one member aged above 45 were identified each year. Catastrophic health expenditure was measured by the ratio of a household's out-of-pocket healthcare payments (OOP) to the household's Capacity to Pay (CTP). A panel logit random-effects model was used to examine correlates with catastrophic health expenditure. RESULTS:The incidence of catastrophic health expenditures for Chinese households with members aged 45 and above in 2011 and 2013 were 12.99% and 15.56%, respectively. The mean gaps (MGs) were 3.16% and 4.88%, respectively, and the mean positive gaps (MPGs) were 24.36% and 31.40%, respectively. The incidences of catastrophic health expenditures were 17.41% and 20.03% in former smoking households, 12.10% and 15.09% in current smoking households, and 12.72% and 13.64% in nonsmoking households. In the panel logit regression model analysis, former smoking households (OR = 1.444, P

Glucocorticoids are the only therapy that has been demonstrated to alter the progress of Duchenne muscular dystrophy (DMD), the most common muscular dystrophy in children. However, glucocorticoids disturb skeletal muscle metabolism and hamper myogenesis and muscle regeneration. The mechanisms involved in the glucocorticoid-mediated suppression of myogenic differentiation are not fully understood. Glycogen synthase kinase-3β (GSK-3β) is considered to play a central role as a negative regulator in myogenic differentiation. Here, we showed that glucocorticoid treatment during the first 48 h in differentiation medium decreased the level of phosphorylated Ser9-GSK-3β, an inactive form of GSK-3β, suggesting that glucocorticoids affect GSK-3β activity. We then investigated whether GSK-3β inhibition could regulate glucocorticoid-mediated suppression of myogenic differentiation in vitro. Two methods were employed to inhibit GSK-3β: pharmacological inhibition with LiCl and GSK-3β gene knockdown. We found that both methods resulted in enhanced myotube formation and increased levels of muscle regulatory factors and muscle-specific protein expression. Importantly, GSK-3β inhibition attenuated glucocorticoid-induced suppression of myogenic differentiation. Collectively, these data suggest the involvement of GSK-3β in the glucocorticoid-mediated impairment of myogenic differentiation. Therefore, the inhibition of GSK-3β may be a strategy for preventing glucocorticoid-induced muscle degeneration.