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Physician Burnout and Its Associated Factors: A Cross‐sectional Study in Shanghai: Zhihui WANG, et al. School of Public Health, Fudan University China— Objectives The aim of this study was to determine the rate of burnout and the contributing factors behind it among physicians in Shanghai. Methods In this cross‐sectional study, a total of 457 physicians from 21 hospitals in Shanghai completed self‐reported questionnaires in June 2008. The Chinese version of the job content questionnaire (C‐JCQ) and the Chinese version of the effort‐reward imbalance questionnaire (C‐ERI) were used to measure occupational stress. The Chinese version of Maslach Burnout Inventory (C‐MBI) was used to measure burnout rate. We then performed regression analysis of physician burnout. Results The MBI model revealed that 277 physicians (60.6%) were experiencing a mild degree of burnout and that 27 physicians (5.9%) were experiencing a severe degree of burnout. In the assessment of occupational stress, most physicians (64.8%) had a demand/control ratio higher than 1, and 21.9% of all physicians had an effort/reward ratio higher than 1, indicating a high level of occupational stress exposure. Regression analyses showed higher levels of burnout among physicians of younger age, less work experience, longer working hours, on shift duty, or from highergrade hospitals. Both the JCQ and ERI models showed good predictive power for physician burnout, with the ERI model performing better. Conclusions Physicians in Shanghai were experiencing a high degree of burnout, which was significantly associated with occupational stress as well as distinctive personal and work characteristics. Interventions aiming at reducing job‐related stress can be effective approaches to prevent burnout among physicians.

The transition to air breathing after birth requires both anatomic and biochemical maturation of the lung. Lung morphogenesis is mediated by complex paracrine interactions between respiratory epithelial cells and mesenchymal cells that direct transcriptional programs guiding patterning and cytodifferentiation of the lung. In the present study, transgenic mice were generated in which the Kruppel-like factor 5 gene (Klf5) was conditionally deleted in respiratory epithelial cells in the fetal lung. Lack of KLF5 inhibited maturation of the lung during the saccular stage of development. Klf5Δ/Δ mice died of respiratory distress immediately after birth. Abnormalities in lung maturation and morphogenesis were observed in the respiratory epithelium, the bronchiolar smooth muscle, and the pulmonary vasculature. Respiratory epithelial cells of both the conducting and peripheral airways were immature. Surfactant phospholipids were decreased and lamellar bodies, the storage form of surfactant, were rarely found. mRNA microarray analysis demonstrated that KLF5 influenced the expression of genes regulating surfactant lipid and protein homeostasis, vasculogenesis, including Vegfa, and smooth muscle cell differentiation. KLF5 regulates genes controlling paracrine interactions during lung morphogenesis, as well as those regulating the maturation of the respiratory epithelium that is required for lung function after birth.