Impact of the COVID-19 kindergarten closure on overweight and obesity among 3- to 7-year-old children.

BACKGROUND: Knowledge on the impact of the temporary kindergarten closure policy under COVID-19 in 2020 on childhood overweight and obesity is inadequate. We aimed to examine differences in rates of overweight and obesity from 2018 to 2021 among kindergarten children aged 3-7 years. METHODS: Overweight was defined as body mass index (BMI) > 1 standard deviation (SD) for age and sex, and obesity was defined as BMI > 2 SD for age and sex. Generalized linear mixed modeling was used for analysis. RESULTS: A total of 44,884 children and 71,216 growth data points from all 57 public kindergartens in Jiading District, Shanghai, China were analyzed. The rates of obesity from 2018 to 2021 were 6.9%, 6.6%, 9.5%, and 7.3% in boys and 2.8%, 2.8%, 4.5%, and 3.1% in girls, respectively. The rates of overweight from 2018 to 2021 were 14.3%, 14.3%, 18.2%, and 15.3% in boys and 10.6%, 10.9%, 13.9%, and 11.6% in girls. The rates of obesity and overweight among kindergarten children in 2020 were significantly higher than those in 2018, 2019, and 2021. Compared to 2020, the odds ratios of the obesity rate in 2018, 2019, and 2021 were 0.67 [95% confidence interval (CI) = 0.58-0.77, P < 0.001], 0.72 (95% CI = 0.64-0.80, P < 0.001) and 0.81 (95% CI = 0.72-0.92, P = 0.001), respectively. The odds ratios of the overweight rate in 2018, 2019, and 2021 were 0.75 (95% CI = 0.69-0.82, P < 0.001), 0.78 (95% CI = 0.72-0.84, P < 0.001), and 0.89 (95% CI = 0.81-0.97, P = 0.008), respectively, compared to 2020. CONCLUSIONS: The rates of overweight and obesity significantly increased among kindergarten children in 2020 after the 5-month kindergarten closure. It was critical to provide guidance to caregivers on fostering a healthy lifestyle for children at home under public health emergencies.

Interaction of Insomnia and Somatization with Post-Traumatic Stress Disorder in Pregnant Women During the COVID-19 Pandemic.

INTRODUCTION: Post-traumatic stress disorder (PTSD) has an adverse impact on the emotional health of prenatal maternal women and their offspring. During the Coronavirus Disease 2019 (COVID-19) pandemic, pregnant women are vulnerable to traumatic events and are prone to PTSD symptoms. The aim of the study was to explore the predictive effects of insomnia and somatization on PTSD in pregnant women by utilizing generalized additive model (GAM). MATERIALS AND METHODS: A total of 1638 pregnant women from three local cities in China underwent online survey on sleep quality, somatization, and PTSD symptoms tested by the Insomnia Severity Index (ISI), the subscale somatization of Symptom Checklist-90 (SCL-90-S) and the Checklist for DSM-5 (PCL-5), respectively. RESULTS: Insomnia was positively correlated with PTSD symptoms in pregnant women (p = 1.79×10-5). Interestingly, insomnia and somatization showed a complex non-primary linear interaction in predicting PTSD (p = 2.00×10-16). CONCLUSION: Our results suggest that insomnia is a prominent predictor of PTSD symptoms in pregnant women in the context of public emergencies. In addition, the effects of insomnia and somatization on PTSD symptoms are characterized by complex non-primary linear relationships.

VEGF receptor 2 (KDR) protects airways from mucus metaplasia through a Sox9-dependent pathway.

Mucus-secreting goblet cells are the dominant cell type in pulmonary diseases, e.g., asthma and cystic fibrosis (CF), leading to pathologic mucus metaplasia and airway obstruction. Cytokines including IL-13 are the major players in the transdifferentiation of club cells into goblet cells. Unexpectedly, we have uncovered a previously undescribed pathway promoting mucous metaplasia that involves VEGFa and its receptor KDR. Single-cell RNA sequencing analysis coupled with genetic mouse modeling demonstrates that loss of epithelial VEGFa, KDR, or MEK/ERK kinase promotes excessive club-to-goblet transdifferentiation during development and regeneration. Sox9 is required for goblet cell differentiation following Kdr inhibition in both mouse and human club cells. Significantly, airway mucous metaplasia in asthmatic and CF patients is also associated with reduced KDR signaling and increased SOX9 expression. Together, these findings reveal an unexpected role for VEGFa/KDR signaling in the defense against mucous metaplasia, offering a potential therapeutic target for this common airway pathology.

Oxidative stress-mediated epidermal growth factor receptor activation regulates PM2.5-induced over-secretion of pro-inflammatory mediators from human bronchial epithelial cells.

BACKGROUND: Exposure to PM2.5 has been associated with increased morbidity and mortality of lung diseases although the underlying mechanisms have not been fully uncovered. Airway inflammation is a critical event in the pathogenesis of lung diseases. This study aimed to examine the role of oxidative stress and epidermal growth factor receptor (EGFR) in PM2.5-induced pro-inflammatory response in a human bronchial epithelial cell line, BEAS-2B. METHODS: BEAS-2B cells were exposed to 0, 20, 50, 100 and 150 µg/ml of PM2.5. Secretion of pro-inflammatory mediators including interleukin-6 (IL-6), IL-8 and IL-1ß was determined using enzyme linked immunosorbent assay. Levels of intracellular reactive oxygen species (ROS) were determined using flow cytometry. Phosphorylation of the EGFR was examined with immunoblotting. RESULTS: PM2.5 exposure increased the secretion of IL-6, IL-8, and IL-1ß in a concentration-dependent fashion. Moreover, exposure to PM2.5 elevated intracellular levels of ROS, and phosphorylation of the EGFR (Y1068). Pretreatment of BEAS-2B cells with either an antioxidant or a specific EGFR inhibitor significantly reduced PM2.5-induced IL-6, IL-8 and IL-1ß secretion, implying that both oxidative stress and EGFR activation were involved in PM2.5-induced pro-inflammatory response. Furthermore, pre-treatment of BEAS-2B cells with an antioxidant significantly blunted PM2.5-induced EGFR activation, suggesting that oxidative stress was required for PM2.5-induced EGFR activation. CONCLUSION: PM2.5 exposure induces pro-inflammatory response in human bronchial epithelial cells through oxidative stress-mediated EGFR activation.