The COVID-19 pandemic and its social stressors have hindered obesity prevention and management. Obesity prevalence has been rising in the US, particularly in Black and Mexican American adolescents. 1 Few population-level studies have examined the effects of COVID-19 on childhood obesity prevalence. An observational study found childhood obesity prevalence in the Philadelphia, Pennsylvania, region increased from 13.7% to 15.4% (2019-2020). 2 The study included all patient visits and analyzed 2 time periods without a control period. Given obesity prevalence had been increasing prior to COVID-19, the observed increase may be overstated. 1 Using the Massachusetts Department of Public Health's disease surveillance system (MDPHnet), we examined obesity prevalence in 3 periods from 2018 to 2020 in a fixed cohort of children and adolescents.Methods | MPDHnet allows authorized users to query the electronic health record systems of 3 practice groups across 59 sites in Massachusetts serving 1.5 million socioeconomically diverse patients. 3 We identified a cohort of individuals aged 2 to 17 years in 2018, with body mass index (BMI) measured from July 1 to December 31, 2018 (historical control period), July 1 to December 31, 2019 (pre-COVID-19), and July 1 to December 31, 2020 (post-COVID-19 initial surge). We assessed obesity prevalence (BMI ≥95th percentile per standardized growth charts 4 ) overall and by sex, age (2-5 years, 6-11 years, 12-20 years) at time of BMI measurement, and race and ethnicity (Asian, Black, Hispanic, White). Race and ethnicity were reported by parents/guardians and captured in each practice's electronic health record (eMethods in the Supplement). We calculated differences in trends by subtracting change in obesity prevalence pre- COVID-19 (2018COVID-19 ( -2019 from the change post-COVID-19 initial surge (2019-2020). Our study did not meet criteria for human subjects research by Massachusetts General Hospital's institutional review board.Results | Among 46 151 included participants, 4197 (9%) were Asian; 4582 (10%), Black; 5862 (13%), Hispanic; 46 (0.1%), Native American; 24 751 (54%) White; and 6713 (15%), unknown race and ethnicity (Table 1). Obesity prevalence increased during 2019 to 2020 to a greater extent than expected based on the increase in pre-COVID-19 years, from 15.1% in 2018 to 15.7% in 2019 and 17.3% in 2020 (differences in trends, 1.1%; 95% CI 0.3%-1.9%). There were greater than expected increases in obesity prevalence among boys aged 6 to 11 years overall (2.8%; 95% CI, 0.8%-4.8%), specifically in Black (6.3%; 95% CI, -1.0%-13.6%) and Hispanic (7.1%; 95% CI, 0.1%-14.1%) subgroups, al-though the former had a wider 95% CI that crossed the null (Table 2).

IMPORTANCEAs smoking continues to decline in many developed countries, the proportion of lung cancers in nonsmokers will rise. This shift may create substantial pressure to further expand lung cancer screening to lower-risk groups.OBJECTIVE To determine the association of lung cancer incidence with the promotion of screening in a largely nonsmoking population. DESIGN, SETTING, AND PARTICIPANTSThis population-based ecological cohort study of stage-specific lung cancer incidence used the Taiwan Cancer Registry to identify women

Biliary atresia (BA), the most common cause of end-stage liver disease and the leading indication for pediatric liver transplantation, is associated with intrahepatic ductular reactions within regions of rapidly expanding periportal biliary fibrosis. While the extent of such biliary fibrosis is a negative predictor of long-term transplant-free survival, the cellular phenotypes involved in the fibrosis are not well established. Using a Rhesus rotavirus (RRV)-induced mouse model of BA, we demonstrate significant expansion of a cell population expressing the putative stem/progenitor cell marker PROMININ-1 (PROM1) adjacent to ductular reactions within regions of periportal fibrosis. PROM1positive (pos) cells express Collagen-1α1. Subsets of PROM1pos cells co-express progenitor cell marker CD49f, epithelial marker E-CADHERIN, biliary marker CYTOKERATIN-19, and mesenchymal markers VIMENTIN and α-SMOOTH MUSCLE ACTIN. Expansion of the PROM1pos cell population is associated with activation of Fibroblast Growth Factor (FGF) and Transforming Growth Factor-β (TGFβ) signaling. In vitro co-treatment of PROM1-expressing Mat1a−/− hepatic progenitor cells with recombinant human FGF10 and TGFβ1 promotes morphologic transformation toward a myofibroblastic cell phenotype with increased expression of myofibroblastic genes Collagen-1α1, Fibronectin, and α–Smooth muscle actin. Infants with BA demonstrate similar expansion of periportal PROM1pos cells with activated SMAD3 signaling in association with increased hepatic expression of FGF10, FGFR1, and FGFR2 as well as mesenchymal genes SLUG and SNAIL. Infants with perinatal subtype of BA have higher tissue levels of PROM1 expression than those with embryonic subtype. Conclusion Expansion of collagen-producing PROM1pos cells within the regions of periportal fibrosis is associated with activated FGF and TGFβ pathways in both experimental and human BA. PROM1pos cells may, therefore, play an important role in the biliary fibrosis of BA.

SummaryBackgroundIncreased visceral adipose tissue (VAT) precedes development of insulin resistance and dyslipidemia in adults. The associations of abdominal adiposity derived from dual‐energy X‐ray absorptiometry (DXA), including VAT, subcutaneous abdominal adipose tissue (SAAT) and total abdominal adipose tissue (TAAT) with cardio‐metabolic risk in adolescents are understudied.ObjectivesWe examined the cross‐sectional associations of DXA‐measured abdominal adiposity with cardio‐metabolic risk and related markers in early adolescence (mean [SD] age 13.0 [0.7] years).MethodsWe collected data from 740 adolescents (374 girls and 366 boys) in Project Viva, a U.S. pre‐birth cohort. We used DXA estimates of VAT, SAAT and TAAT area. We conducted overall and sex‐stratified linear regression models, adjusting for age, sex (in overall models), race/ethnicity, puberty score and body mass index (BMI) z‐score.ResultsMean BMI z‐score was 0.59 (1.28). After adjustment, greater VAT (per 1 SD score) was associated with higher metabolic risk z‐score (β 0.14 units; 95% CI 0.08, 0.20), higher log high‐sensitivity C‐reactive protein (β 0.51 mg/L; 0.36, 0.66) and log leptin (β 0.36 ng/mL; 0.27, 0.44), and lower log adiponectin (β −0.08 ug/mL; −0.13, −0.02). SAAT and TAAT showed similar associations as VAT with comparable or greater effect sizes.ConclusionIn early adolescence, DXA‐measured VAT, SAAT and TAAT are associated with cardio‐metabolic risk and related markers, independent of current BMI. Among two adolescents with the same BMI, there is an associated higher cardio‐metabolic risk in the adolescent with greater DXA‐measured abdominal adiposity.