School-based recruitment of youth for a research purpose is problematic, as one has to deal with multiple ethical and practical constraints. This study reports on predictors of schools' and families' participation in a longitudinal study of tobacco use among 11-year-old children. School size, but not tobacco policy, was linked to participation. High parental education and average social status in the residence area were associated with parental consent. Given the social background, prevalence of parental tobacco use was close to the expected. Compliance of responsible adults in youth research cannot be predicted on the basis of simple behavioural models.
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http://dx.doi.org/10.1093/eurpub/13.1.75 | DOI Listing |
PLoS One
January 2025
Faculty of Medicine and Health Technology, Department of Ophthalmology, Tampere University, Tampere, Finland.
Background: The long-term patterns in first-line glaucoma medication are not well established. Exploring these in longitudinal and population-based settings would provide information for the healthcare systems to plan glaucoma care accordingly.
Objective: To evaluate patterns in first-line glaucoma monotherapy in Finland during 1995-2019 based on nationwide survey and register data.
Pulmonology
December 2025
State Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & National Center for Respiratory Medicine & Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Interleukin-1β is one of the major cytokines involved in the initiation and persistence of airway inflammation in chronic obstructive pulmonary disease (COPD). However, the association between plasma interleukin-1β and lung function decline remains unclear. We aimed to explore the association between plasma interleukin-1β and lung function decline.
View Article and Find Full Text PDFJ Nephrol
January 2025
Department of Nephrology, Beaumont Hospital, Dublin, Ireland.
Background: Autosomal dominant polycystic kidney disease (ADPKD) is caused primarily by pathogenic variants in the PKD1 and PKD2 genes. Although the type of ADPKD variant can influence disease severity, rare, hypomorphic PKD1 variants have also been reported to modify disease severity or cause biallelic ADPKD. This study examines whether rare, additional, potentially protein-altering, non-pathogenic PKD1 variants contribute to ADPKD phenotypic outcomes.
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