Introduction and Aims Transdermal alcohol sensors allow objective, continuous monitoring and have potential to expand current research on adolescent and young adult alcohol use. The purpose of this manuscript is to evaluate the feasibility and reliability of transdermal alcohol sensor use among female adolescents as compared to female young adults. Design and Methods This trial included 59 female adolescents and young adults aged 14–24 years who reported drinking during the previous month. All participants were asked to wear a Giner Wrist Transdermal Alcohol Sensor (WrisTAS)‐7 over a 1 month prospective study. Participants came to the research lab weekly to complete a detailed self‐report of behaviours, including day of drinking events, amounts and types of alcohol use and length of drinking events. Estimates of blood alcohol concentration (eBAC) were computed from self‐report data using the Matthew and Miller, NHTSA and Zhang equations. Daily transdermal alcohol concentration (TAC) peaks and calculated eBAC peak data were analysed with paired‐samples t‐tests and repeated measures correlations for validity comparisons. Results All participants (100%, n = 59) completed the trial, however, two participants were removed due to greater than 50% of missing transdermal alcohol sensor data. Of the 57 participants, the data included 1,722 days of continuous alcohol monitoring. Missing data was recorded more frequently among female adolescents at about (11.78%) as compared to female young adults (8.59%; χ2 = −18.40, P < 0.001). Participant self‐report of drinking occurred with greater frequency (374 events) than detected by the WrisTAS transdermal alcohol sensors (243 events). On days when self‐report and sensor data indicated a drinking event, participants' eBAC was moderately correlated with TAC, after accounting for repeated measures. Discussion and Conclusions This study finds that transdermal alcohol sensors are moderately reliable when sensor data is paired with self‐report. This objective data collection method may improve the ability to collect alcohol curves among adolescents.
Dried plum supplementation has been shown to enhance bone formation while suppressing bone resorption. Evidence from previous studies has demonstrated that these responses can be attributed in part to the fruit's polyphenolic compounds. The purpose of this study was to identify the most bioactive polyphenolic fractions of dried plum with a focus on their osteogenic activity and to investigate their mechanisms of action under normal and inflammatory conditions. Utilizing chromatographic techniques, six fractions of polyphenolic compounds were prepared from a crude extract of dried plum. Initial screening assays revealed that two fractions (DP-FrA and DP-FrB) had the greatest osteogenic potential. Subsequent experiments using primary bone-marrow-derived osteoblast cultures demonstrated these two fractions enhanced extracellular alkaline phosphatase (ALP), an indicator of osteoblast activity, and mineralized nodule formation under normal conditions. Both fractions enhanced bone morphogenetic protein (BMP) signaling, as indicated by increased Bmp2 and Runx2 gene expression and protein levels of phosphorylated Smad1/5. DP-FrB was most effective at up-regulating Tak1 and Smad1, as well as protein levels of phospho-p38. Under inflammatory conditions, TNF-α suppressed ALP and tended to decrease nodule formation (P=.0674). This response coincided with suppressed gene expression of Bmp2 and the up-regulation of Smad6, an inhibitor of BMP signaling. DP-FrA and DP-FrB partially normalized these responses. Our results show that certain fractions of polyphenolic compounds in dried plum up-regulate osteoblast activity by enhancing BMP signaling, and when this pathway is inhibited by TNF-α, the osteogenic response is attenuated.
Background: Clinical and preclinical studies have shown that dietary supplementation with dried plum improves bone health. These osteoprotective effects are a result, in part, of the antiresorptive properties of the fruit, which appear to be mediated by its polyphenolic compounds. Objective: This study was designed to determine if certain fractions of the polyphenolic compounds in dried plums are responsible for the antiresorptive effects and whether they alter mitogen-activated protein kinase (MAPK) and calcium signaling, which are essential to osteoclast differentiation and activity, under normal and inflammatory conditions. Methods: Six polyphenolic fractions were derived from the total polyphenolic extract of dried plum based on solubility. Initial screening, with the use of the Raw 264.7 monocyte and macrophage cell line, showed that 3 fractions had the most marked capacity to downregulate osteoclast differentiation. This response was confirmed in 2 of the fractions by using primary bone marrow–derived cultures and in all subsequent experiments to determine how osteoclast differentiation and function were altered with a focus on these 2 fractions in primary cultures. Data were analyzed by using ANOVA followed by post hoc analyses. Results: Both of the polyphenol fractions decreased osteoclast differentiation and activity coincident with downregulating nuclear factor of activated T cells, cytoplasmic, calcineurin-dependent 1 (Nfatc1), which is required for osteoclast differentiation. Calcium signaling, essential for the auto-amplification of Nfatc1, was suppressed by the polyphenolic fractions under normal conditions as indicated by suppressed mRNA expression of costimulatory receptors osteoclast-associated receptor (Oscar), signaling regulatory protein β1 (Sirpb1), and triggering receptor expressed on myeloid cells 2 (Trem2). In contrast, in the presence of tumor necrosis factor α (TNF-α), only Sirpb1 was downregulated. In addition to calcium signaling, phosphorylation of extracellular signal–regulated kinase (Erk) and p38 MAPK, involved in the expression and activation of Nfatc1, was also suppressed by the polyphenolic fractions. Conclusion: These results show that certain types of polyphenolic compounds from dried plum downregulate calcium and MAPK signaling, resulting in suppression of Nfatc1 expression, which ultimately decreases osteoclast formation and activity.
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