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Recently, bulk drag coefficient (~CD) formulations used to quantify wave energy dissipation by Rhizophora mangroves were developed from laboratory data; however, these formulations have not yet been validated with field data. Additionally, due to the complex geometry of mangrove trees within forests and spatial variability, common criteria for determining the adequate geometric characteristics of mangrove forests are lacking and are required to obtain accurate definitions for ~CD. This paper addresses these knowledge gaps by proposing a newly integrated ~CD formulation based on the comprehensive characterization of a Rhizophora mangle forest combined with wave measurements in field, and by using numerical modeling for the calibration process. The field campaign consisted of 23 continuous days of recorded wave data and spatial distribution observations of the geometric characteristics of the mangrove forest. The variation in frontal area per unit height per square meter (Ahm) along the mangrove forest was reported for three zones with different densities identified along the study transect, with decreasing root density from the vegetation edge to the forest interior. On average, the incident wave height decreased by 34% at 63 m in mangrove forests, and the wave attenuation ratios (r) varied between 0.001 and 0.01 m-1. To estimate the ~CD values associated with these wave height attenuation ratios, the Simulating Waves Nearshore (SWAN) numerical model was used to calibrate the model results with the field observations. The variation in the tree frontal area along the mangrove forest and the wave conditions at the site are considered during the calibration process. To further characterize ~CD for this type of mangrove species, the ~CD values acquired from the calibration together with the values reported in the literature from laboratory experiments are presented as a function of the Keulegan-Carpenter number (KC). Root diameter is defined as the characteristic length according to the inherent geometric characteristics of a Rhizophora sp. forest. The new formulation allows us to predictably estimate ~CD values that can be used as inputs in drag force-based models to estimate the attenuation of wave energy produced by Rhizophora sp. forests. [ABSTRACT FROM AUTHOR]

Adolescents' experiences with social media are complex and can impact their mental well-being differently. Our study aimed to understand how neurobiological sensitivities may moderate the association between different social media experiences and depressive symptoms. In a multi-wave study, 80 adolescents (Mage = 13.06, SD = .58) took part in an fMRI task designed to gauge the neural responses when viewing accepted and rejected peers within their own social networks (wave 1). We also collected self-reported measures of positive (digital social connection) and negative (digital pressure) experiences on social media and depressive symptoms (waves 2 and 3). Our findings revealed that there were no significant associations between digital social connection, digital pressure, and depressive symptoms one year later. However, the association between digital social connection and depressive symptoms was moderated by neural responsivity. Specifically, for adolescents with reduced sensitivity to their rejected peers in the VS, rTPJ, and vmPFC, digital social connection was associated with reduced depressive symptoms one year later. These results emphasize the importance of individual differences in how adolescents' brains respond to rejected peers in shaping the impact of online experiences on their mental well-being., (© The Author(s) 2024. Published by Oxford University Press.)

The widespread use of potent androgen receptor signaling inhibitors (ARSIs) has led to an increasing emergence of AR-independent castration-resistant prostate cancer (CRPC), typically driven by loss of AR expression, lineage plasticity, and transformation to prostate cancers (PCs) that exhibit phenotypes of neuroendocrine or basal-like cells. The anti-apoptotic protein BCL2 is upregulated in neuroendocrine cancers and may be a therapeutic target for this aggressive PC disease subset. There is an unmet clinical need, therefore, to clinically characterize BCL2 expression in metastatic CRPC (mCRPC), determine its association with AR expression, uncover its mechanisms of regulation, and evaluate BCL2 as a therapeutic target and/or biomarker with clinical utility. Here, using multiple PC biopsy cohorts and models, we demonstrate that BCL2 expression is enriched in AR-negative mCRPC, associating with shorter overall survival and resistance to ARSIs. Moreover, high BCL2 expression associates with lineage plasticity features and neuroendocrine marker positivity. We provide evidence that BCL2 expression is regulated by DNA methylation, associated with epithelial-mesenchymal transition, and increased by the neuronal transcription factor ASCL1. Finally, BCL2 inhibition had antitumor activity in some, but not all, BCL2-positive PC models, highlighting the need for combination strategies to enhance tumor cell apoptosis and enrich response.