"Letting Go and Staying Connected": Substance Use Outcomes from a Developmentally Targeted Intervention for Parents of College Students.

We present results of a randomized, controlled, efficacy trial of a handbook intervention for parents of first-year college students. The aim of the interactive intervention was to decrease risk behaviors by increasing family protective factors. The handbook, based in self-determination theory and the social development model, provided evidence-based and developmentally targeted suggestions for parents to engage with their students in activities designed to support successful adjustment to college. We recruited 919 parent-student dyads from incoming students enrolled at a university in the U.S. Pacific Northwest and randomly assigned them to control and intervention conditions. We sent handbooks to intervention parents in June before students' August matriculation. Research assistants trained in motivational interviewing contacted parents to encourage use of the handbook. Control parents and students received treatment as usual. Participants completed baseline surveys during their final semester in high school (time 1) and their first semester at college (time 2). Self-reported frequency of alcohol, cannabis, and simultaneous use increased across both handbook and control students. In intent-to-treat analyses, odds of increased use were consistently lower and of similar magnitude for students in the intervention condition than in the control condition, and odds of first-time use were also lower in the intervention condition. Contact from research assistants predicted parents' engagement, and parent and student report of active engagement with handbook predicted lower substance use among intervention than control students across the transition to college. We developed a low-cost, theory-based handbook to help parents support their young adult children as they transition to independent college life. Students whose parents used the handbook were less likely to initiate or increase substance use than students in the control condition during their first semester in college.ClinicalTrials.gov Identifier: NCT03227809.

Prostasin is a glycosylphosphatidylinositol-anchored active serine protease.

A recombinant human prostasin serine protease was expressed in several human cell lines. Subcellular fractionation showed that this serine protease is synthesized as a membrane-bound protein while a free-form prostasin is secreted into the culture medium. Prostasin was identified in nuclear and membrane fractions. Membrane-bound prostasin can be released by phosphatidylinositol-specific phospholipase C treatment, or labeled by [(3)H]ethanolamine, indicating a glycosylphosphatidylinositol anchorage. A prostasin-binding protein was identified in mouse and human seminal vesicle fluid. Both the secreted and the membrane-bound prostasin were able to form a covalently linked 82-kDa complex when incubated with seminal vesicle fluid. The complex formation between prostasin and the prostasin-binding protein was inhibited by a prostasin antibody, heparin, and serine protease inhibitors. Prostasin's serine protease activity was inhibited when bound to the prostasin-binding protein in mouse seminal vesicle fluid. This study indicates that prostasin is an active serine protease in its membrane-bound form.

Fields of aberrant CpG island hypermethylation in Barrett's esophagus and associated adenocarcinoma.

Esophageal adenocarcinoma (EAC) is thought to develop through a multistage process in which Barrett's metaplasia progresses through low- and high-grade dysplasia to invasive cancer. Transcriptional silencing of tumor suppressor genes by promoter CpG island hypermethylation has been observed in many types of human cancer. Analysis of CpG island hypermethylation in EAC has thus far been limited to the CDKN2A (p16) gene. In this study, we extend the methylation analysis of EAC to include three other genes, APC, CDH1 (E-cadherin), and ESR1 (ER, estrogen receptor alpha), in addition to CDKN2A. Molecular analysis can provide insight into the complex relationships between tissues with different histologies in Barrett's esophagus and associated adenocarcinoma. Therefore, we have mapped the spatial distribution of methylation patterns in six esophagectomy cases in detail. Hypermethylation of the four CpG islands was analyzed by the MethyLight technique in 107 biopsies derived from these six patients for a total of 428 methylation analyses. Our results show that normal esophageal squamous epithelium is unmethylated at all four CpG islands. CDH1 is unmethylated in most other tissue types as well. Hypermethylation of ESR1 is seen at high frequency in inflammatory reflux esophagitis and at all subsequent stages, whereas APC and CDKN2A hypermethylation is found in Barrett's metaplasia, dysplasia, and EAC. When it occurs, hypermethylation of APC, CDKN2A, and ESR1 is usually found in a large contiguous field, suggesting either a concerted methylation change associated with metaplasia or a clonal expansion of cells with abnormal hypermethylation.

Linking economic hardship to adolescent aggression.

The relationship between economic hardship and adolescent aggression has been explored from various perspectives. Using survey and observational data on two-parent families in a midwestern rural county, the study identifies four important mechanisms that link economic hardship to the aggressive behavior of adolescents. Economic pressure stemming from low income, financial loss, and unstable work, adversely affects the marital relationship through the negativity of fathers. Negative marital interactions increase irritable parenting, making adolescent aggression more likely.