Examination of self-determination theory constructs as mediators of the effect of motivational interviewing on tobacco cessation outcomes

Title from PDF of title page viewed June 17, 2021Dissertation advisor: Kym BennettVitaIncludes bibliographical references (pages 43-61)Thesis (Ph.D.)--Department of Psychology. University of Missouri--Kansas City, 2021Despite an abundance of evidence supporting the efficacy of motivational interviewing for health behavior change, little is known about how it works. This study conducted a secondary analysis of autonomous motivation as a mediator of motivational interviewing’s effects in a recently completed randomized controlled clinical trial comparing motivational interviewing to health education on smoking quit attempts (KC Quest). Results of the parent trial unexpectedly revealed that motivational interviewing was not more effective than health education for inducing quit attempts of smoking cessation. While the mechanism through with the interventions is still unknown it remains feasible that motivational interviewing led to quit attempts and cessation by increasing autonomous motivation while health education was effective through a different mechanism. Interventions consisted of motivational interviewing (n=90) and health education (n=92). The primary outcome was the occurrence of any quit attempt defined as a serious quit attempt of at least 24 hours (Biener & Abrams, 1991; Marlatt, Curry, & Gordon, 1988) by Week 26. The Treatment Self-Regulation Questionnaire (TSRQ), developed from self-determination theory (SDT:Deci & Ryan, 1985), assesses the degree of autonomous self-regulation regarding why people engage or would engage in healthy behavior. Change scores from baseline to week 26 in the Autonomous (AR) and Controlled regulation (CR) subscales were computed for use in the mediation modeling. Log-binomial regression mediation examining each mediator separately revealed neither AR nor CR mediated effects of motivational interviewing or health education on quit attempts. A strength of the KC Quest enrollment was the inclusion of a racially diverse group of participants (67.2% Black) most adversely effected by smoking co-morbidities. Our current study did not detect a difference in smoking outcomes based on motivation mediators among Black participants. An important implication of this study is that while self-regulation failed to explain how, motivational interviewing and health education both increased quit attempts. There is a need for future investigations to examine other SDT constructs, such as relatedness and competence, as potential mediators of smoking interventions.Introduction -- Literature review -- Methods -- Analysis -- Results -- Discussion -- Appendix A. Treatment self-regulation questionnair

Role of X11 and ubiquilin as In Vivo Regulators of the Amyloid Precursor Protein in Drosophila

The Amyloid Precursor Protein (APP) undergoes sequential proteolytic cleavages through the action of β- and γ-secretase, which result in the generation of toxic β-amyloid (Aβ) peptides and a C-terminal fragment consisting of the intracellular domain of APP (AICD). Mutations leading to increased APP levels or alterations in APP cleavage cause familial Alzheimer's disease (AD). Thus, identification of factors that regulate APP steady state levels and/or APP cleavage by γ-secretase is likely to provide insight into AD pathogenesis. Here, using transgenic flies that act as reporters for endogenous γ-secretase activity and/or APP levels (GAMAREP), and for the APP intracellular domain (AICDREP), we identified mutations in X11L and ubiquilin (ubqn) as genetic modifiers of APP. Human homologs of both X11L (X11/Mint) and Ubqn (UBQLN1) have been implicated in AD pathogenesis. In contrast to previous reports, we show that overexpression of X11L or human X11 does not alter γ-secretase cleavage of APP or Notch, another γ-secretase substrate. Instead, expression of either X11L or human X11 regulates APP at the level of the AICD, and this activity requires the phosphotyrosine binding (PTB) domain of X11. In contrast, Ubqn regulates the levels of APP: loss of ubqn function leads to a decrease in the steady state levels of APP, while increased ubqn expression results in an increase in APP levels. Ubqn physically binds to APP, an interaction that depends on its ubiquitin-associated (UBA) domain, suggesting that direct physical interactions may underlie Ubqn-dependent regulation of APP. Together, our studies identify X11L and Ubqn as in vivo regulators of APP. Since increased expression of X11 attenuates Aβ production and/or secretion in APP transgenic mice, but does not act on γ-secretase directly, X11 may represent an attractive therapeutic target for AD

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Impact of meningococcal ACWY conjugate vaccines on pharyngeal carriage in adolescents: evidence for herd protection from the UK MenACWY programme

Objective: Serogroup W and Y invasive meningococcal disease increased globally from 2000 onwards. Responding to a rapid increase in serogroup W clonal complex 11 (W:cc11) invasive meningococcal disease, the UK replaced an adolescent booster dose of meningococcal C conjugate vaccine with quadrivalent MenACWY conjugate vaccine in 2015. By 2018, the vaccine coverage in the eligible school cohorts aged 14 to 19 years was 84%. We assessed the impact of the MenACWY vaccination programme on meningococcal carriage. Methods: An observational study of culture-defined oropharyngeal meningococcal carriage prevalence before and after the start of the MenACWY vaccination programme in UK school students, aged 15 to 19 years, using two cross-sectional studies: 2014 to 2015 “UKMenCar4” and 2018 “Be on the TEAM” (ISRCTN75858406). Results: A total of 10 625 participants preimplementation and 13 434 postimplementation were included. Carriage of genogroups C, W, and Y (combined) decreased from 2.03 to 0.71% (OR 0.34 [95% CI 0.27–0.44], p < 0.001). Carriage of genogroup B meningococci did not change (1.26% vs 1.23% [95% CI 0.77–1.22], p = 0.80) and genogroup C remained rare (n = 7/10 625 vs 17/13 488, p = 0.135). The proportion of serogroup positive isolates (i.e. those expressing capsule) decreased for genogroup W by 53.8% (95% CI –5.0 to 79.8, p = 0.016) and for genogroup Y by 30.1% (95% CI 8.9–46·3, p = 0.0025). Discussion: The UK MenACWY vaccination programme reduced carriage acquisition of genogroup and serogroup Y and W meningococci and sustained low levels of genogroup C carriage. These data support the use of quadrivalent MenACWY conjugate vaccine for indirect (herd) protection

Proceedings of the 13th annual conference of INEBRIA

CITATION: Watson, R., et al. 2016. Proceedings of the 13th annual conference of INEBRIA. Addiction Science & Clinical Practice, 11:13, doi:10.1186/s13722-016-0062-9.The original publication is available at https://ascpjournal.biomedcentral.comENGLISH SUMMARY : Meeting abstracts.https://ascpjournal.biomedcentral.com/articles/10.1186/s13722-016-0062-9Publisher's versio