ABSTRACT
Background: The incidence of dual diagnosis (DD) (i.e. substance use disorders [SUD] and co-occurring mental disorders) is widespread; however, they vary widely in permutation and combination. As a result, establishing effective and empirically supported interventions for this clinical population remains challenging. Aim: This study aimed to examine current literature on the treatment outcomes for patients with DD. Method: A systematic review of randomised controlled trials (RCTs) published between 2009 and 2018 was conducted for two broad intervention categories identified by the literature: non-integrated and integrated treatment. Multiple electronic databases were searched using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines (PRISMA). Results: The search generated a total of 743 studies, of which 11 satisfied the inclusion criteria. These studies were thematically synthesised into two main analytical themes: 'treatment outcomes' and 'reported strengths and limitations of DD treatment'. Specifically, integrated treatment held an advantage over non-integrated treatment in significantly improving psychiatric symptomatology. However, no significant benefits were found between integrated and non-integrated treatment regarding substance misuse and treatment retention. Conclusion: Overall, the results provided insufficient evidence to support the enhanced efficacy of integrated or non-integrated treatment over the other in treating patients with DD. Contribution: The study's findings were used to provide recommendations to inform the clinical psychological service delivery of dual diagnosis treatment in South Africa and also to identify gaps in the literature and highlight areas for future research.
ABSTRACT
The role of CaMK II in regulating GLUT4 expression in response to intermittent exercise was investigated. Wistar rats completed 5 x 17-min bouts of swimming after receiving 5 mg/kg KN93 (a CaMK II inhibitor), KN92 (an analog of KN93 that does not inhibit CaMK II), or an equivalent volume of vehicle. Triceps muscles that were harvested at 0, 6, or 18 h postexercise were assayed for 1) CaMK II phosphorylation by Western blot, 2) acetylation of histone H3 at the Glut4 MEF2 site by chromatin immunoprecipitation (ChIP) assay, 3) bound MEF2A at the Glut4 MEF2 cis-element by ChIP, and 4) GLUT4 expression by RT-PCR and Western blot. Compared with controls, exercise caused a twofold increase in CaMK II phosphorylation. Immunohistochemical stains indicated increased CaMK II phosphorylation in nuclear and perinuclear regions of the muscle fiber. Acetylation of histone H3 in the region surrounding the MEF2 binding site on the Glut4 gene and the amount of MEF2A that bind to the site increased approximately twofold postexercise. GLUT4 mRNA and protein increased approximately 2.2- and 1.8-fold, respectively, after exercise. The exercise-induced increases in CaMK II phosphorylation, histone H3 acetylation, MEF2A binding, and GLUT4 expression were attenuated or abolished when KN93 was administered to rats prior to exercise. KN92 did not affect the increases in pCaMK II and GLUT4. These data support the hypothesis that CaMK II activation by exercise increases GLUT4 expression via increased accessibility of MEF2A to its cis-element on the gene.
