Exploring an increased role for Australian community pharmacy in mental health professional service delivery: evaluation of the literature

Background: Australian general practitioners primarily treat mental health problems by prescribing medication dispensed by community pharmacists. Pharmacists therefore have regular interactions with mental health consumers and carers.Aims: This narrative review explored the potential role of community pharmacy in mental health services.Method: Medline, CINAHL, ProQuest, Emerald, PsycINFO, Science Direct, PubMed, Web of Knowledge and IPA were utilised. The Cochrane Library as well as grey literature and “lay” search engines such as GoogleScholar were also searched.Results: Four systematic reviews and ten community pharmacy randomised controlled trials were identified. Various relevant reviews outlining the impact of community pharmacy based disease state or medicines management services were also identified.Conclusion: International studies involving professional service interventions for mental health consumers could be contextualised for the Australian setting. Australian studies of pharmacy professional services for chronic physical health conditions provided further guidance for the expansion of community pharmacy mental health professional services

Group-Based Parent Training Interventions for Parents of Children with Autism Spectrum Disorders: a Literature Review

© 2018, Springer Science+Business Media, LLC, part of Springer Nature. Parents of children with autism spectrum disorders should have access to interventions to help them understand and support their child. This literature review examines the existing evidence for group-based parent training interventions that support parents of children with autism. From the literature, core intervention processes and outcomes are identified and include parenting and parent behaviour, parent health, child behaviour and peer and social support. Results show a positive trend for intervention effectiveness, but findings are limited by low-quality studies and heterogeneity of intervention content, outcomes and outcome measurement. Future research should focus on specifying effective intervention ingredients and modes of delivery, consistent and reliable outcome measurement, and improving methodological rigour to build a more robust evidence base

Multimodal characterization of the visual network in Huntington's disease gene carriers

Objective A sensorimotor network structural phenotype predicted motor task performance in a previous study in Huntington’s disease (HD) gene carriers. We investigated in the visual network whether structure – function – behaviour relationship patterns, and the effects of the HD mutation, extended beyond the sensorimotor network. Methods We used multimodal visual network MRI structural measures (cortical thickness and white matter connectivity), plus visual evoked potentials and task performance (Map Search; Symbol Digit Modalities Test) in healthy controls and HD gene carriers. Results Using principal component (PC) analysis, we identified a structure – function relationship common to both groups. PC scores differed between groups indicating white matter disorganization (higher RD, lower FA) and slower, and more disperse, VEP signal transmission (higher VEP P100 latency and lower VEP P100 amplitude) in HD than controls while task performance was similar. Conclusions HD may be associated with reduced white matter organization and efficient visual network function but normal task performance. Significance These findings indicate that structure – function relationships in the visual network, and the effects of the HD mutation, share some commonalities with those in the sensorimotor network. However, implications for task performance differ between the two networks suggesting the influence of network specific factors

Characterising white matter in Huntington's disease

Background: Investigating early white matter (WM) change in Huntington’s Disease (HD) can improve our understanding of the way in which disease spreads from the striatum. Objectives: Here, we provide a detailed characterisation of pathology-related WM change in HD. We first examined WM microstructure using diffusion-weighted imaging, then investigated both underlying biological properties of WM and products of WM damage including iron, myelin plus neurofilament light (NfL), a biofluid marker of axonal degeneration – in parallel with the mutant huntingtin protein (mHTT). Methods: We examined WM change in HD gene-carriers from the HD-CSF cohort, baseline visit. We used standard diffusion MRI to measure metrics including fractional anisotropy (FA), a marker of WM integrity, and diffusivity; a novel diffusion model (NODDI) to measure axonal density and organisation; T1 and T2 weighted structural MRI images to derive proxy iron content and myelin-contrast measures; and biofluid concentrations of NfL (in CSF and plasma) and mHTT (in CSF). Results: HD gene-carriers displayed reduced FA and increased diffusivity compared to controls, both of which were also associated with disease progression, CSF and mHTT levels. HD gene-carriers also displayed proxy measures of reduced myelin-contrast and iron in the striatum. Conclusion: Collectively, these findings present a more complete characterisation of HD-related microstructural brain changes. Correlation between reduced FA, increased axonal orientation and biofluid markers suggest that axonal breakdown is associated with increased WM degeneration, while higher quantitative T2 signal and lower myelin-contrast may indicate a process of demyelination limited to the striatum

mRNA processing in mutant zebrafish lines generated by chemical and CRISPR-mediated mutagenesis produces unexpected transcripts that escape nonsense-mediated decay.

As model organism-based research shifts from forward to reverse genetics approaches, largely due to the ease of genome editing technology, a low frequency of abnormal phenotypes is being observed in lines with mutations predicted to lead to deleterious effects on the encoded protein. In zebrafish, this low frequency is in part explained by compensation by genes of redundant or similar function, often resulting from the additional round of teleost-specific whole genome duplication within vertebrates. Here we offer additional explanations for the low frequency of mutant phenotypes. We analyzed mRNA processing in seven zebrafish lines with mutations expected to disrupt gene function, generated by CRISPR/Cas9 or ENU mutagenesis methods. Five of the seven lines showed evidence of altered mRNA processing: one through a skipped exon that did not lead to a frame shift, one through nonsense-associated splicing that did not lead to a frame shift, and three through the use of cryptic splice sites. These results highlight the need for a methodical analysis of the mRNA produced in mutant lines before making conclusions or embarking on studies that assume loss of function as a result of a given genomic change. Furthermore, recognition of the types of adaptations that can occur may inform the strategies of mutant generation

TADPOLE Challenge: Accurate Alzheimer's disease prediction through crowdsourced forecasting of future data

The TADPOLE Challenge compares the performance of algorithms at predicting the future evolution of individuals at risk of Alzheimer's disease. TADPOLE Challenge participants train their models and algorithms on historical data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. Participants are then required to make forecasts of three key outcomes for ADNI-3 rollover participants: clinical diagnosis, ADAS-Cog 13, and total volume of the ventricles -- which are then compared with future measurements. Strong points of the challenge are that the test data did not exist at the time of forecasting (it was acquired afterwards), and that it focuses on the challenging problem of cohort selection for clinical trials by identifying fast progressors. The submission phase of TADPOLE was open until 15 November 2017; since then data has been acquired until April 2019 from 219 subjects with 223 clinical visits and 150 Magnetic Resonance Imaging (MRI) scans, which was used for the evaluation of the participants' predictions. Thirty-three teams participated with a total of 92 submissions. No single submission was best at predicting all three outcomes. For diagnosis prediction, the best forecast (team Frog), which was based on gradient boosting, obtained a multiclass area under the receiver-operating curve (MAUC) of 0.931, while for ventricle prediction the best forecast (team EMC1), which was based on disease progression modelling and spline regression, obtained mean absolute error of 0.41% of total intracranial volume (ICV). For ADAS-Cog 13, no forecast was considerably better than the benchmark mixed effects model (BenchmarkME), provided to participants before the submission deadline. Further analysis can help understand which input features and algorithms are most suitable for Alzheimer's disease prediction and for aiding patient stratification in clinical trials.Comment: 10 pages, 1 figure, 4 tables. arXiv admin note: substantial text overlap with arXiv:1805.0390

Submerged in the mainstream? A case study of an immigrant learner in a New Zealand primary classroom

Immigrant children from diverse language backgrounds face not only linguistic challenges when enrolled in mainstream English-medium classrooms, but also difficulties adjusting to an unfamiliar learning community. The culture of primary school classrooms in New Zealand typically reflects conventions across three dimensions: interactional, instructional task performance and cognitive-academic development. All three dimensions are underpinned by the culturally specific discourse conventions involved in language socialisation. New learners may be helped by classmates or their teacher to understand and successfully use these conventions, but left on their own they may sink rather than swim. This is a case study of one Taiwanese 11-year old boy, 'John', who entered a New Zealand primary classroom midway through the school year. John's basic conversational ability was sound, but he did not possess the interactive classroom skills needed to operate in the new culture of learning. Selected from a wider study of the classroom, transcript data from audio-recorded excerpts of John's interactions over several months with his teacher and classmates are interpreted from perspectives derived from sociocultural and language socialisation theories. The article concludes with a brief consideration of the extent to which John constructed, or was constrained from constructing meaningful learning experiences, and suggestions for further research and reflection

Cross-sectional and longitudinal voxel-based grey matter asymmetries in Huntington's disease

Huntington's disease (HD) is a progressive neurodegenerative disorder that can be genetically confirmed with certainty decades before clinical onset. This allows the investigation of functional and structural changes in HD many years prior to disease onset, which may reveal important mechanistic insights into brain function, structure and organization in general. While regional atrophy is present at early stages of HD, it is still unclear if both hemispheres are equally affected by neurodegeneration and how the extent of asymmetry affects domain-specific functional decline. Here, we used whole-brain voxel-based analysis to investigate cross-sectional and longitudinal hemispheric asymmetries in grey matter (GM) volume in 56 manifest HD (mHD), 83 pre-manifest HD (preHD), and 80 healthy controls (HC). Furthermore, a regression analysis was used to assess the relationship between neuroanatomical asymmetries and decline in motor and cognitive measures across the disease spectrum. The cross-sectional analysis showed striatal leftward-biased GM atrophy in mHD, but not in preHD, relative to HC. Longitudinally, no net 36-month change in GM asymmetries was found in any of the groups. In the regression analysis, HD-related decline in quantitative-motor (Q-Motor) performance was linked to lower GM volume in the left superior parietal cortex. These findings suggest a stronger disease effect targeting the left hemisphere, especially in those with declining motor performance. This effect did not change over a period of three years and may indicate a compensatory role of the right hemisphere in line with recent functional imaging studies