Evaluation of the Reducing Reoffending Change Fund

The aim of this evaluation was to assess the extent to which the Public Social Partnerships model delivers effective mentoring services that reduce the risk of reoffending. It was carried out by Ciaran Mulholland, Jane Eunson, Lorraine Murray and Louise Bowen (Ipsos MORI Scotland) in collaboration with Professor Gill McIvor, Dr Margaret Malloch, Professor Bill Whyte, Dr Steve Kirkwood and Professor Fergus McNeill

Evaluation of the Reducing Reoffending Change Fund

The independent evaluation of the Reducing Reoffending Change Fund (RRCF) assessed the extent to which the Public Social Partnership (PSP) model delivers effective mentoring services that reduce the risk of reoffending and support reintegration, and concluded that there is a strong case for the continuation and expansion of mentoring services

Evaluation of the Reducing Reoffending Change Fund: Research Findings

This report presents the findings of an independent evaluation of the Reducing Reoffending Change Fund (RRCF). This was undertaken by Ipsos MORI Scotland between September 2013 and November 2015. The aim of the evaluation was to provide a comprehensive assessment of the extent to which the Public Social Partnership (PSP) model delivers effective mentoring services that reduce the risk of reoffending and support reintegration. The report concludes that mentoring is an effective approach which helps mentees to learn and implement constructive, non-criminal ways of addressing problems in their lives and to reduce risk factors associated with offending behaviour, and that there is a strong case for the continuation and expansion of mentoring services

Clinical, genetic and expression studies of human CNS channelopathies

SIGLEAvailable from British Library Document Supply Centre- DSC:DXN057477 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Variable K+ channel subunit dysfunction in inherited mutations of KCNA1

Mutations of KCNA1, which codes for the K+ channel subunit hKv1.1, are associated with the human autosomal dominant disease episodic ataxia type 1 (EA1). Five recently described mutations are associated with a broad range of phenotypes: neuromyotonia alone or with seizures, EA1 with seizures, or very drug-resistant EA1. Here we investigated the consequences of each mutation for channel assembly, trafficking, gating and permeation. We related data obtained from co-expression of mutant and wild-type hKv1.1 to the results of expressing mutant-wild-type fusion proteins, and combined electrophysiological recordings in Xenopus oocytes with a pharmacological discrimination of the contribution of mutant and wild-type subunits to channels expressed at the membrane. We also applied confocal laser scanning microscopy to measure the level of expression of either wild-type or mutant subunits tagged with green fluorescent protein (GFP). R417stop truncates most of the C-terminus and is associated with severe drug-resistant EA1. Electrophysiological and pharmacological measurements indicated that the mutation impairs both tetramerisation of R417stop with wild-type subunits, and membrane targeting of heterotetramers. This conclusion was supported by confocal laser scanning imaging of enhanced GFP (EGFP)-tagged hKv1.1 subunits. Co-expression of R417stop with wild-type hKv1.2 subunits yielded similar results to co-expression with wild-type hKv1.1. Mutations associated with typical EA1 (V404I) or with neuromyotonia alone (P244H) significantly affected neither tetramerisation nor trafficking, and only altered channel kinetics. Two other mutations associated with a severe phenotype (T226R, A242P) yielded an intermediate result. The phenotypic variability of KCNA1 mutations is reflected in a wide range of disorders of channel assembly, trafficking and kinetics