The National Exercise Referral Framework

A 2013 Review of the HSE funded GP Exercise Referral Programme (GPERP) highlighted the need for a new National Exercise Referral Framework (NERF). The evidence suggests that exercise referral is an effective targeted health intervention for specific patients and with the increasing prevalence of chronic disease it is imperative that we examine, design and progress the implementation of scalable, sustainable evidence-based, interventions, integrated across the health system to improve the health and wellbeing of the population. The development of this proposed National Exercise Referral Framework, commissioned by Health Promotion and Improvement, was led by DCU involving a multi-disciplinary Working Group and supported by a HSE Cross-Divisional Group. We are grateful to the Working Group and in particular to Dr Catherine Woods and the team in DCU for their extensive work and commitment to this project. There are a number of practical steps now required to determine the feasibility of the proposed framework as a national model namely, identification of a sustainable funding model; design and development of chronic disease care pathways and a phased implementation plan that would build on the existing programmes. The Health & Wellbeing Division of the HSE will lead the next phase of this project

Shell growth and repair in the gastropod, Tegula funebralis

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Quantitative 18F-FDG PET-CT scan characteristics correlate with tuberculosis treatment response

Abstract Background There is a growing interest in the use of F-18 FDG PET-CT to monitor tuberculosis (TB) treatment response. Tuberculosis lung lesions are often complex and diffuse, with dynamic changes during treatment and persisting metabolic activity after apparent clinical cure. This poses a challenge in quantifying scan-based markers of burden of disease and disease activity. We used semi-automated, whole lung quantification of lung lesions to analyse serial FDG PET-CT scans from the Catalysis TB Treatment Response Cohort to identify characteristics that best correlated with clinical and microbiological outcomes. Results Quantified scan metrics were already associated with clinical outcomes at diagnosis and 1 month after treatment, with further improved accuracy to differentiate clinical outcomes after standard treatment duration (month 6). A high cavity volume showed the strongest association with a risk of treatment failure (AUC 0.81 to predict failure at diagnosis), while a suboptimal reduction of the total glycolytic activity in lung lesions during treatment had the strongest association with recurrent disease (AUC 0.8 to predict pooled unfavourable outcomes). During the first year after TB treatment lesion burden reduced; but for many patients, there were continued dynamic changes of individual lesions. Conclusions Quantification of FDG PET-CT images better characterised TB treatment outcomes than qualitative scan patterns and robustly measured the burden of disease. In future, validated metrics may be used to stratify patients and help evaluate the effectiveness of TB treatment modalities

Chorea-acanthocytosis: genetic linkage to chromosome 9q21.

Chorea-acanthocytosis (CHAC) is a rare autosomal recessive disorder characterized by progressive neurodegeneration and unusual red-cell morphology (acanthocytosis), with onset in the third to fifth decade of life. Neurological impairment with acanthocytosis (neuroacanthocytosis) also is seen in abetalipoproteinemia and X-linked McLeod syndrome. Whereas the molecular etiology of McLeod syndrome has been defined (Ho et al. 1994), that of CHAC is still unknown. In the absence of cytogenetic rearrangements, we initiated a genomewide scan for linkage in 11 families, segregating for CHAC, who are of diverse geographical origin. We report here that the disease is linked, in all families, to a 6-cM region of chromosome 9q21 that is flanked by the recombinant markers GATA89a11 and D9S1843. A maximum two-point LOD score of 7.1 (theta = .00) for D9S1867 was achieved, and the linked region has been confirmed by homozygosity-by-descent, in offspring from inbred families. These findings provide strong evidence for the involvement of a single locus for CHAC and are the first step in positional cloning of the disease gene