Development of a framework for radiographer online clinical education (FORCE): the specifc strand of nuclear medicine within this european project

The overall aim of the FORCE project is to develop virtual web-based learning resources where Radiography undergraduates can engage in interactive, problem-based development of radiographic knowledge, ability and professional awareness. This European-funded project is internally divided in three diferent strands (Radiology Diagnostic Imaging, Radiotherapy and Nuclear Medicine). The aim of this presentation is to present the global project, mainly focusing developments, achievements and challenges within the Nuclear Medicine specifc strand.info:eu-repo/semantics/publishedVersio

Exploring the Relationship Between Schizophrenia and Cardiovascular Disease:A Genetic Correlation and Multivariable Mendelian Randomization Study

Individuals with schizophrenia have a reduced life-expectancy compared to the general population, largely due to an increased risk of cardiovascular disease (CVD). Clinical and epidemiological studies have been unable to unravel the nature of this relationship. We obtained summary-data of genome-wide-association studies of schizophrenia (N = 130 644), heart failure (N = 977 323), coronary artery disease (N = 332 477), systolic and diastolic blood pressure (N = 757 601), heart rate variability (N = 46 952), QT interval (N = 103 331), early repolarization and dilated cardiomyopathy ECG patterns (N = 63 700). We computed genetic correlations and conducted bi-directional Mendelian randomization (MR) to assess causality. With multivariable MR, we investigated whether causal effects were mediated by smoking, body mass index, physical activity, lipid levels, or type 2 diabetes. Genetic correlations between schizophrenia and CVD were close to zero (−0.02–0.04). There was evidence that liability to schizophrenia causally increases heart failure risk. This effect remained consistent with multivariable MR. There was also evidence that liability to schizophrenia increases early repolarization pattern, largely mediated by BMI and lipids. Finally, there was evidence that liability to schizophrenia increases heart rate variability, a direction of effect contrasting clinical studies. There was weak evidence that higher systolic blood pressure increases schizophrenia risk. Our finding that liability to schizophrenia increases heart failure is consistent with the notion that schizophrenia involves a systemic dysregulation of the body with detrimental effects on the heart. To decrease cardiovascular mortality among individuals with schizophrenia, priority should lie with optimal treatment in early stages of psychosis

Education models used across Europe to train therapeutic radiographers/radiotherapists : a cross-case study

Interviews with radiotherapy (RT) stakeholders were completed across four European countries to identify the educational models used across Europe and how they affect competencies of Therapeutic Radiographers/Radiotherapists (TR/RTTs). The stakeholders identified the following educational models: • Programmes below European Qualifications Framework (EQF) level 6 (EQF4 or EQF5) • RT-only BSc programmes (EQF6) • Multiple-specialism BSc programmes (EQF6) • RT-only apprenticeships (EQF6) • Multiple-specialism BSc followed by an MSc (EQF6→EQF7) • Integrated masters (EQF7) • RT-only pre-registration MSc (EQF7) • ‘Common trunk’ model (EQF6 or EQF7) Each educational model has its set of advantages and disadvantages, but most models can be used to achieve the same essential competencies of TR/RTTs. Some models showed weaknesses in their ability to develop adequate RT competencies (low EQF level, low RT-specific content). Regulating the standards of practice at national level ensures that essential competencies are developed across all course programmes, improving the care to RT patients.peer-reviewe

Activation of Ventral Tegmental Area 5-HT2C Receptors Reduces Incentive Motivation

FUNDING AND DISCLOSURE The research was funded by Wellcome Trust (WT098012) to LKH; and National Institute of Health (DK056731) and the Marilyn H. Vincent Foundation to MGM. The University of Michigan Transgenic Core facility is partially supported by the NIH-funded University of Michigan Center for Gastrointestinal Research (DK034933). The remaining authors declare no conflict of interest. ACKNOWLEDGMENTS We thank Dr Celine Cansell, Ms Raffaella Chianese and the staff of the Medical Research Facility for technical assistance. We thank Dr Vladimir Orduña for the scientific advice and technical assistance.Peer reviewedPublisher PD

Quantitative analysis of performance on a progressive-ratio schedule: effects of reinforcer type, food deprivation and acute treatment with Δ⁹-tetrahydrocannabinol (THC)

Rats’ performance on a progressive-ratio schedule maintained by sucrose (0.6 M, 50 μl) and corn oil (100%, 25 μl) reinforcers was assessed using a model derived from Killeen’s (1994) theory of scheduled-controlled behaviour, ‘Mathematical Principles of Reinforcement’. When the rats were maintained at 80% of their free-feeding body weights, the parameter expressing incentive value, a, was greater for the corn oil than for the sucrose reinforcer; the response-time parameter, δ, did not differ between the reinforcer types, but a parameter derived from the linear waiting principle (Tₒ), indicated that the minimum post-reinforcement pause was longer for corn oil than for sucrose. When the rats were maintained under free-feeding conditions, a was reduced, indicating a reduction of incentive value, but δ was unaltered. Under the food-deprived condition, the CB1 cannabinoid receptor agonist Δ⁹-tetrahydrocannabinol (THC: 0.3, 1 and 3 mg kg-1) increased the value of sucrose; none of the other parameters was affected by THC. The results provide new information about the sensitivity of the model’s parameters to deprivation and reinforcer quality, and suggest that THC selectively enhances the incentive value of sucrose

Genetic predisposition for sudden cardiac death in myocardial ischaemia: the Arrhythmia Genetics in the NEtherlandS study

Sudden cardiac death from ventricular fibrillation during myocardial infarction is a leading cause of total and cardiovascular mortality. This multifactorial, complex condition clusters in families, suggesting a substantial genetic cause. We carried out a genomewide association study (GWAS) for sudden cardiac death, in the AGNES (Arrhythmia Genetics in the Netherlands) population, consisting of patients with (cases) and without (controls) ventricular fibrillation during a first ST-elevation myocardial infarction. The most significant association was found at chromosome 21q21 (rs2824292; odds ratio = 1.78, 95% CI 1.47–2.13, P = 3.3 × 10−10), 98 kb proximal of the CXADR gene, encoding the Coxsackie and adenovirus receptor. This locus has not previously been implicated in arrhythmia susceptibility. Further research on the mechanism of this locus will ultimately provide novel insight into arrhythmia mechanisms in this condition

Recurrent and Founder Mutations in the Netherlands: the Long-QT Syndrome

Background and objective The long-QT syndrome (LQTS) is associated with premature sudden cardiac deaths affecting whole families and is caused by mutations in genes encoding for cardiac proteins. When the same mutation is found in different families (recurrent mutations), this may imply either a common ancestor (founder) or multiple de novo mutations. We aimed to review recurrent mutations in patients with LQTS. Methods By use of our databases, we investigated the number of mutations that were found recurrently (at least three times) in LQT type 1-3 patients in the Netherlands. We studied familial links in the apparently unrelated probands, and we visualised the geographical distribution of these probands. Our results were compared with published literature of founder effects in LQTS outside the Netherlands. Results We counted 14 recurrent LQT mutations in the Netherlands. There are 326 identified carriers of one of these mutations. For three of these mutations, familial links were found between apparently unrelated probands. Conclusion Whereas true LQT founder mutations are described elsewhere in the world, we cannot yet demonstrate a real founder effect of these recurrent mutations in the Netherlands. Further studies on the prevalence of these mutations are indicated, and haplotype-sharing of the mutation carriers is pertinent to provide more evidence for founder mutation-based LQTS pathology in our countr