From Lurker to Active Participant

The original publication is available from www.springerlink.com. Sloep, P. B., & Kester, L. (2009). From Lurker to Active Participant. In R. Koper (Ed)., Learning Network Services for Professional Development (pp. 17-26). Berlin, Germany: Springer Verlag.In this chapter we will specifically go into the question of how prospective Learning Network users may be convinced of these benefits, for that is likely to be the necessary condition for their active participation in any Learning Network. Their question would be ‘Why should I participate?’, this chapter inventories an-swers to that question, which are then translated into a few guidelines for those contemplating to set up a particular, topic-bound Learning Network. Two kinds of answer are distinguished. Proximate answers, which affect the decision to partici-pate here and now; and ultimate answers, which motivate participation, but only in the long run, after the decision to participate has already been taken. Both are im-portant, the former to persuade people to participate, the latter to persuade people to keep participating. Before going into them, we’ll introduce a concrete example to add some realism to the discussion.The work on this publication has been sponsored in part by the TENCompetence Integrated Project that is funded by the European Commission's 6th Framework Programme, priority IST/Technology Enhanced Learning. Contract 027087 [http://www.tencompetence.org

'Education, education, education' : legal, moral and clinical

This article brings together Professor Donald Nicolson's intellectual interest in professional legal ethics and his long-standing involvement with law clinics both as an advisor at the University of Cape Town and Director of the University of Bristol Law Clinic and the University of Strathclyde Law Clinic. In this article he looks at how legal education may help start this process of character development, arguing that the best means is through student involvement in voluntary law clinics. And here he builds upon his recent article which argues for voluntary, community service oriented law clinics over those which emphasise the education of students

The development of Scotland’s Curriculum for Excellence: Amnesia and Déjà Vu

Scotland’s new Curriculum for Excellence (CfE) has been widely acknowledged as the most significant educational development in a generation, with the potential to transform learning and teaching in Scottish schools. In common with recent developments elsewhere, CfE seeks to re-engage teachers with processes of curriculum development, to place learning at the heart of the curriculum and to change engrained practices of schooling. This article draws upon well-established curriculum theory (notably the work of both Lawrence Stenhouse and A.V. Kelly) to analyse the new curriculum. We argue that by neglecting to take account of such theory, the curricular offering proposed by CfE is subject to a number of significant structural contradictions which may affect the impact that it ultimately exerts on learning and teaching; in effect, by ignoring the lessons of the past, CfE runs the risk of undermining the potential for real change

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies

Loss-of-function ABCC8 mutations in pulmonary arterial hypertension

Background: In pulmonary arterial hypertension (PAH), pathological changes in pulmonary arterioles progressively raise pulmonary artery pressure and increase pulmonary vascular resistance, leading to right heart failure and high mortality rates. Recently, the first potassium channelopathy in PAH, because of mutations in KCNK3, was identified as a genetic cause and pharmacological target. Methods: Exome sequencing was performed to identify novel genes in a cohort of 99 pediatric and 134 adult-onset group I PAH patients. Novel rare variants in the gene identified were independently identified in a cohort of 680 adult-onset patients. Variants were expressed in COS cells and function assessed by patch-clamp and rubidium flux analysis. Results: We identified a de novo novel heterozygous predicted deleterious missense variant c.G2873A (p.R958H) in ABCC8 in a child with idiopathic PAH. We then evaluated all individuals in the original and a second cohort for rare or novel variants in ABCC8 and identified 11 additional heterozygous predicted damaging ABCC8 variants. ABCC8 encodes SUR1 (sulfonylurea receptor 1)—a regulatory subunit of the ATP-sensitive potassium channel. We observed loss of ATP-sensitive potassium channel function for all ABCC8 variants evaluated and pharmacological rescue of all channel currents in vitro by the SUR1 activator, diazoxide. Conclusions: Novel and rare missense variants in ABCC8 are associated with PAH. Identified ABCC8 mutations decreased ATP-sensitive potassium channel function, which was pharmacologically recovered