Recognition of Experience Based Education and Learning (REBEL)

The RECOGNITION OF EXPERIENCE-BASED EDUCATION and LEARNING (REBEL) framework is designed to assist learning reflection and evaluation in the context of informal and non-formal lived and educational experiences. The REBEL competencies and capabilities tool: The competencies and capabilities tool is a method that offers a variety of structures for evaluating learning gain. It can be used in relation to an individual’s lived experiences as well as their engagement and participation in both non-formal and formal education. The system is composed of 108 descriptors relating to transferable competencies and capabilities. The tool enhances student awareness of their strengths and positive behaviors, and their personal and professional development needs. Flexible learning and access: The REBEL system can facilitate and support the process of application for the Accreditation of Prior Experience and Learning. As such, it can supplement or replace a part of the existing curriculum of a course or assist students without standard qualifications in their applications for HE courses. Current developments with Camden Council are focused on the Extended Project Qualification and the REBEL tool is being deployed to reinforce learner confidence and enable third party endorsements (kite-marked certification). Development: The REBEL competencies and capabilities tool is open source and was devised and tested in partnership and with the support of: University of Salford, SOLIDAR foundation, Observal (the Observatory of Validated Learning at Universidad Valladolid), La Ligue de L’Enseignement (France), Workers Educational Association (UK), Trade Union UnionLearn (TUC), and the Open Design and Manufacture EU Strategic Network

Cortactin deficiency is associated with reduced neutrophil recruitment but increased vascular permeability in vivo

Cortactin is required for endothelial barrier function and leukocyte recruitment in vivo

Reduced inflammatory hyperalgesia with preservation of acute thermal nociception in mice lacking cGMP-dependent protein kinase I

cGMP-dependent protein kinase I (PKG-I) has been suggested to contribute to the facilitation of nociceptive transmission in the spinal cord presumably by acting as a downstream target of nitric oxide. However, PKG-I activators caused conflicting effects on nociceptive behavior. In the present study we used PKG-I(-/-) mice to further assess the role of PKG-I in nociception. PKG-I deficiency was associated with reduced nociceptive behavior in the formalin assay and zymosan-induced paw inflammation. However, acute thermal nociception in the hot-plate test was unaltered. After spinal delivery of the PKG inhibitor, Rp-8-Br-cGMPS, nociceptive behavior of PKG-I(+/+) mice was indistinguishable from that of PKG-I(-/-) mice. On the other hand, the PKG activator, 8-Br-cGMP (250 nmol intrathecally) caused mechanical allodynia only in PKG-I(+/+) mice, indicating that the presence of PKG-I was essential for this effect. Immunofluorescence studies of the spinal cord revealed additional morphological differences. In the dorsal horn of 3- to 4-week-old PKG-I(-/-) mice laminae I-III were smaller and contained fewer neurons than controls. Furthermore, the density of substance P-positive neurons and fibers was significantly reduced. The paucity of substance P in laminae I-III may contribute to the reduction of nociception in PKG-I(-/-) mice and suggests a role of PKG-I in substance P synthesis

Protein folds vs. protein folding: Differing questions, different challenges

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