Confident and competent?: helping students to develop their practice based skills

The Competence in Practice Assessment (CiPA) Tool was designed and developed to support student self-assessment in a social care or health setting. It is one of many artefacts created as part of the Centre for Excellence in Teaching and Learning called ‘Assessment and Learning in Practice Settings’. Demonstration of competence is essential for courses leading to professional registration. This presentation will chart the development and evaluation of the CiPA tool into responsive software that students can self complete at stages throughout their course: In doing this we demonstrate how a research project became the springboard for the development of student centred learning and teaching innovation. 14 students from a range of health and social work courses, who responded to a job advertisement, worked in multiprofessional collaborative groups to design feedback, reflective prompts and resource links in response to students’ self assessment ratings. This was then built into a simple software package by a computing placement student. The result is that students complete the tool [with potential for PC, web or Mobile access] by assessing their perception of their own competency at their current stage in the course. The software provides them with feedback designed to support their own assessment and suggest actions: this is confidential and thus a safe activity, but linked to Personal Development Planning and so able to be incorporated into their record of professional growth, preparation for further placement experience and readiness for qualification. Taking responsibility for one’s own learning, and developing self assessment skills are parts of becoming a competent practitioner in any profession; thus whilst the questions as they stand relate to health and social care professions, the design principles apply to any placement experience, leading to opportunities for creative development of the tool

Immune modulation to improve tissue engineering outcomes for cartilage repair in the osteoarthritic joint

Osteoarthritis (OA), the most common form of arthritis, is a disabling degenerative joint disease affecting synovial joints and is associated with cartilage destruction, inflammation of the synovial membrane, and subchondral bone remodeling. Inflammation of the synovial membrane may arise secondary to degenerative processes in articular cartilage (AC), or may be a primary occurrence in OA pathogenesis. However, synovial inflammation plays a key role in the pathogenesis and disease progression of OA through the production of pro-inflammatory mediators, and is associated with cartilage destruction and pain. The triggers that initiate activation of the immune response in OA are unknown, but crosstalk between osteoarthritic chondrocytes, cartilage degradation products, and the synovium may act to perpetuate this response. Increasing evidence has emerged highlighting an important role for pro-inflammatory mediators and infiltrating inflammatory cell populations in the progression of the disease. Tissue engineering strategies hold great potential for the repair of damaged AC in an osteoarthritic joint. However, an in-depth understanding of how OA-associated inflammation impacts chondrocyte and progenitor cell behavior is required to achieve efficient cartilage regeneration in a catabolic osteoarthritic environment. In this review, we will discuss the role of inflammation in OA, and investigate novel immune modulation strategies that may prevent disease progression and facilitate successful cartilage regeneration for the treatment of OA

Immune modulation to improve tissue engineering outcomes for cartilage repair in the osteoarthritic joint

Osteoarthritis (OA), the most common form of arthritis, is a disabling degenerative joint disease affecting synovial joints and is associated with cartilage destruction, inflammation of the synovial membrane, and subchondral bone remodeling. Inflammation of the synovial membrane may arise secondary to degenerative processes in articular cartilage (AC), or may be a primary occurrence in OA pathogenesis. However, synovial inflammation plays a key role in the pathogenesis and disease progression of OA through the production of pro-inflammatory mediators, and is associated with cartilage destruction and pain. The triggers that initiate activation of the immune response in OA are unknown, but crosstalk between osteoarthritic chondrocytes, cartilage degradation products, and the synovium may act to perpetuate this response. Increasing evidence has emerged highlighting an important role for pro-inflammatory mediators and infiltrating inflammatory cell populations in the progression of the disease. Tissue engineering strategies hold great potential for the repair of damaged AC in an osteoarthritic joint. However, an in-depth understanding of how OA-associated inflammation impacts chondrocyte and progenitor cell behavior is required to achieve efficient cartilage regeneration in a catabolic osteoarthritic environment. In this review, we will discuss the role of inflammation in OA, and investigate novel immune modulation strategies that may prevent disease progression and facilitate successful cartilage regeneration for the treatment of OA

Learning to Classify Morals and Conventions: Artificial Intelligence in Terms of the Economics of Convention

Artificial Intelligence (AI) and its relation with societies has become an increasingly interesting subject of study for the social sciences. Nevertheless, there is still an important lack of interdisciplinary and empirical research applying social theories to the field of AI. We here aim to shed light on the interactions between humans and autonomous systems and analyse the moral conventions, which underly these interactions and cause moments of conflict and cooperation. For this purpose we employ the Economics of Convention (EC), originally developed in the context of economic processes of production and management involving humans, objects and machines. We create a dataset from three relevant text sources and perform a qualitative exploration of its content. Then, we train a combination of Machine Learning (ML) classifiers on this dataset, which achieve an average classification accuracy of 83.7%. A qualitative and quantitative evaluation of the predicted conventions reveals, inter alia, that the Industrial and Inspired conventions tend to co-exist in the AI domain. This is the first time, ML classifiers are used to study the EC in different AI-related text types. Our analysis of a larger dataset is especially beneficial for the social sciences

vIL-10-overexpressing human MSCs modulate naïve and activated T lymphocytes following induction of collagenase-induced osteoarthritis

Recent efforts in osteoarthritis (OA) research have highlighted synovial inflammation and involvement of immune cells in disease onset and progression. We sought to establish the in-vivo immune response in collagenase-induced OA and investigate the ability of human mesenchymal stem cells (hMSCs) overexpressing viral interleukin 10 (vIL-10) to modulate immune populations and delay/prevent disease progression. Eight-week-old male C57BL/6 mice were injected with 1 U type VII collagenase over two consecutive days. At day 7, 20,000 hMSCs overexpressing vIL-10 were injected into the affected knee. Control groups comprised of vehicle, 20,000 untransduced or adNull-transduced MSCs or virus alone. Six weeks later knees were harvested for histological analysis and popliteal and inguinal lymph nodes for flow cytometric analysis. At this time there was no significant difference in knee OA scores between any of the groups. A trend toward more damage in animals treated with hMSCs was observed. Interestingly there was a significant reduction in the amount of activated CD4 and CD8 T cells in the vIL-10-expressing hMSC group. vIL-10-overexpressing hMSCs can induce long-term reduction in activated T cells in draining lymph nodes of mice with collagenase-induced OA. This could lead to reduced OA severity or disease progression over the long term

Differentiation of vascular stem cells contributes to ectopic calcification of atherosclerotic plaque

The cellular and molecular basis of vascular calcification (VC) in atherosclerosis is not fully understood. Here, we investigate role of resident/circulating progenitor cells in VC and contribution of inflammatory plaque environment to this process. Vessel-derived stem/progenitor cells (VSCs) and mesenchymal stem cells (MSCs) isolated from atherosclerotic ApoE(-/-) mice showed significantly more in vitro osteogenesis and chondrogenesis than cells generated from control C57BL/6 mice. To assess their ability to form bone in vivo, cells were primed chondrogenically or cultured in control medium on collagen glycosaminoglycan scaffolds in vitro prior to subcutaneous implantation in ApoE(-/-) and C57BL/6 mice using a crossover study design. Atherosclerotic ApoE(-/-) MSCs and VSCs formed bone when implanted in C57BL/6 mice. In ApoE(-/-) mice, these cells generated more mature bone than C57BL/6 cells. The atherosclerotic in vivo environment alone promoted bone formation by implanted C57BL/6 cells. Un-primed C57BL/6 VSCs were unable to form bone in either mouse strain. Treatment of ApoE(-/-) VSC chondrogenic cultures with interleukin (IL)-6 resulted in significantly increased glycosaminoglycan deposition and expression of characteristic chondrogenic genes at 21 days. In conclusion, resident vascular cells from atherosclerotic environment respond to the inflammatory milieu and undergo calcification. IL-6 may have a role in aberrant differentiation of VSCs contributing to vascular calcification in atherosclerosis. Stem Cells2016;34:913-92

Differentiation of vascular stem cells contributes to ectopic calcification of atherosclerotic plaque

The cellular and molecular basis of vascular calcification (VC) in atherosclerosis is not fully understood. Here, we investigate role of resident/circulating progenitor cells in VC and contribution of inflammatory plaque environment to this process. Vessel-derived stem/progenitor cells (VSCs) and mesenchymal stem cells (MSCs) isolated from atherosclerotic ApoE(-/-) mice showed significantly more in vitro osteogenesis and chondrogenesis than cells generated from control C57BL/6 mice. To assess their ability to form bone in vivo, cells were primed chondrogenically or cultured in control medium on collagen glycosaminoglycan scaffolds in vitro prior to subcutaneous implantation in ApoE(-/-) and C57BL/6 mice using a crossover study design. Atherosclerotic ApoE(-/-) MSCs and VSCs formed bone when implanted in C57BL/6 mice. In ApoE(-/-) mice, these cells generated more mature bone than C57BL/6 cells. The atherosclerotic in vivo environment alone promoted bone formation by implanted C57BL/6 cells. Un-primed C57BL/6 VSCs were unable to form bone in either mouse strain. Treatment of ApoE(-/-) VSC chondrogenic cultures with interleukin (IL)-6 resulted in significantly increased glycosaminoglycan deposition and expression of characteristic chondrogenic genes at 21 days. In conclusion, resident vascular cells from atherosclerotic environment respond to the inflammatory milieu and undergo calcification. IL-6 may have a role in aberrant differentiation of VSCs contributing to vascular calcification in atherosclerosis. Stem Cells 2016;34:913-923.Irish Research Council for Science, Engineering and Technology and Science Foundation Ireland under Grant No. 09/SRC/B179

Additional file 3: Figure S3. of vIL-10-overexpressing human MSCs modulate naïve and activated T lymphocytes following induction of collagenase-induced osteoarthritis

AdIL-10-transduced MSCs do not reduce the levels of pro-inflammatory monocytes at 6 weeks post injection. A CD11b and Ly6C expression by myeloid cells isolated from the popliteal and inguinal lymph nodes at 6 weeks post treatment, as detected by flow cytometry. For the popliteal lymph nodes, data points represent n = 4, pooled from eight animals. Data points in the AdIL-10 group represent n = 5, with three samples pooled from two animals and two single samples. For inguinal lymph nodes, data points represent n = 2, pooled from eight animals. Data points in the AdIL-10 group represent n = 3, with one sample pooled from four animals, one sample pooled from three animals and one single sample. B Serum levels of MCP-1 at 6 weeks post treatment, as quantified utilising a chemiluminescent array. (PDF 47 kb

Additional file 1: Figure S1. of vIL-10-overexpressing human MSCs modulate naĂŻve and activated T lymphocytes following induction of collagenase-induced osteoarthritis

Timeline illustrating the induction of OA in mice followed by injection of five different treatment conditions at day 7. Six weeks after treatment animals were euthanised and the joints harvested for histological scoring. Lymph nodes and blood were taken for flow cytometric and multiplex ELISA analyses respectively. (PDF 9 kb