An overview of the nature of the preparation of practice educators in five health care disciplines

Practice education is a core element of all educational programmes that prepare health care professionals for academic award and registration to practice. Ensuring quality and effectiveness involves partnership working between Higher Education Institutions (HEI’s) and health care providers, social care communities, voluntary and independent sectors offering client care throughout the United Kingdom and Republic of Ireland. Clearly practitioners who support, supervise and assess learners for entry to their respective professions need to be well prepared and supported in their roles as practice educators. However it would appear that the nature of this support and preparation varies across disciplines and that good practice is not easily shared. With this in mind, the Making Practice Based Learning Work (MPBLW) project aims to make practitioners more effective at supporting and supervising students in the workplace across a range of health care disciplines namely Dietetics, Nursing, Occupational Therapy, Physiotherapy and Radiology. The Department of Employment and Learning (Northern Ireland) and the Higher Education Funding Council for England has funded this collaborative project involving staff from Ulster, Northumbria and Bournemouth Universities. The outcomes for each phase of the project are: Phase One: • Identify and document good practice on how practitioners are prepared for their educational role. Phase Two: • Develop and evaluate learning materials for use by practitioners across five health care disciplines. • Make learning materials available in a number of efficient media, e.g. paper, electronic, CD-ROM and web-based. • Develop a programme applicable to interprofessional and uniprofessional contexts. • Widen access for a multicultural workforce. Phase Three: • Embed best educational practice through the establishment of an academicpractitioner network. • Disseminate a range of materials and processes across the wider academic and health and social care communities

Crystal Structure Of (3e)-3-(2,4-dinitrophenoxymethyl)-4-phenylbut-3-en-2-one

In the title compound, C17H14N2O6, the conformation about the C=C double bond [1.345(2)Å] is E, with the ketone moiety almost coplanar [C-C-C-C torsion angle = 9.5(2)°] along with the phenyl ring [C-C-C-C = 5.9(2)°]. The aromatic rings are almost perpendicular to each other [dihedral angle = 86.66(7)°]. The 4-nitro moiety is approximately coplanar with the benzene ring to which it is attached [O-N-C-C = 4.2(2)°], whereas the one in the ortho position is twisted [O-N-C-C = 138.28(13)°]. The molecules associate via C-H⋯O interactions, involving both O atoms from the 2-nitro group, to form a helical supramolecular chain along [010]. Nitro-nitro N⋯O interactions [2.8461(19)Å] connect the chains into layers that stack along [001].709o1051o1052Altomare, A., Burla, M.C., Camalli, M., Cascarano, G.L., Giacovazzo, C., Guagliardi, A., Moliterni, A.G.G., Spagna, R., (1999) J. Appl. Cryst, 32, pp. 115-119Brandenburg, K., (2006) DIAMOND, , Crystal Impact GbR, Bonn, Germany(2009) APEX2 and SAINT, , Bruker Bruker AXS Inc., Madison, Wisconsin, USA(2010) ChemAxon, , http://www.chemaxon.com, MarvinsketchDaszkiewicz, M., (2013) CrystEngComm, 15, pp. 10427-10430Farrugia, L.J., (2012) J. Appl. Cryst, 45, pp. 849-854Gans, J., Shalloway, D., (2001) J. Mol. Graph. Mode, 119, pp. 557-559De Paula, B.R.S., Zampieri, D.S., Rodrigues, J.A.R., Moran, P.J.S., (2013) Tetrahedron Asymmetry, 24, pp. 973-981Rodrigues, J.A.R., Moran, P.J.S., Conceicaõ, G.J.A., Fardelone, L.C., (2004) Food Technol. Biotechno, 142, pp. 295-303Sheldrick, G.M., (1996) SADABS, , University of Göttingen, GermanySheldrick, G.M., (2008) Acta Cryst A, 64, pp. 112-122Westrip, S.P., (2010) J. Appl. Cryst, 43, pp. 920-925Zukerman-Schpector, J., Maganhi, S.H., Moran, P.J.S., De Paula, B.R.S., Nucci, P.R., Tiekink, E.R.T., (2014) Acta Cryst. e, 70, pp. o1020-o102

Crystal Structure Of (3e)-3-[(4-nitrophenoxy) Methyl]-4-phenylbut-3-en-2-one

In the title compound, C17H15NO4, the conformation about the C=C double bond [1.348(2)Å] is E with the ketone group almost co-planar [C-C-C-C torsion angle = 7.2(2)°] but the phenyl group twisted away [C-C-C-C = 160.93(17)°]. The terminal aromatic rings are almost perpendicular to each other [dihedral angle = 81.61(9)°] giving the molecule an overall U-shape. The crystal packing feature benzene-C-H⋯O(ketone) contacts that lead to supramolecular helical chains along the b axis. These are connected by π-π interactions between benzene and phenyl rings [inter-centroid distance = 3.6648(14)Å], resulting in the formation of a supramolecular layer in the bc plane.709o1020o1021Altomare, A., Burla, M.C., Camalli, M., Cascarano, G.L., Giacovazzo, C., Guagliardi, A., Moliterni, A.G.G., Spagna, R., (1999) J. Appl. Cryst32, pp. 115-119Brandenburg, K., (2006) DIAMOND, , Crystal Impact GbR, Bonn, Germany(2009) APEX2 and SAINT, , Bruker Bruker AXS Inc., Madison, Wisconsin, USA(2010) Marvinsketch, , http://www.chemaxon.com, ChemaxonFarrugia, L.J., (2012) J. Appl. Cryst45, pp. 849-854De Paula, B.R.S., Zampieri, D.S., Rodrigues, J.A.R., Moran, P.J.S., (2013) Tetrahedron: Asymmetry24, pp. 973-981Rodrigues, J.A.R., Moran, P.J.S., Conceicaõ, G.J.A., Fardelone, L.C., (2004) Food Technol. Biotechnol42, pp. 295-303Sheldrick, G.M., (1996) SADABS, , University of Göttingen, GermanySheldrick, G.M., (2008) Acta Cryst A64, pp. 112-122Westrip, S.P., (2010) J. Appl. Cryst43, pp. 920-92

Gene × environment interactions in schizophrenia: evidence from genetic mouse models

The study of gene × environment, as well as epistatic interactions in schizophrenia, has provided important insight into the complex etiopathologic basis of schizophrenia. It has also increased our understanding of the role of susceptibility genes in the disorder and is an important consideration as we seek to translate genetic advances into novel antipsychotic treatment targets. This review summarises data arising from research involving the modelling of gene × environment interactions in schizophrenia using preclinical genetic models. Evidence for synergistic effects on the expression of schizophrenia-relevant endophenotypes will be discussed. It is proposed that valid and multifactorial preclinical models are important tools for identifying critical areas, as well as underlying mechanisms, of convergence of genetic and environmental risk factors, and their interaction in schizophrenia

Olfactory threshold selectively predicts positive psychometric schizotypy

Olfactory impairment might be useful as a non-invasive pre-morbid biological marker of psychosis. People with schizophrenia show consistent impairments, but an association between olfaction and schizotypy in non-clinical populations is inconclusive and has been somewhat controversial. This is important as impairment in patients may be artefacts of antipsychotic medication. Meta-analyses indicate small effect sizes in non-clinical populations, suggesting prior negative studies may have been underpowered to demonstrate them.We measured olfaction and psychometrically-defined schizotypy in a sample of 739 non-clinical volunteers [mean age 23.1]. Subsets reported whether they had a history of mental illness in the family or smoked. We used (sniffin’ sticks) to measure threshold detection, discrimination and identification of odours. O-LIFE was used to measure schizotypy.Lower olfactory-threshold selectively predicted higher scores on the positive dimension, unusual experiences. This association was most evident in sub-groups reporting history of mental illness in the family and/or smoking. There was a weak trend for an association between identification and introvertive anhedonia and discrimination and cognitive disorganization in those with a history of mental illness in the family.These data support the idea that olfaction merits further investigation as a biomarker for psychosis and that olfactory-threshold detection in particular has potential to selectively predict unusual experiences. Variability in previous studies may have been exacerbated by including different proportions of participants with history of mental illness in the family and/or smoking. We propose that non-clinical participants be stratified by these factors in futurestudies of olfaction and potentially any study that measures psychometric schizotypy

Abnormal clock gene expression and locomotor activity rhythms in two month-old female APPSwe/PS1dE9 mice

In addition to cognitive decline, Alzheimer’s disease (AD) is also characterized by agitation and disruptions in activity and sleep. These symptoms typically occur in the evening or at night and have been referred to as ‘sundowning’. These symptoms are especially difficult for carers and there are no specific drug treatments. There is increasing evidence that these symptoms reflect an underlying pathology of circadian rhythm generation and transmission. We investigated whether a transgenic mouse model relevant to AD (APPswe/PS1dE9) exhibits circadian alterations in locomotor activity and expression of clock genes involved in the regulation of the circadian cycle. Female mice at 2 months of age were investigated in their home cage. Results show that the APPswe/PS1dE9 transgene alters levels and patterns in circadian rhythm of locomotor activity. Expression of the clock genes Per1, Per2, Cry1 and Cry2 was found to increase at night compared to day in wild-type control mice in the medulla/pons. This effect was blunted for Cry1 and Cry2 gene expression in APPswe/PS1dE9. In summary, this study suggests altered circadian regulation of locomotor activity is abnormal in female APPswe/PS1dE9 mice and that this alteration has biomolecular analogies in a widely available model of AD. Furthermore, the early age at which these effects are manifest suggests that these circadian effects may precede plaque development. The APPswe/PS1dE9 mouse genetic model may have potential to serve as a tool in understanding the neuropathology of circadian abnormalities in AD and as a model system to test novel therapeutic agents for these symptoms

Urocortin 2 inhibits human aortic smooth muscle cell proliferation via corticotrophin releasing hormone receptor-2 in abdominal aortic aneurysm

Introduction: A key feature of abdominal aortic aneurysm is the loss of proliferation and paucity of vascular smooth muscle cells, the major cells within the aortic tunica media. It has been suggested that urocortin 2 (UCN2), a selective ligand for corticotrophin releasing factor receptor 2 (CRFR2) may play a beneficial role in various cardiovascular diseases. However, the role of this peptide in abdominal aortic aneurysm has not been studied in detail. Here we assessed the hypothesis that urocortin 2 promotes an aneurysm phenotype in human aortic smooth muscles in vitro via CRFR2. Experimental Procedure: We assessed the release of UCN2 from explants of human tissue biopsies in vitro (Aortic aneurysm thrombus, n = 14; aortic aneurysm body, n = 11; femoral atheroma control, n = 6) using ELISA. We investigated the effect of incubating human aortic smooth muscle cells with recombinant UCN2 or aneurysm thrombus explants secretions at a UCN2 dose of 0, 10 and 100 nM for 24 and 48 hours (n = 6 per group x 3 experiments). Cell proliferation was determined by the alamarBlue® cell viability reagent. Results were analyzed and presented as mean ± SEM relative to the control. We also investigated the impact of blocking CRFR2 on UCN2 induced changes on these cells. Results: Secretion of UCN2 was significantly higher from aneurysm thrombus (n = 14, p = 0.0020) and aneurysm body (n = 11, p = 0.0104) compared to femoral atheroma. Human aortic smooth muscle cells proliferation was dose dependently inhibited by recombinant UCN2 (p = 0.0172) and aortic aneurysm thrombus conditioned medium (p = 0.0273) after 24 hours. This effect of recombinant UCN2 was abrogated significantly by prior incubation with the CRFR2 blocker Astressin-2B (p = 0.0043). Similar effects were seen on incubating cells for 48 hours. Conclusion: UCN2 is released in high concentrations by aortic aneurysm thrombus. UCN2 inhibits aortic vascular smooth muscle cell proliferation in vitro via CRFR2. This effect may be relevant to the pathogenesis of abdominal aortic aneurysm

Urocortin 2 inhibits human aortic smooth muscle cell proliferation via corticotrophin releasing hormone receptor-2 in abdominal aortic aneurysm

Introduction: A key feature of abdominal aortic aneurysm is the loss of proliferation and paucity of vascular smooth muscle cells, the major cells within the aortic tunica media. It has been suggested that urocortin 2 (UCN2), a selective ligand for corticotrophin releasing factor receptor 2 (CRFR2) may play a beneficial role in various cardiovascular diseases. However, the role of this peptide in abdominal aortic aneurysm has not been studied in detail. Here we assessed the hypothesis that urocortin 2 promotes an aneurysm phenotype in human aortic smooth muscles in vitro via CRFR2. Experimental Procedure: We assessed the release of UCN2 from explants of human tissue biopsies in vitro (Aortic aneurysm thrombus, n = 14; aortic aneurysm body, n = 11; femoral atheroma control, n = 6) using ELISA. We investigated the effect of incubating human aortic smooth muscle cells with recombinant UCN2 or aneurysm thrombus explants secretions at a UCN2 dose of 0, 10 and 100 nM for 24 and 48 hours (n = 6 per group x 3 experiments). Cell proliferation was determined by the alamarBlue® cell viability reagent. Results were analyzed and presented as mean ± SEM relative to the control. We also investigated the impact of blocking CRFR2 on UCN2 induced changes on these cells. Results: Secretion of UCN2 was significantly higher from aneurysm thrombus (n = 14, p = 0.0020) and aneurysm body (n = 11, p = 0.0104) compared to femoral atheroma. Human aortic smooth muscle cells proliferation was dose dependently inhibited by recombinant UCN2 (p = 0.0172) and aortic aneurysm thrombus conditioned medium (p = 0.0273) after 24 hours. This effect of recombinant UCN2 was abrogated significantly by prior incubation with the CRFR2 blocker Astressin-2B (p = 0.0043). Similar effects were seen on incubating cells for 48 hours. Conclusion: UCN2 is released in high concentrations by aortic aneurysm thrombus. UCN2 inhibits aortic vascular smooth muscle cell proliferation in vitro via CRFR2. This effect may be relevant to the pathogenesis of abdominal aortic aneurysm