292 research outputs found

    Teaching health science students foundation motivational interviewing skills: use of motivational interviewing treatment integrity and self-reflection to approach transformative learning

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    © 2015 Schoo et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http:// creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.BACKGROUND: Many undergraduate and graduate-entry health science curricula have incorporated training in motivational interviewing (MI). However, to effectively teach skills that will remain with students after they graduate is challenging. The aims of this study were to find out self-assessed MI skills of health students and whether reflecting on the results can promote transformative learning. METHODS: Thirty-six Australian occupational therapy and physiotherapy students were taught the principles of MI, asked to conduct a motivational interview, transcribe it, self-rate it using the Motivational Interviewing Treatment Integrity (MITI) tool and reflect on the experience. Student MI skills were measured using the reported MITI subscores. Student assignments and a focus group discussion were analysed to explore the student experience using the MITI tool and self-reflection to improve their understanding of MI principles. RESULTS: Students found MI challenging, although identified the MITI tool as useful for promoting self-reflection and to isolate MI skills. Students self-assessed their MI skills as competent and higher than scores expected from beginners. CONCLUSIONS: The results inform educational programs on how MI skills can be developed for health professional students and can result in transformative learning. Students may over-state their MI skills and strategies to reduce this, including peer review, are discussed. Structured self-reflection, using tools such as the MITI can promote awareness of MI skills and compliment didactic teaching methods

    Density Profiles in Random Quantum Spin Chains

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    We consider random transverse-field Ising spin chains and study the magnetization and the energy-density profiles by numerically exact calculations in rather large finite systems (L128L\le 128). Using different boundary conditions (free, fixed and mixed) the numerical data collapse to scaling functions, which are very accurately described by simple analytic expressions. The average magnetization profiles satisfy the Fisher-de Gennes scaling conjecture and the corresponding scaling functions are indistinguishable from those predicted by conformal invariance.Comment: 4 pages RevTeX, 4 eps-figures include

    Evidence of mild founder LMOD3 mutations causing nemaline myopathy 10 in Germany and Austria

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    Objective To expand the clinical and genetic spectrum of nemaline myopathy 10 by a series of Austrian and German patients with a milder disease course and missense mutations in LMOD3. Methods We characterized the clinical features and the genetic status of 4 unrelated adolescent or adult patients with nemaline myopathy. Results The 4 patients showed a relatively mild disease course. They all have survived into adulthood, 3 of 4 have remained ambulatory, and all showed marked facial weakness. Muscle biopsy specimens gave evidence of nemaline bodies. All patients were unrelated but originated from Austria (Tyrol and Upper Austria) and Southern Germany (Bavaria). All patients carried the missense variant c.1648C>T, p.(Leu550Phe) in the LMOD3 gene, either on both alleles or in trans with another missense variant (c.1004A>G, p.Gln335Arg). Both variants were not reported previously. Conclusions In 2014, a severe form of congenital nemaline myopathy caused by disrupting mutations in LMOD3 was identified and denoted as NEM10. Unlike the previously reported patients, who had a severe clinical picture with a substantial risk of early death, our patients showed a relatively mild disease course. As the missense variant c.1648C>T is located further downstream compared to all previously published LMOD3 mutations, it might be associated with higher protein expression compared to the reported loss-of-function mutations. The apparent clusters of 2 mild mutations in Germany and Austria in 4 unrelated families may be explained by a founder effect

    Mutations in Subunits of the Activating Signal Cointegrator 1 Complex Are Associated with Prenatal Spinal Muscular Atrophy and Congenital Bone Fractures

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    Transcriptional signal cointegrators associate with transcription factors or nuclear receptors and coregulate tissue-specific gene transcription. We report on recessive loss-of-function mutations in two genes (TRIP4 and ASCC1) that encode subunits of the nuclear activating signal cointegrator 1 (ASC-1) complex. We used autozygosity mapping and whole-exome sequencing to search for pathogenic mutations in four families. Affected individuals presented with prenatal-onset spinal muscular atrophy (SMA), multiple congenital contractures (arthrogryposis multiplex congenita), respiratory distress, and congenital bone fractures. We identified homozygous and compound-heterozygous nonsense and frameshift TRIP4 and ASCC1 mutations that led to a truncation or the entire absence of the respective proteins and cosegregated with the disease phenotype. Trip4 and Ascc1 have identical expression patterns in 17.5-day-old mouse embryos with high expression levels in the spinal cord, brain, paraspinal ganglia, thyroid, and submandibular glands. Antisense morpholino-mediated knockdown of either trip4 or ascc1 in zebrafish disrupted the highly patterned and coordinated process of α-motoneuron outgrowth and formation of myotomes and neuromuscular junctions and led to a swimming defect in the larvae. Immunoprecipitation of the ASC-1 complex consistently copurified cysteine and glycine rich protein 1 (CSRP1), a transcriptional cofactor, which is known to be involved in spinal cord regeneration upon injury in adult zebrafish. ASCC1 mutant fibroblasts downregulated genes associated with neurogenesis, neuronal migration, and pathfinding (SERPINF1, DAB1, SEMA3D, SEMA3A), as well as with bone development (TNFRSF11B, RASSF2, STC1). Our findings indicate that the dysfunction of a transcriptional coactivator complex can result in a clinical syndrome affecting the neuromuscular system

    Разработка технических средств и технологий гравийной обсыпки прифильтровой зоны нефтяных скважин

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    Борьба с пескопроявлениями в скважинах – процесс, который может потребовать достаточно больших затрат времени и финансов, однако он необходим для правильного функционирования оборудования. Можно выделить два возможных направления решения проблемы: технологические и механические. Технологические методы основаны на изучении механических свойств породы пласта в начальных условиях и их изменений при нарушении равновесного состояния термогидродинамической системы. Механические методы являются наиболее простыми и доступными, поэтому получили наибольшее распространение. К ним относится оборудование нефтяных скважин противопесочными фильтрами различной конструкции.Sand production is undesirable during production of hydrocarbon as it can cause many different problems both topside and downhole. There are several methods available in the industry today to control sand production. In general, sand control methods can be categorized as either mechanical or chemical. The mechanical means hinders formation sand using down-hole filters such as liners, screens or gravel packs

    Grid-Adapted FUN3D Computations for the Second High Lift Prediction Workshop

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    Contributions of the unstructured Reynolds-averaged Navier-Stokes code FUN3D to the 2nd AIAA CFD High Lift Prediction Workshop are described, and detailed comparisons are made with experimental data. Using workshop-supplied grids, results for the clean wing configuration are compared with results from the structured code CFL3D Using the same turbulence model, both codes compare reasonably well in terms of total forces and moments, and the maximum lift is similarly over-predicted for both codes compared to experiment. By including more representative geometry features such as slat and flap brackets and slat pressure tube bundles, FUN3D captures the general effects of the Reynolds number variation, but under-predicts maximum lift on workshop-supplied grids in comparison with the experimental data, due to excessive separation. However, when output-based, off-body grid adaptation in FUN3D is employed, results improve considerably. In particular, when the geometry includes both brackets and the pressure tube bundles, grid adaptation results in a more accurate prediction of lift near stall in comparison with the wind-tunnel data. Furthermore, a rotation-corrected turbulence model shows improved pressure predictions on the outboard span when using adapted grids

    Incidence rates of progressive childhood encephalopathy in Oslo, Norway: a population based study

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    <p>Abstract</p> <p>Background</p> <p>Progressive encephalopathy (PE) in children is a heterogeneous group of diseases mainly composed of metabolic diseases, but it consists also of neurodegenerative disorders where neither metabolic nor other causes are found. We wanted to estimate the incidence rate and aetiology of PE, as well as the age of onset of the disease.</p> <p>Methods</p> <p>We included PE cases born between 1985 and 2003, living in Oslo, and registered the number presenting annually between 1985 and 2004. Person-years at risk between 0 and 15 years were based on the number of live births during the observation period which was divided into four 5-year intervals. We calculated incidence rates according to age at onset which was classified as neonatal (0–4 weeks), infantile (1–12 months), late infantile (1–5 years), and juvenile (6–12 years).</p> <p>Results</p> <p>We found 84 PE cases representing 28 diagnoses among 1,305,997 person years, giving an incidence rate of 6.43 per 100,000 person years. The age-specific incidence rates per 100,000 were: 79.89 (<1 year), 8.64 (1–2 years), 1.90 (2–5 years), and 0.65 (>5 years). 66% (55/84) of the cases were metabolic, 32% (27/54) were neurodegenerative, and 2% (2/84) had HIV encephalopathy. 71% (60/84) of the cases presented at < 1 year, 24% (20/84) were late infantile presentations, and 5% (4/84) were juvenile presentations. Neonatal onset was more common in the metabolic (46%) (25/55) compared to the neurodegenerative group (7%) (2/27). 20% (17/84) of all cases were classified as unspecified neurodegenerative disease.</p> <p>Conclusion</p> <p>The overall incidence rate of PE was 6.43 per 100,000 person years. There was a strong reduction in incidence rates with increasing age. Two-thirds of the cases were metabolic, of which almost half presented in the neonatal period.</p

    Genetic and expression studies of SMN2 gene in Russian patients with spinal muscular atrophy type II and III

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    <p>Abstract</p> <p>Background</p> <p>Spinal muscular atrophy (SMA type I, II and III) is an autosomal recessive neuromuscular disorder caused by mutations in the survival motor neuron gene (<it>SMN1</it>). <it>SMN2 </it>is a centromeric copy gene that has been characterized as a major modifier of SMA severity. SMA type I patients have one or two <it>SMN2 </it>copies while most SMA type II patients carry three <it>SMN2 </it>copies and SMA III patients have three or four <it>SMN2 </it>copies. The <it>SMN1 </it>gene produces a full-length transcript (FL-SMN) while <it>SMN2 </it>is only able to produce a small portion of the FL-SMN because of a splice mutation which results in the production of abnormal SMNΔ7 mRNA.</p> <p>Methods</p> <p>In this study we performed quantification of the <it>SMN2 </it>gene copy number in Russian patients affected by SMA type II and III (42 and 19 patients, respectively) by means of real-time PCR. Moreover, we present two families consisting of asymptomatic carriers of a homozygous absence of the <it>SMN1 </it>gene. We also developed a novel RT-qPCR-based assay to determine the FL-SMN/SMNΔ7 mRNA ratio as SMA biomarker.</p> <p>Results</p> <p>Comparison of the <it>SMN2 </it>copy number and clinical features revealed a significant correlation between mild clinical phenotype (SMA type III) and presence of four copies of the <it>SMN2 </it>gene. In both asymptomatic cases we found an increased number of <it>SMN2 </it>copies in the healthy carriers and a biallelic <it>SMN1 </it>absence. Furthermore, the novel assay revealed a difference between SMA patients and healthy controls.</p> <p>Conclusions</p> <p>We suggest that the <it>SMN2 </it>gene copy quantification in SMA patients could be used as a prognostic tool for discrimination between the SMA type II and SMA type III diagnoses, whereas the FL-SMN/SMNΔ7 mRNA ratio could be a useful biomarker for detecting changes during SMA pharmacotherapy.</p
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