En sammenlignende undersøgelse af praktikforløb og færdighedstræning i tre videregående uddannelser

Praktikforløb i videregående uddannelser er blevet et politisk indsatsområde, og der er i sundhedsuddannelserne også et internationalt forskningsfokus på emnet. I denne artikel vil vi beskrive og sammenligne rammerne for praktikforløb og færdighedstræning på idræts-, læge- og sygeplejerskeuddannelsen. Artiklen tager afsæt i Heggens skelnen mellem begreberne professionsidentitet og professionel identitet. Den studerendes opfattelse af sig selv som professionsudøver må ud fra dette afsæt udvikles via tilegnelse af både en særlig videnskabelig funderet teoretisk viden, særlig praktisk ekspertise, samt en særlig etisk og social forpligtelse til at arbejde for medborgernes bedste. I den konkrete sammenligning af idræts-, læge- og syge-plejerskeuddannelserne konkluderes, at både færdighedstræning og praktik vægtes højt, men at både omfang, struktur, placering og læringsmål varierer betydeligt. Det må have væsensforskellige konsekvenser for de studerendes tilegnelse af viden, færdigheder og holdninger og dermed for deres professionelle identitetsudvikling. Vi kan ikke afgøre om professionsidentitetsforståelsen er årsag eller virkning, men der ser ud til at være et samspil mellem uddannelsernes undervisningsformer og professionsidentitet. In this paper we describe and compare workplace learning and skills training in medicine, nursing and sports science education. The paper builds on Heggen’s concepts concerning the identity of a profession versus a personal professional identity. Based on this, a student’s perception of herself as a professional develops from learning a particular scientific knowledge-base, a particular set of practical skills and a particular ethical and social obligation to work for the community. We concluded that all three educations studied attach great importance to workplace learning and skills training, but the extent, the structure, the timing and the learning outcomes differ considerably. This must have consequences for the students’ learning, their knowledge, skills and attitudes and for the development of their personal professional identity

Nanotitanium dioxide toxicity in mouse lung is reduced in sanding dust from paint

<p>Abstract</p> <p>Background</p> <p>Little is known of how the toxicity of nanoparticles is affected by the incorporation in complex matrices. We compared the toxic effects of the titanium dioxide nanoparticle UV-Titan L181 (NanoTiO₂), pure or embedded in a paint matrix. We also compared the effects of the same paint with and without NanoTiO₂.</p> <p>Methods</p> <p>Mice received a single intratracheal instillation of 18, 54 and 162 μg of NanoTiO₂or 54, 162 and 486 μg of the sanding dust from paint with and without NanoTiO₂. DNA damage in broncheoalveolar lavage cells and liver, lung inflammation and liver histology were evaluated 1, 3 and 28 days after intratracheal instillation. Printex 90 was included as positive control.</p> <p>Results</p> <p>There was no additive effect of adding NanoTiO₂to paints: Therefore the toxicity of NanoTiO₂was reduced by inclusion into a paint matrix. NanoTiO₂induced inflammation in mice with severity similar to Printex 90. The inflammatory response of NanoTiO₂and Printex 90 correlated with the instilled surface area. None of the materials, except of Printex 90, induced DNA damage in lung lining fluid cells. The highest dose of NanoTiO₂caused DNA damage in hepatic tissue 1 day after intratracheal instillation. Exposure of mice to the dust from paints with and without TiO₂was not associated with hepatic histopathological changes. Exposure to NanoTiO₂or to Printex 90 caused slight histopathological changes in the liver in some of the mice at different time points.</p> <p>Conclusions</p> <p>Pulmonary inflammation and DNA damage and hepatic histopathology were not changed in mice instilled with sanding dust from NanoTiO₂paint compared to paint without NanoTiO₂. However, pure NanoTiO₂caused greater inflammation than NanoTiO₂embedded in the paint matrix.</p

No Cytotoxicity or Genotoxicity of Graphene and Graphene Oxide in Murine Lung Epithelial FE1 Cells in Vitro

International audienceGraphene and graphene oxide receive much attention these years, because they add attractive properties to a wide range of applications and products. Several studies have shown toxicological effects of other carbon-based nanomaterials such as carbon black nanoparticles and carbon nanotubes in vitro and in vivo. Here, we report in-depth physicochemical characterization of three commercial graphene materials, one graphene oxide (GO) and two reduced graphene oxides (rGO) and assess cytotoxicity and genotoxicity in the murine lung epithelial cell line FE1. The studied GO and rGO mainly consisted of 2-3 graphene layers with lateral sizes of 1-2 mu m. GO had almost equimolar content of C, O, and H while the two rGO materials had lower contents of oxygen with C/O and C/H ratios of 8 and 12.8, respectively. All materials had low levels of endotoxin and low levels of inorganic impurities, which were mainly sulphur, manganese, and silicon. GO generated more ROS than the two rGO materials, but none of the graphene materials influenced cytotoxicity in terms of cell viability and cell proliferation after 24 hr. Furthermore, no genotoxicity was observed using the alkaline comet assay following 3 or 24 hr of exposure. We demonstrate that chemically pure, few-layered GO and rGO with comparable lateral size (> 1 mu m) do not induce significant cytotoxicity or genotoxicity in FE1 cells at relatively high doses (5-200 mu g/ml). Environ. Mol. Mutagen. 57:469-482, 2016. (c) 2016 The Authors. Environmental and Molecular Mutagenesis Published by Wiley Periodicals, Inc

Epoxy composite dusts with and without carbon nanotubes cause similar pulmonary responses, but differences in liver histology in mice following pulmonary deposition

Inorganic chemical composition given as elemental weight% measured by standardless WDXRF. The three epoxy materials were measured as solid disks (4 cm in diameter, 1 cm high). For comparison, the results for CNT powder, previously published in [25], were added to the figure. Displayed axis 99.7 – 100 %. (PPTX 71 kb

Effects of physicochemical properties of TiO2 nanomaterials for pulmonary inflammation, acute phase response and alveolar proteinosis in intratracheally exposed mice

Nanomaterial (NM) characteristics may affect the pulmonary toxicity and inflammatory response, including specific surface area, size, shape, crystal phase or other surface characteristics. Grouping of TiO2 in hazard assessment might be challenging because of variation in physicochemical properties. We exposed C57BL/6 J mice to a single dose of four anatase TiO2 NMs with various sizes and shapes by intratracheal instillation and assessed the pulmonary toxicity 1, 3, 28, 90 or 180 days post-exposure. The quartz DQ12 was included as benchmark particle. Pulmonary responses were evaluated by histopathology, electron microscopy, bronchoalveolar lavage (BAL) fluid cell composition and acute phase response. Genotoxicity was evaluated by DNA strand break levels in BAL cells, lung and liver in the comet assay. Multiple regression analyses were applied to identify specific TiO2 NMs properties important for the pulmonary inflammation and acute phase response. The TiO2 NMs induced similar inflammatory responses when surface area was used as dose metrics, although inflammatory and acute phase response was greatest and more persistent for the TiO2 tube. Similar histopathological changes were observed for the TiO2 tube and DQ12 including pulmonary alveolar proteinosis indicating profound effects related to the tube shape. Comparison with previously published data on rutile TiO2 NMs indicated that rutile TiO2 NMs were more inflammogenic in terms of neutrophil influx than anatase TiO2 NMs when normalized to total deposited surface area. Overall, the results suggest that specific surface area, crystal phase and shape of TiO2 NMs are important predictors for the observed pulmonary effects of TiO2 NMs.Peer reviewe

Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk

BACKGROUND: Particulate air pollution is associated with cardiovascular disease. Acute phase response is causally linked to cardiovascular disease. Here, we propose that particle-induced pulmonary acute phase response provides an underlying mechanism for particle-induced cardiovascular risk. METHODS: We analysed the mRNA expression of Serum Amyloid A (Saa3) in lung tissue from female C57BL/6J mice exposed to different particles including nanomaterials (carbon black and titanium dioxide nanoparticles, multi- and single walled carbon nanotubes), diesel exhaust particles and airborne dust collected at a biofuel plant. Mice were exposed to single or multiple doses of particles by inhalation or intratracheal instillation and pulmonary mRNA expression of Saa3 was determined at different time points of up to 4 weeks after exposure. Also hepatic mRNA expression of Saa3, SAA3 protein levels in broncheoalveolar lavage fluid and in plasma and high density lipoprotein levels in plasma were determined in mice exposed to multiwalled carbon nanotubes. RESULTS: Pulmonary exposure to particles strongly increased Saa3 mRNA levels in lung tissue and elevated SAA3 protein levels in broncheoalveolar lavage fluid and plasma, whereas hepatic Saa3 levels were much less affected. Pulmonary Saa3 expression correlated with the number of neutrophils in BAL across different dosing regimens, doses and time points. CONCLUSIONS: Pulmonary acute phase response may constitute a direct link between particle inhalation and risk of cardiovascular disease. We propose that the particle-induced pulmonary acute phase response may predict risk for cardiovascular disease