Las historias de vida en la formación inicial del profesorado de educación física

En este trabajo se plantea la utilización de las ¿Historias de Vida¿ en la Formación del Profesorado de Educación Física como punto de partida en el desarrollo de procesos de formación del profesorado reflexivos y críticos. En un primer apartado realizamos una revisión sobre el estado de la cuestión a partir de los trabajos realizados en nuestro área curricular. En un segundo apartado explicamos como las historias de vida sirven como técnica de introspección y toma de conciencia de sus creencias y planteamientos sobre Educación Física Escolar. En este sentido la utilización de historias de vida en la Formación Inicial del Profesorado de Educación Física es extraordinariamente interesante como punto de partida a la hora de comprender mejor el sentido de las diferentes asignaturas y la necesidad de ir elaborando sus propios modelos como profesores de Educación Física

A Physically-Based Fractional Diffusion Model for Semi-Dilute Suspensions of Rods in a Newtonian Fluid

[EN] The rheological behaviour of suspensions involving interacting (functionalized) rods remains nowadays incompletely understood, in particular with regard to the evolution of the elastic modulus with the applied frequency in small-amplitude oscillatory flows. In a previous work, we addressed this issue by assuming a fractional diffusion mechanism, however the approach followed was purely phenomenological. The present work revisits the topic from a phys ical viewpoint, with the aim of justifying the fractional nature of diffusion. After accomplishing this first objective, we explore by means of numerical ex periments the consequences of the proposed fractional modelling approach in linear and non-linear rheology.Nadal, E.; Aguado-López, JV.; Abisset-Chavanne, E.; Chinesta Soria, FJ.; Keunings, R.; Cueto, E. (2017). A Physically-Based Fractional Diffusion Model for Semi-Dilute Suspensions of Rods in a Newtonian Fluid. Applied Mathematical Modelling. 51:58-67. https://doi.org/10.1016/j.apm.2017.06.009S58675

Redox and Catalytic Properties of Promoted NiO Catalysts for the Oxidative Dehydrogenation of Ethane

[EN] NiO and metal-promoted NiO catalysts (M-NiO, with a M/(M+Ni) atomic ratio of 0.08, with M = Nb, Sn, or La) have been prepared, tested in the oxidative dehydrogenation (ODH) of ethane, and characterized by means of XRD, TPR, HRTEM, Raman, XPS, and in situ XAS (using H-2/He, air or C2H6/He mixtures). The selectivity to ethylene during the ODH of ethane decreases according to the following trend: Nb NiO Sn NiO > La NiO > NiO, whereas the catalyst reducibility (determined by both TPR and XAS using H-2/He mixtures) shows the opposite trend. However, different reducibility and catalytic behavior in the absence of oxygen (ethane/He mixtures) have been observed, especially when comparing Nb- and Sn-promoted NiO samples. These differences can be ascribed mainly to a different phase distribution of the promoter. The results presented here are discussed in terms of the nature of active and selective sites for ODH of ethane in selective and unselective catalysts, but also the role of promoters and the importance of their phase distribution.The authors would like to acknowledge the DGICYT in Spain CTQ2012-37925-C03-2, CTQ2015-68951-C3-1-R, and CTQ2015-68951-C3-3-R. Authors thank European Synchrotron Radiation Facility, ESRF (Project CH-4512; BM25-SpLine Beamlime). Authors from ITQ also thank Project SEV-2016-0683 for financial support. D.D. thanks MINECO and Severo Ochoa Excellence Program for his fellowship (SVP-2014-068669). B.S. also thanks UV-INV-AE16-484416. Finally, the authors thank the Electron Microscopy Service of Universitat Politecnica de Valencia for their support.Delgado-Muñoz, D.; Solsona Espriu, BE.; Ykrelef, A.; Rodriguez-Gomez, A.; Caballero, A.; Rodríguez-Aguado, E.; Rodriguez-Castellón, E.... (2017). Redox and Catalytic Properties of Promoted NiO Catalysts for the Oxidative Dehydrogenation of Ethane. The Journal of Physical Chemistry C. 121(45):25132-25142. https://doi.org/10.1021/acs.jpcc.7b07066S25132251421214

Genome-wide association study of treatment-related toxicity two years following radiotherapy for breast cancer

Càncer de mama; Toxicitat crònica; RadiogenòmicaBreast cancer; Chronic toxicity; RadiogenomicsCáncer de mama; Toxicidad crónica; RadiogenómicaBackground and purpose Up to a quarter of breast cancer patients treated by surgery and radiotherapy experience clinically significant toxicity. If patients at high risk of adverse effects could be identified at diagnosis, their treatment could be tailored accordingly. This study was designed to identify common single nucleotide polymorphisms (SNPs) associated with toxicity two years following whole breast radiotherapy. Materials and Methods A genome-wide association study (GWAS) was performed in 1,640 breast cancer patients with complete SNP, clinical, treatment and toxicity data, recruited across 18 European and US centres into the prospective REQUITE cohort study. Toxicity data (CTCAE v4.0) were collected at baseline, end of radiotherapy, and annual follow-up. A total of 7,097,340 SNPs were tested for association with the residuals of toxicity endpoints, adjusted for clinical, treatment co-variates and population substructure. Results Quantile-quantile plots showed more associations with toxicity above the p < 5 × 10-5 level than expected by chance. Eight SNPs reached genome-wide significance. Nipple retraction grade ≥ 2 was associated with the rs188287402 variant (p = 2.80 × 10-8), breast oedema grade ≥ 2 with rs12657177 (p = 1.12 × 10-10), rs75912034 (p = 1.12 × 10-10), rs145328458 (p = 1.06 × 10-9) and rs61966612 (p = 1.23 × 10-9), induration grade ≥ 2 with rs77311050 (p = 2.54 × 10-8) and rs34063419 (p = 1.21 × 10-8), and arm lymphoedema grade ≥ 1 with rs643644 (p = 3.54 × 10-8). Heritability estimates across significant endpoints ranged from 25% to 39%. Our study did not replicate previously reported SNPs associated with breast radiation toxicity at the pre-specified significance level. Conclusions This GWAS for long-term breast radiation toxicity provides further evidence for significant association of common SNPs with distinct toxicity endpoints.REQUITE received funding from the European Union's Seventh Framework Programme for research, technological development, and demonstration under grant agreement no. 601826. We thank all patients who participated in the REQUITE study and all the *members of the REQUITE project consortium in: Belgium: Ghent University Hospital; KU Leuven. France: ICM Montpellier, CHU Nîmes (Department of Radiation Oncology, CHU Nîmes, Nîmes, France). Germany: Zentrum für Strahlentherapie Freiburg (Dr. Petra Stegmaier); Städtisches Klinikum Karlsruhe (Dr. Bernhard Neu); ViDia Christliche Kliniken Karlsruhe (Prof. Johannes Claßen); Klinikum der Stadt Ludwigshafen GmbH (PD Dr. Thomas Schnabel); Universitätsklinikum Mannheim: Anette Kipke, Stefanie Kolb, Anke Keller and Christiane Zimmermann; Strahlentherapie Speyer (Dr. Jörg Schäfer). The researchers at DKFZ also thank Anusha Müller, Irmgard Helmbold, Thomas Heger, and Sabine Behrens. Petra Seibold was supported by ERA PerMed JCT2018 funding (ERAPERMED2018-244, BMBF #01KU1912) and BfS funding (#3619S42261). Italy: Fondazione IRCCS Istituto Nazionale dei Tumori, Milano; Candiolo Cancer Institute – FPO, IRCCS. Tiziana Rancati was partially funded by Fondazione Italo Monzino. Spain: Barcelona: Vall d'Hebron Hospital Universitari, Vall d'Hebron Barcelona Hospital Campus; VHIO acknowledge the Cellex Foundation for providing research facilities and the CERCA Programme/Generalitat de Catalunya for institutional support. Sara Gutiérrez-Enríquez is supported by ERAPerMed JTC2018 funding (ERAPERMED2018-244 and SLT011/18/00005) and the Government of Catalonia (2021SGR01112). Santiago: Complexo Hospitalario Universitario de Santiago. Ana Vega is supported by Spanish Instituto de Salud Carlos III (ISCIII) funding, an initiative of the Spanish Ministry of Economy and Innovation partially supported by European Regional Development FEDER Funds (PI22/00589, PI19/01424, PI16/00046, PI13/ 02030, PI10/00164; INT20/00071, INT17/00133, INT16/00154, INT15/00070), through the Autonomous Government of Galicia (Consolidation and structuring program: IN607B), by ERAPerMed JTC2018 funding (ERAPERMED2018-244) and by the AECC (PRYES211091VEGA). UK: University Hospitals of Leicester NHS Trust: Theresa Beaver, Sara Barrows, Monika Kaushik, Frances Kenny, Jaroslaw Krupa, Kelly V Lambert, Simon M Pilgrim, Sheila Shokuhi, Kalliope Valassidou, Kiran Kancherla, Kufre Sampson, Ahmed Osman and Kaitlin Walker. Harkeran K Jandu is supported by the Wellcome Trust Genetic Epidemiology and Public Health Genomics Doctoral Training Partnership (Grant Number: 218505/Z/19/Z). Tim Rattay was funded by a National Institute of Health Research (NIHR) Clinical Lectureship (CL 2017-11-002). He was previously funded by an NIHR Doctoral Research Fellowship (DRF 2014-07-079). This publication presents independent research funded by the NIHR. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. University of Manchester: Catharine West and Rebecca Elliott are supported by the NIHR Manchester Biomedical Research Centre and Catharine West is supported by Cancer Research UK (C1094/A18504, C147/A25254). USA: Mount Sinai Hospital, New York

Picasso’s 1917 paint materials and their influence on the condition of four paintings

This work aims to investigate the correlation between the painting materials used by Picasso to create four artworks in Barcelona in 1917 and their actual conditions. Specifically, a range of crack types and patterns was observed in the painted layers. The paintings, kept together in Picasso’s family house until they were donated to the Museu Picasso in 1970, had significant differences in their condition, even though they present several similarities in the choice of materials, technique and in their conservation history. A multi-analytical approach was adopted to characterise the painted layers by X-ray fluorescence spectroscopy, fibre optic reflectance spectroscopy in the 350–2200 nm range, gas chromatography-mass spectrometry, and Fourier transform infrared spectroscopy. The obtained results have been combined with those from a previous analytical campaign focused on the study of grounds and canvases of these four paintings and with visual examination of the cracks to establish hypotheses about the differences in degradation. This combined overview of non-invasive documentation techniques, chemical analysis and observations of the mechanical damage has provided an insight into the possible contribution each layer could have played in the damage observed in the four canvas paintings

Treatment time and circadian genotype interact to influence radiotherapy side-effects. A prospective European validation study using the REQUITE cohort

Breast cancer; Circadian rhythm; RadiotherapyCáncer de mama; Ritmo circadiano; RadioterapiaCàncer de mama; Ritme circadià; RadioteràpiaBackground Circadian rhythm impacts broad biological processes, including response to cancer treatment. Evidence conflicts on whether treatment time affects risk of radiotherapy side-effects, likely because of differing time analyses and target tissues. We previously showed interactive effects of time and genotypes of circadian genes on late toxicity after breast radiotherapy and aimed to validate those results in a multi-centre cohort. Methods Clinical and genotype data from 1690 REQUITE breast cancer patients were used with erythema (acute; n=340) and breast atrophy (two years post-radiotherapy; n=514) as primary endpoints. Local datetimes per fraction were converted into solar times as predictors. Genetic chronotype markers were included in logistic regressions to identify primary endpoint predictors. Findings Significant predictors for erythema included BMI, radiation dose and PER3 genotype (OR 1.27(95%CI 1.03-1.56); P < 0.03). Effect of treatment time effect on acute toxicity was inconclusive, with no interaction between time and genotype. For late toxicity (breast atrophy), predictors included BMI, radiation dose, surgery type, treatment time and SNPs in CLOCK (OR 0.62 (95%CI 0.4-0.9); P < 0.01), PER3 (OR 0.65 (95%CI 0.44-0.97); P < 0.04) and RASD1 (OR 0.56 (95%CI 0.35-0.89); P < 0.02). There was a statistically significant interaction between time and genotypes of circadian rhythm genes (CLOCK OR 1.13 (95%CI 1.03-1.23), P < 0.01; PER3 OR 1.1 (95%CI 1.01-1.2), P < 0.04; RASD1 OR 1.15 (95%CI 1.04-1.28), P < 0.008), with peak time for toxicity determined by genotype. Interpretation Late atrophy can be mitigated by selecting optimal treatment time according to circadian genotypes (e.g. treat PER3 rs2087947C/C genotypes in mornings; T/T in afternoons). We predict triple-homozygous patients (14%) reduce chance of atrophy from 70% to 33% by treating in mornings as opposed to mid-afternoon. Future clinical trials could stratify patients treated at optimal times compared to those scheduled normally.EU-FP7

(Pre)treatment risk factors for late fatigue and fatigue trajectories following radiotherapy for breast cancer

Breast cancer; Fatigue; RadiotherapyCáncer de mama; Fatiga; RadioterapiaCàncer de mama; Fatiga; RadioteràpiaFatigue is common in breast-cancer survivors. Our study assessed fatigue longitudinally in breast cancer patients receiving adjuvant radiotherapy (RT) and aimed to identify risk factors associated with long-term fatigue and underlying fatigue trajectories. Fatigue was measured in a prospective multicenter cohort (REQUITE) using the Multidimensional Fatigue Inventory (MFI-20) and analyzed using mixed models. Multivariable logistic models identified factors associated with fatigue dimensions at 2 years post-RT and latent class growth analysis identified individual fatigue trajectories. A total of 1443, 1302, 1203 and 1098 patients completed the MFI-20 at baseline, end of RT, after 1 and 2 years. Overall, levels of fatigue significantly increased from baseline to end of RT for all fatigue dimensions (P < .05) and returned to baseline levels after 2 years. A quarter of patients were assigned to latent trajectory high (23.7%) and moderate (24.8%) fatigue classes, while 46.3% and 5.2% to the low and decreasing fatigue classes, respectively. Factors associated with multiple fatigue dimensions at 2 years include age, BMI, global health status, insomnia, pain, dyspnea and depression. Fatigue present at baseline was consistently associated with all five MFI-20 fatigue dimensions (ORGeneralFatigue = 3.81, P < .001). From latent trajectory analysis, patients with a combination of factors such as pain, insomnia, depression, younger age and endocrine therapy had a particularly high risk of developing early and persistent high fatigue years after treatment. Our results confirmed the multidimensional nature of fatigue and will help clinicians identify breast cancer patients at higher risk of having persistent/late fatigue so that tailored interventions can be delivered.We thank all patients who participated in the REQUITE study and all the REQUITE staff involved in this project. Belgium: Ghent University Hospital; KU Leuven. France: ICM Montpellier, CHU Nîmes (Department of Radiation Oncology, CHU Nîmes, Nîmes, France). Germany: Zentrum für Strahlentherapie Freiburg (Dr. Petra Stegmaier); Städtisches Klinikum Karlsruhe (Dr. Bernhard Neu); ViDia Christliche Kliniken Karlsruhe (Prof. Johannes Claßen); Klinikum der Stadt Ludwigshafen GmbH (PD Dr. Thomas Schnabel); Universitätsklinikum Mannheim: Anette Kipke and Christiane Zimmermann; Strahlentherapie Speyer (Dr. Jörg Schäfer). The researchers at DKFZ also thank Anusha Müller, Irmgard Helmbold, Thomas Heger, Sabine Behrens, Axel Benner, Nicholas Schreck. Petra Seibold is supported by ERA PerMed 2018 funding (BMBF #01KU1912) and BfS funding (#3619S42261). Italy: Fondazione IRCCS Istituto Nazionale dei Tumori, Milano; Candiolo Cancer Institute – FPO, IRCCS. Tiziana Rancati was partially funded by Fondazione Italo Monzino. The Netherlands: Sylvie Canisius at Maastro Clinics, Maastricht. Spain: Barcelona: Vall d'Hebron Hospital Universitari, Vall d'Hebron Barcelona Hospital Campus; VHIO acknowledge the Cellex Foundation for providing research facilities and thank CERCA Programme/Generalitat de Catalunya for institutional support. Sara Gutiérrez-Enríquez is supported by ERAPerMed JTC2018 funding (ERAPERMED2018-244 and SLT011/18/00005). Santiago: Complexo Hospitalario Universitario de Santiago. Ana Vega: supported by Spanish Instituto de Salud Carlos III (ISCIII) funding, an initiative of the Spanish Ministry of Economy and Innovation partially supported by European Regional Development FEDER Funds (PI22/00589, PI19/01424; INT20/00071); the ERAPerMed JTC2018 funding (AC18/00117); the Autonomous Government of Galicia (Consolidation and structuring program: IN607B), by the Fundación Mutua Madrileña (call 2018) and by the AECC (PRYES211091VEGA); UK: University Hospitals of Leicester NHS Trust; Theresa Beaver, Kaitlin Walker and Sara Barrows. Dr Tim Rattay was funded by a National Institute of Health Research (NIHR) Clinical Lectureship (CL 2017-11-002) and is currently supported by the NIHR Leicester Biomedical Research Centre. He was previously funded by a National Institute of Health Research (NIHR) Doctoral Research Fellowship (DRF 2014-07-079). This publication presents independent research funded by the NIHR. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Manchester: Catharine West and Rebecca Elliott are supported by NIHR Manchester Biomedical Research Centre and Catharine West is supported by Cancer Research UK (C1094/A18504, C147/A25254). USA: Mount Sinai Hospital, New York. Open Access funding enabled and organized by Projekt DEAL

Ab Initio Calculation of the Lattice Distortions induced by Substitutional Ag- and Cu- Impurities in Alkali Halide Crystals

An ab initio study of the doping of alkali halide crystals (AX: A = Li, Na, K, Rb; X = F, Cl, Br, I) by ns2 anions (Ag- and Cu-) is presented. Large active clusters with 179 ions embedded in the surrounding crystalline lattice are considered in order to describe properly the lattice relaxation induced by the introduction of substitutional impurities. In all the cases considered, the lattice distortions imply the concerted movement of several shells of neighbors. The shell displacements are smaller for the smaller anion Cu-, as expected. The study of the family of rock-salt alkali halides (excepting CsF) allows us to extract trends that might be useful at a predictive level in the study of other impurity systems. Those trends are presented and discussed in terms of simple geometric arguments.Comment: LaTeX file. 8 pages, 3 EPS pictures. New version contains calculations of the energy of formation of the defects with model clusters of different size

Large-scale meta-genome-wide association study reveals common genetic factors linked to radiation-induced acute toxicities across cancer types

Meta-genome; Toxicities; CancerMetagenoma; Toxicidades; CáncerMetagenoma; Toxicitats; CàncerBackground This study was designed to identify common genetic susceptibility and shared genetic variants associated with acute radiation-induced toxicity across 4 cancer types (prostate, head and neck, breast, and lung). Methods A genome-wide association study meta-analysis was performed using 19 cohorts totaling 12 042 patients. Acute standardized total average toxicity (STATacute) was modelled using a generalized linear regression model for additive effect of genetic variants, adjusted for demographic and clinical covariates (rSTATacute). Linkage disequilibrium score regression estimated shared single-nucleotide variation (SNV—formerly SNP)–based heritability of rSTATacute in all patients and for each cancer type. Results Shared SNV-based heritability of STATacute among all cancer types was estimated at 10% (SE = 0.02) and was higher for prostate (17%, SE = 0.07), head and neck (27%, SE = 0.09), and breast (16%, SE = 0.09) cancers. We identified 130 suggestive associated SNVs with rSTATacute (5.0 × 10‒8 < P < 1.0 × 10‒5) across 25 genomic regions. rs142667902 showed the strongest association (effect allele A; effect size ‒0.17; P = 1.7 × 10‒7), which is located near DPPA4, encoding a protein involved in pluripotency in stem cells, which are essential for repair of radiation-induced tissue injury. Gene-set enrichment analysis identified ‘RNA splicing via endonucleolytic cleavage and ligation’ (P = 5.1 × 10‒6, P = .079 corrected) as the top gene set associated with rSTATacute among all patients. In silico gene expression analysis showed that the genes associated with rSTATacute were statistically significantly up-regulated in skin (not sun exposed P = .004 corrected; sun exposed P = .026 corrected). Conclusions There is shared SNV-based heritability for acute radiation-induced toxicity across and within individual cancer sites. Future meta–genome-wide association studies among large radiation therapy patient cohorts are worthwhile to identify the common causal variants for acute radiotoxicity across cancer types.E.N. was supported by a scholarship for a PhD from the University of Groningen, Groningen, The Netherlands. T.D. is funded as an Academic Clinical Fellow by the National Institute for Health Research, UK. D.J.T. is supported by a grant from The Taylor Family Foundation and Cancer Research UK [C19941/A30286]. M.L.K.C. is supported by the National Medical Research Council Singapore Clinician Scientist Award (NMRC/CSA-INV/0027/2018), National Research Foundation Proton Competitive Research Program (NRF-CRP17-2017-05), Ministry of Education Tier 3 Academic Research Fund (MOE2016-T3-1-004), the Duke-NUS Oncology Academic Program Goh Foundation Proton Research Programme, NCCS Cancer Fund, and the Kua Hong Pak Head and Neck Cancer Research Programme. G.C.B. is supported by Cancer research UK RadNet Cambridge [C17918/A28870]. RADIOGEN research was supported by Spanish Instituto de Salud Carlos III (ISCIII) funding, an initiative of the Spanish Ministry of Economy and Innovation partially supported by European Regional Development FEDER Funds (INT20/00071, INT15/00070, INT17/00133, INT16/00154; PI19/01424; PI16/00046; PI13/02030; PI10/00164); by AECC grant PRYES211091VEGA and through the Autonomous Government of Galicia (Consolidation and structuring program: IN607B). C.N.A. and L.M.H.S. received funding from the Danish Cancer Society (grant R231-A14074-B2537). T.R. was funded by a National Institutes of Health Research (NIHR) Clinical Lectureship (CL 2017-11-002) and is supported by the NIHR Leicester Biomedical Research Centre. This publication presents independent research funded by the NIHR. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. REQUITE received funding from the European Union’s Seventh Framework Programme for research, technological development, and demonstration under grant agreement No. 601826. S.G.E. is supported by the government of Catalonia 2021SGR01112. L.D. was supported by the European Union Horizon 2020 research and innovation programs BRIDGES (grant No. 634935)