Physics demos for all UVEG degrees: a unique project in Spain

The Physics Demo Project at the University of Valencia (www.uv.es/fisicademos) has developed a collection of physics demonstrations to be used during lectures. It consists of more than 130 experimental demos about different physics topics. More than 30 professors borrow them whenever they lecture on physics in any of our 40 courses in 17 different science or technical degrees, involving 246 ECTS and more than 3500 students. Each demo kit with a simple experimental set displays a particular physics phenomenon. An on-line user guide highlights the main physics principles involved, instructions on how to use it and advices of how to link it to the theoretical concepts or to technical applications. Demo lectures (and collections) are a usual and widespread practice in many countries but not in Spain. This unique initiative aims at the recovery of this practice by involving a growing collaborative team of users and with the aid of educational innovation projects. Here we explain the project content, organization and recent developments. Our experience, together with the positive students comments, allows us to draw the following conclusions: demos introduce the real sensible world in the lecture hall, providing the necessary link between concepts and everyday life, and becoming, again, something more than "chalk and talk"

Dopaminergic control of ADAMTS2 expression through cAMP/CREB and ERK: molecular effects of antipsychotics

© The Author(s) 2019.A better understanding of the molecular mechanisms that participate in the development and clinical manifestations of schizophrenia can lead to improve our ability to diagnose and treat this disease. Previous data strongly associated the levels of deregulated ADAMTS2 expression in peripheral blood mononuclear cells (PBMCs) from patients at first episode of psychosis (up) as well as in clinical responders to treatment with antipsychotic drugs (down). In this current work, we performed an independent validation of such data and studied the mechanisms implicated in the control of ADAMTS2 gene expression. Using a new cohort of drug-naïve schizophrenia patients with clinical follow-up, we confirmed that the expression of ADAMTS2 was highly upregulated in PBMCs at the onset (drug-naïve patients) and downregulated, in clinical responders, after treatment with antipsychotics. Mechanistically, ADAMTS2 expression was activated by dopaminergic signalling (D1-class receptors) and downstream by cAMP/CREB and mitogen-activated protein kinase (MAPK)/ERK signalling. Incubation with antipsychotic drugs and selective PKA and MEK inhibitors abrogated D1-mediated activation of ADAMTS2 in neuronal-like cells. Thus, D1 receptors signalling towards CREB activation might participate in the onset and clinical responses to therapy in schizophrenia patients, by controlling ADAMTS2 expression and activity. The unbiased investigation of molecular mechanisms triggered by antipsychotic drugs may provide a new landscape of novel targets potentially associated with clinical efficacy.This work was supported by: SAF2016-76046-R and SAF2013-46292-R (MINECO and FEDER) to B.C.F., PI16/00156 (isciii and FEDER) to J.P.V., LUCHAMOS POR LA VIDA project to F.R.J. and J.P.V., SAF2017-83702-R (MINECO and FEDER), Red TERCEL RD12/0019/0024 (ISCIII) and GVA-PROMETEO 2018/041 (Generalitat Valenciana) to S.M. J.P.V. is supported by the RyC research programme (RYC-2013-14097) and F.R.J. by the predoctoral research programme (BES-2014-070615), from MINECO and FEDER

Seguimiento de las guías españolas para el manejo del asma por el médico de atención primaria: un estudio observacional ambispectivo

Objetivo Evaluar el grado de seguimiento de las recomendaciones de las versiones de la Guía española para el manejo del asma (GEMA 2009 y 2015) y su repercusión en el control de la enfermedad. Material y métodos Estudio observacional y ambispectivo realizado entre septiembre del 2015 y abril del 2016, en el que participaron 314 médicos de atención primaria y 2.864 pacientes. Resultados Utilizando datos retrospectivos, 81 de los 314 médicos (25, 8% [IC del 95%, 21, 3 a 30, 9]) comunicaron seguir las recomendaciones de la GEMA 2009. Al inicio del estudio, 88 de los 314 médicos (28, 0% [IC del 95%, 23, 4 a 33, 2]) seguían las recomendaciones de la GEMA 2015. El tener un asma mal controlada (OR 0, 19, IC del 95%, 0, 13 a 0, 28) y presentar un asma persistente grave al inicio del estudio (OR 0, 20, IC del 95%, 0, 12 a 0, 34) se asociaron negativamente con tener un asma bien controlada al final del seguimiento. Por el contrario, el seguimiento de las recomendaciones de la GEMA 2015 se asoció de manera positiva con una mayor posibilidad de que el paciente tuviera un asma bien controlada al final del periodo de seguimiento (OR 1, 70, IC del 95%, 1, 40 a 2, 06). Conclusiones El escaso seguimiento de las guías clínicas para el manejo del asma constituye un problema común entre los médicos de atención primaria. Un seguimiento de estas guías se asocia con un control mejor del asma. Existe la necesidad de actuaciones que puedan mejorar el seguimiento por parte de los médicos de atención primaria de las guías para el manejo del asma. Objective: To assess the degree of compliance with the recommendations of the 2009 and 2015 versions of the Spanish guidelines for managing asthma (Guía Española para el Manejo del Asma [GEMA]) and the effect of this compliance on controlling the disease. Material and methods: We conducted an observational ambispective study between September 2015 and April 2016 in which 314 primary care physicians and 2864 patients participated. Results: Using retrospective data, we found that 81 of the 314 physicians (25.8%; 95% CI 21.3–30.9) stated that they complied with the GEMA2009 recommendations. At the start of the study, 88 of the 314 physicians (28.0%; 95% CI 23.4–33.2) complied with the GEMA2015 recommendations. Poorly controlled asthma (OR, 0.19; 95% CI 0.13–0.28) and persistent severe asthma at the start of the study (OR, 0.20; 95% CI 0.12–0.34) were negatively associated with having well-controlled asthma by the end of the follow-up. In contrast, compliance with the GEMA2015 recommendations was positively associated with a greater likelihood that the patient would have well-controlled asthma by the end of the follow-up (OR, 1.70; 95% CI 1.40–2.06). Conclusions: Low compliance with the clinical guidelines for managing asthma is a common problem among primary care physicians. Compliance with these guidelines is associated with better asthma control. Actions need to be taken to improve primary care physician compliance with the asthma management guidelines

Effects of ocular hypertension in the visual system of pigmented mice.

To study the effects of ocular hypertension (OHT) on the visual system of C57BL/6 pigmented mice, the limbal and episcleral veins of the left eye were laser photocoagulated (LP). LP increased the intraocular pressure during the first five days (d), reaching basal values at 7d. To investigate the effect of OHT on the retinal ganglion cell (RGC) retrograde axonal transport, hydroxistilbamidine methanesulfonate (OHSt) was applied to both superior colliculi (SCi) and the retinas were dissected 2 or 4 weeks after LP. To determine RGC survival, these same retinas were immunoreacted against Brn3a (general RGC population) and melanopsin (intrinsically photosensitive RGCs, m+RGCs). To study whether OHT affected non-RGC neurons in the ganglion cell layer (GCL), RGCs were immunodetected with Brn3a and all GCL nuclei counterstained with DAPI in a group of animals examined 4 weeks post-LP. Innervation of the SCi was examined at 10 days, 8 or 14 weeks after LP with the orthogradely transported cholera toxin subunit-B. OHT resulted in diffuse and sectorial loss of OHSt+RGCs (50% at 2 weeks and 62% at 4 weeks) and in a comparable loss of Brn3a+RGCs at the same time intervals. m+RGCs decreased to 59% at 2 weeks and to 46% at 4 weeks, such loss was diffuse, did not parallel the sectorial loss of the general RGC population and was more severe in the superior-temporal retina. In the GCL, cell loss is selective for RGCs and does not affect other non-RGC neurons. The retinotectal innervation appeared significantly reduced at 10 days (55.7%) and did not progress further up to 14 weeks (46.6%). Thus, LP-induced OHT results in retrograde degeneration of RGCs and m+RGCs, as well as in the loss of CTB-labelled retinotectal terminals

Intraocular pressure values.

<p><b>A</b>: Graph showing the temporal course of IOP from 24h till 14 weeks after laser photocoagulation (LP). In the left eye (LE) there is a significant increase of the IOP at 24h, 48h and 5 days compared to the contralateral right eye (RE) and to prelaser (PRE) values. IOP values are back to normal from 1 week to 14 weeks, the latest time analyzed. In <b>B</b> are shown the IOP values during the first week post-LP measured at shorter intervals. One hour after LP, IOP has already increased significantly in the left eye. n = number of animals analyzed.</p

Correlation analysis.

<p>Correlation between the number of Brn3a⁺RGCs vs OHSt⁺RGCs (<b>A</b>) and mRGCs vs OHSt-RGCs (<b>B</b>) for each analyzed retina (open circles) at 2 and 4 weeks after OHT induction. The r² value for each regression line is shown at the bottom right of each graph.</p

Experimental design.

<p>Both retinas from each mouse were studied, the left treated ones, and their right contralateral to the lesion, which were used as control.</p><p>Experimental design.</p

Sectorial loss of RGCs after OHT.

<p>Distribution of traced- (A-F), Brn3a⁺ (A'-F') and melanopsin⁺ (A'',F'') RGCs at 2 (<b>A-C''</b>) and 4 weeks (<b>D-F''</b>) after the induction of ocular hypertension (OHT). Maps labelled with the same letter are from the same retina (<b>A-A''</b>, <b>B-B''</b> and so on). <b>A-F'</b>: isodensity maps. <b>A''-F''</b>: neighbour maps. Colour scale for isodensity maps in A goes from purple (0 RGCs/mm²) to red (≥4,800 RGCs/mm²), and for neighbour maps in A'' goes from purple (1–2 neighbours in a radius of 0.165 mm) to red (≥11 neighbours in the same radius). At the bottom of each map is shown the number of RGCs or mRGCs counted in its respective retina. S: superior, V: ventral, N: nasal, T: temporal. Bar scale in A: 500 μm.</p

Primary antibodies used in this work.

<p>Primary antibodies used in this work.</p