Clase magistral vs aprendizaje basado en problemas en una asignatura troncal

Hace cuatro años que en la asignatura troncal de Farmacologia I de la Licenciatura de Farmacia de la Universidad de Barcelona hemos introducido sesiones de Aprendizaje Basado en Problemas (ABP). En uno de estos ABPs dedicado a las tetraciclinas (antibióticos) hemos evaluado, mediante una encuesta, la aceptación por parte del alumno de esta estrategia docente, así como sus resultados (nota de test) vs una clase tradicional de un grupo farmacológico paralelo (antibióticos aminoglucósidos). Todos los grupos (media de 5 individuos por grupo) resolvieron correctamente el problema. A la pregunta “Te gusta más estudiar un grupo farmacológico mediante un ABP que con una clase tradicional” el 90,9% contestó que sí, aunque la mayoría de los alumnos añadieron el comentario de que preferirían una clase adicional complementaria. El 86,4 % reconoce que este sistema ha mejorado su capacidad de razonamiento. El 80% es partidario de sustituir alguna clase tradicional por un ABP. Cuando se realizó un test de 10 preguntas sobre aminoglucósidos explicado en una clase magistral durante la misma semana y otro test de 10 preguntas sobre tetraciclinas (objeto del ABP) las notas medias fueron de 4,4 ± 2,87 vs 8,0 ± 2,01 (p<0.001). Vemos pues que el aprendizaje ha sido correcto y mejor que en una clase tradicional, a pesar de la sensación de desestructuración que el alumno tiene.Eje: Educación universitaria: Experiencias educativasRed de Universidades con Carreras en Informática (RedUNCI

Elaboración de un entorno web para una asignatura optativa

El objetivo del trabajo ha sido el mejorar el rendimiento académico práctico y favorecer la autoformación en una asignatura optativa de la Licenciatura en Farmacia, la Farmacología Experimental. Para ello se han elaborado unos materiales en formato electrónico de apoyo a las clases teóricas y prácticas. Se ha creado un entorno virtual “html” denominado “Guía Digital de Prácticas” conteniendo: Información dividida en pequeñas unidades que supongan un trabajo de no más de 30 minutos; la inclusión de ejercicios en cada submenú y la posibilidad de autoevaluación. La integración del material de “e-learning” ha mejorado de forma notable el rendimiento de los alumnos más en las habilidades prácticas que en los conocimientos teóricosEje: Educación universitaria: Experiencias uso NTICRed de Universidades con Carreras en Informática (RedUNCI

Clase magistral vs aprendizaje basado en problemas en una asignatura troncal

Hace cuatro años que en la asignatura troncal de Farmacologia I de la Licenciatura de Farmacia de la Universidad de Barcelona hemos introducido sesiones de Aprendizaje Basado en Problemas (ABP). En uno de estos ABPs dedicado a las tetraciclinas (antibióticos) hemos evaluado, mediante una encuesta, la aceptación por parte del alumno de esta estrategia docente, así como sus resultados (nota de test) vs una clase tradicional de un grupo farmacológico paralelo (antibióticos aminoglucósidos). Todos los grupos (media de 5 individuos por grupo) resolvieron correctamente el problema. A la pregunta “Te gusta más estudiar un grupo farmacológico mediante un ABP que con una clase tradicional” el 90,9% contestó que sí, aunque la mayoría de los alumnos añadieron el comentario de que preferirían una clase adicional complementaria. El 86,4 % reconoce que este sistema ha mejorado su capacidad de razonamiento. El 80% es partidario de sustituir alguna clase tradicional por un ABP. Cuando se realizó un test de 10 preguntas sobre aminoglucósidos explicado en una clase magistral durante la misma semana y otro test de 10 preguntas sobre tetraciclinas (objeto del ABP) las notas medias fueron de 4,4 ± 2,87 vs 8,0 ± 2,01 (p<0.001). Vemos pues que el aprendizaje ha sido correcto y mejor que en una clase tradicional, a pesar de la sensación de desestructuración que el alumno tiene.Eje: Educación universitaria: Experiencias educativasRed de Universidades con Carreras en Informática (RedUNCI

Elaboración de un entorno web para una asignatura optativa

El objetivo del trabajo ha sido el mejorar el rendimiento académico práctico y favorecer la autoformación en una asignatura optativa de la Licenciatura en Farmacia, la Farmacología Experimental. Para ello se han elaborado unos materiales en formato electrónico de apoyo a las clases teóricas y prácticas. Se ha creado un entorno virtual “html” denominado “Guía Digital de Prácticas” conteniendo: Información dividida en pequeñas unidades que supongan un trabajo de no más de 30 minutos; la inclusión de ejercicios en cada submenú y la posibilidad de autoevaluación. La integración del material de “e-learning” ha mejorado de forma notable el rendimiento de los alumnos más en las habilidades prácticas que en los conocimientos teóricosEje: Educación universitaria: Experiencias uso NTICRed de Universidades con Carreras en Informática (RedUNCI

Sonogashira diversification of unprotected halotryptophans, halotryptophan containing tripeptides; and generation of a new to nature bromo-natural product and its diversification in water

The blending together of synthetic chemistry with natural product biosynthesis represents a potentially powerful approach to synthesis; to enable this, further synthetic tools and methodologies are needed. To this end, we have explored the first Sonogashira cross-coupling to halotryptophans in water. Broad reaction scope is demonstrated and we have explored the limits of the scope of the reaction. We have demonstrated this methodology to work excellently in the modification of model tripeptides. Furthermore, through precursor directed biosynthesis, we have generated for the first time a new to nature brominated natural product bromo-cystargamide, and demonstrated the applicability of our reaction conditions to modify this novel metabolite

Repeated administration of N-ethyl-pentedrone induces increased aggression and impairs social exploration after withdrawal in mice

N-ethyl-pentedrone (NEPD, 2-(ethylamino)-1-phenyl-1-pentanone) is one of the latest synthetic cathinone derivatives that emerged into the illicit drug market. This drug has psychostimulant properties and has been related with several intoxications and even fatalities. However, information about the consequences of its acute and repeated consumption is lacking. Thus, the aim of our study was to investigate the behavioral effects after both acute and repeated NEPD exposure as well as the neurochemical changes. Male OF1 mice were treated with an acute dose (1, 3 or 10 mg/kg, i.p.) or received repeated injections of these doses (twice/day, 5 days) of NEPD. Shortly after drug-exposure or during drug-withdrawal, anxiety-like behavior, aggressiveness, social interaction, depressive-like symptoms, body weight and temperature were assessed. Also, monoamine synthesis enzymes, levels of neurotransmitters and their precursors and main metabolites, as well as ΔFosB, were determined in striatum and prefrontal cortex from post-mortem tissue. Acute administration of NEPD induced anxiolytic effects and reduced social exploration whereas during withdrawal after repeated administration the anxiolytic effect had vanished, and the reduced social exploration was still present and accompanied with increased aggressive behavior. Moreover, NEPD (10 mg/kg) induced slight hyperthermia and reduced weight gain during the repeated administration, whereas increased locomotor activity and lack of depressive symptoms were found during withdrawal. This was accompanied by increased plasma corticosterone and decrease in striatal dopamine. Finally, the long-lasting and robust increase in ΔFosB levels found in striatum after NEPD chronic exposure suggests a high risk of dependence. The increased aggressivity and locomotor activity, together with this potential of inducing dependence justify a warning about the risks of consumption of NEPD if translated to humans. Keywords: Addiction; Aggressive behavior; Monoamine levels; N-ethyl-pentedrone; Synthetic cathinones

New outcomes of Lewis base addition to diboranes(4): electronic effects override strong steric disincentives

Two surprising new outcomes of the reaction of Lewis bases with dihalodiboranes(4) are presented, including sp2–sp3 diboranes in which the Lewis base unit is bound to a highly sterically congested boron atom, and a rearranged double base adduct. The results provide a fuller understanding of the reactivity of diboranes, a poorly-understood class of molecule of critical importance to synthetic organic chemistry

Mephedrone pharmacokinetics after intravenous and oral administration in rats: relation to pharmacodynamics

Fe d'errates disponible a: http://​dx.​doi.​org/​10.​1007/​s00213-013-3283-6Rationale Mephedrone (4-methylmethcathinone) is a still poorly known drug of abuse, alternative to ecstasy or cocaine. Objective The major aims were to investigate the pharmacokineticsa and locomotor activity of mephedrone in rats and provide a pharmacokinetic/pharmacodynamic model. Methods Mephedrone was administered to male Sprague-Dawley rats intravenously (10 mg/kg) and orally (30 and 60 mg/kg). Plasma concentrations and metabolites were characterized using LC/MS and LC-MS/MS fragmentation patterns. Locomotor activity was monitored for 180-240 min. Results Mephedrone plasma concentrations after i.v. administration fit a two-compartment model (α=10.23 h−1, β=1.86 h−1). After oral administration, peak mephedrone concentrations were achieved between 0.5 and 1 h and declined to undetectable levels at 9 h. The absolute bioavailability of mephedrone was about 10 % and the percentage of mephedrone protein binding was 21.59±3.67%. We have identified five phase I metabolites in rat blood after oral administration. The relationship between brain levels and free plasma concentration was 1.85±0.08. Mephedrone induced a dose-dependent increase in locomotor activity, which lasted up to 2 h. The pharmacokinetic-pharmacodynamic model successfully describes the relationship between mephedrone plasma concentrations and its psychostimulant effect. Conclusions We suggest a very important first-pass effect for mephedrone after oral administration and an easy access to the central nervous system. The model described might be useful in the estimation and prediction of the onset, magnitude,and time course of mephedrone pharmacodynamics as well as to design new animal models of mephedrone addiction and toxicity

Prevention of methamphetamine-induced microglial cell death by TNF-α and IL-6 through activation of the JAK-STAT pathway

<p><b>Abstract</b></p> <p><b>Background</b></p> <p>It is well known that methamphetamine (METH) is neurotoxic and recent studies have suggested the involvement of neuroinflammatory processes in brain dysfunction induced by misuse of this drug. Indeed, glial cells seem to be activated in response to METH, but its effects on microglial cells are not fully understood. Moreover, it has been shown that cytokines, which are normally released by activated microglia, may have a dual role in response to brain injury. This led us to study the toxic effect of METH on microglial cells by looking to cell death and alterations of tumor necrosis factor-alpha (TNF-α) and interleukine-6 (IL-6) systems, as well as the role played by these cytokines.</p> <p><b>Methods</b></p> <p>We used the N9 microglial cell line, and cell death and proliferation were evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling assay and incorporation of bromodeoxyuridine, respectively. The TNF-α and IL-6 content was quantified by enzyme-linked immunosorbent assay, and changes in TNF receptor 1, IL-6 receptor-alpha, Bax and Bcl-2 protein levels by western blotting. Immunocytochemistry analysis was also performed to evaluate alterations in microglial morphology and in the protein expression of phospho-signal transducer and activator of transcription 3 (pSTAT3).</p> <p><b>Results</b></p> <p>METH induced microglial cell death in a concentration-dependent manner (EC₅₀ = 1 mM), and also led to significant morphological changes and decreased cell proliferation. Additionally, this drug increased TNF-α extracellular and intracellular levels, as well as its receptor protein levels at 1 h, whereas IL-6 and its receptor levels were increased at 24 h post-exposure. However, the endogenous proinflammatory cytokines did not contribute to METH-induced microglial cell death. On the other hand, exogenous low concentrations of TNF-α or IL-6 had a protective effect. Interestingly, we also verified that the anti-apoptotic role of TNF-α was mediated by activation of IL-6 signaling, specifically the janus kinase (JAK)-STAT3 pathway, which in turn induced down-regulation of the Bax/Bcl-2 ratio.</p> <p><b>Conclusions</b></p> <p>These findings show that TNF-α and IL-6 have a protective role against METH-induced microglial cell death via the IL-6 receptor, specifically through activation of the JAK-STAT3 pathway, with consequent changes in pro- and anti-apoptotic proteins.</p

Mitochondrial Fragmentation Is Involved in Methamphetamine-Induced Cell Death in Rat Hippocampal Neural Progenitor Cells

Methamphetamine (METH) induces neurodegeneration through damage and apoptosis of dopaminergic nerve terminals and striatal cells, presumably via cross-talk between the endoplasmic reticulum and mitochondria-dependent death cascades. However, the effects of METH on neural progenitor cells (NPC), an important reservoir for replacing neurons and glia during development and injury, remain elusive. Using a rat hippocampal NPC (rhNPC) culture, we characterized the METH-induced mitochondrial fragmentation, apoptosis, and its related signaling mechanism through immunocytochemistry, flow cytometry, and Western blotting. We observed that METH induced rhNPC mitochondrial fragmentation, apoptosis, and inhibited cell proliferation. The mitochondrial fission protein dynamin-related protein 1 (Drp1) and reactive oxygen species (ROS), but not calcium (Ca2+) influx, were involved in the regulation of METH-induced mitochondrial fragmentation. Furthermore, our results indicated that dysregulation of ROS contributed to the oligomerization and translocation of Drp1, resulting in mitochondrial fragmentation in rhNPC. Taken together, our data demonstrate that METH-mediated ROS generation results in the dysregulation of Drp1, which leads to mitochondrial fragmentation and subsequent apoptosis in rhNPC. This provides a potential mechanism for METH-related neurodegenerative disorders, and also provides insight into therapeutic strategies for the neurodegenerative effects of METH