Una llum d'esperança : alumnes repetidors com a monitors de pràctiques. Experiència a segon curs de la Llicenciatura en Medicina

Amb l'ànim d'ajudar als estudiants que tenen problemes a la assignatura "Estructura Microscòpica d'Aparells i Sistemes Humans" de 2n curs de la llicenciatura de Medicina i que la suspenen reiteradamet, el curs 2005-2006 vam iniciar un nou projecte d'innovació docent basat en l'èxit de l'experiència dels professors i monitors de l'assignatura de Neuroanatomia de segon curs de Llicenciatura en medicina durant el curs 2004-2005

ABP integral en histología (teoria i pràctiques), una experiència amb èxit a la Facultat de Medicina

A la nostra Unitat tenim la responsabilitat de dues assignatures de la Llicenciatura de Medicina: (1) Histologia Mèdica (HM), semestral, troncal de 1r curs de 4,5 crèdits (3 crèdits teòrics i 1,5 crèdits pràctics). Al curs 2006-07 es varen matricular 387 estudiants. (2) Estructura Microscòpica d'Aparells I Sistemes Humans (EMASH), anyal, troncal de 2n curs de 9 crèdits (4,5 crèdits teòrics i 4,5 crèdits pràctics. Al curs 2006-07 es varen matricular 298 estudiants.En els darrers anys el nostre objectiu ha sigut migrar des de un mètode docent tradicional de classes magistrals fins a un mètode tipus ABP (Aprenentatge Basat en Problemes) integral (teoria i pràctiques), que a més a més seguís les directius del Protocol de Bolònia per tal d'integrar aquestes assignatures a un nou programa docent de la Llicenciatura a l' EEES (Espai Europeu d'Educació Superior)

Differential modulation of TREM2 protein during postnatal brain development in mice

During postnatal development, microglia, the resident innate immune cells of the central nervous system are constantly monitoring the brain parenchyma, cleaning the cell debris, the synaptic contacts overproduced and also maintaining the brain homeostasis. In this context, the postnatal microglia need some control over the innate immune response. One such molecule recently described to be involved in modulation of immune response is TREM2 (triggering receptor expressed on myeloid cells 2). Although some studies have observed TREM2 mRNA in postnatal brain, the regional pattern of the TREM2 protein has not been described. We therefore characterized the distribution of TREM2 protein in mice brain from Postnatal day (P) 1 to 14 by immunostaining. In our study, TREM2 protein was expressed only in microglia/macrophages and is developmentally downregulated in a region-dependent manner. Its expression persisted in white matter, mainly in caudal corpus callosum, and the neurogenic subventricular zone for a longer time than in grey matter. Additionally, the phenotypes of the TREM2+ microglia also differ; expressing CD16/32, MHCII and CD86 (antigen presentation markers) and CD68 (phagocytic marker) in different regions as well as with different intensity till P7. The mannose receptor (CD206) colocalized with TREM2 only at P1-P3 in the subventricular zone and cingulum, while others persisted at low intensities till P7. Furthermore, the spatiotemporal expression pattern and characterization of TREM2 indicate towards its other plausible roles in phagocytosis, progenitor's fate determination or microglia phenotype modulation during postnatal development. Hence, the increase of TREM2 observed in pathologies may recapitulate their function during postnatal development, as a better understanding of this period may open new pathway for future therapies

Neuroprotection from NMDA excitotoxic lesion by Cu/Zn superoxide dismutase gene delivery to the postnatal rat brain by a modular protein vector

Background: Superoxide mediated oxidative stress is a key neuropathologic mechanism in acute central nervous system injuries. We have analyzed the neuroprotective efficacy of the transient overexpression of antioxidant enzyme Cu/Zn Superoxide dismutase (SOD) after excitotoxic injury to the immature rat brain by using a recently constructed modular protein vector for non-viral gene delivery termed NLSCt. For this purpose, animals were injected with the NLSCt vector carrying the Cu/Zn SOD or the control GFP transgenes 2 hours after intracortical N-methyl-D-aspartate (NMDA) administration, and daily functional evaluation was performed. Moreover, 3 days after, lesion volume, neuronal degeneration and nitrotyrosine immunoreactivity were evaluated. Results: Overexpression of Cu/Zn SOD transgene after NMDA administration showed improved functional outcome and a reduced lesion volume at 3 days post lesion. In secondary degenerative areas, increased neuronal survival as well as decreased numbers of degenerating neurons and nitrotyrosine immunoreactivity was seen. Interestingly, injection of the NLSCt vector carrying the control GFP transgene also displayed a significant neuroprotective effect but less pronounced. Conclusion: When the appropriate levels of Cu/Zn SOD are expressed transiently after injury using the non-viral modular protein vector NLSCt a neuroprotective effect is seen. Thus recombinant modular protein vectors may be suitable for in vivo gene therapy, and Cu/Zn SOD should be considered as an interesting therapeutic transgene

Cu/Zn superoxide dismutase expression in the postnatal rat brain following an excitotoxic injury

BACKGROUND: In the nervous system, as in other organs, Cu/Zn superoxide dismutase (Cu/Zn SOD) is a key antioxidant enzyme involved in superoxide detoxification in normal cellular metabolism and after cell injury. Although it has been suggested that immature brain has a different susceptibility to oxidative damage than adult brain, the distribution and cell-specific expression of this enzyme in immature brain and after postnatal brain damage has not been documented. METHODS: In this study, we used immunohistochemistry and western blot to analyze the expression of Cu/Zn SOD in intact immature rat brain and in immature rat brain after an NMDA-induced excitotoxic cortical injury performed at postnatal day 9. Double immunofluorescence labelling was used to identify Cu/Zn SOD-expressing cell populations. RESULTS: In intact immature brain, Cu/Zn SOD enzyme was widely expressed at high levels in neurons mainly located in cortical layers II, III and V, in the sub-plate, in the pyriform cortex, in the hippocampus, and in the hypothalamus. Glial fibrillary acidic protein-positive cells only showed Cu/Zn SOD expression in the glia limitans and in scattered cells of the ventricle walls. No expression was detected in interfascicular oligodendroglia, microglia or endothelial cells. Following excitotoxic damage, neuronal Cu/Zn SOD was rapidly downregulated (over 2–4 hours) at the injection site before neurodegeneration signals and TUNEL staining were observed. Later, from 1 day post-lesion onward, an upregulation of Cu/Zn SOD was found due to increased expression in astroglia. A further increase was observed at 3, 5 and 7 days that corresponded to extensive induction of Cu/Zn SOD in highly reactive astrocytes and in the astroglial scar. CONCLUSION: We show here that, in the intact immature brain, the expression of Cu/Zn SOD was mainly found in neurons. When damage occurs, a strong and very rapid downregulation of this enzyme precedes neuronal degeneration, and is followed by an upregulation of Cu/Zn SOD in astroglial cells

Una llum d'esperança : alumnes repetidors com a monitors de pràctiques. Experiència a segon curs de la Llicenciatura en Medicina

Amb l'ànim d'ajudar als estudiants que tenen problemes a la assignatura "Estructura Microscòpica d'Aparells i Sistemes Humans" de 2n curs de la llicenciatura de Medicina i que la suspenen reiteradamet, el curs 2005-2006 vam iniciar un nou projecte d'innovació docent basat en l'èxit de l'experiència dels professors i monitors de l'assignatura de Neuroanatomia de segon curs de Llicenciatura en medicina durant el curs 2004-2005

Proliferation dynamics of germinative zone cells in the intact and excitotoxically lesioned postnatal rat brain

Background: The forebrain subventricular zone (SVZ)-olfactory bulb pathway and hippocampal subgranular zone (SGZ) generate neurons into adulthood in the mammalian brain. Neurogenesis increases after injury to the adult brain, but few studies examine the effect of injury on neural and glial precursors in the postnatal brain. To characterize the spatio-temporal dynamics of cell proliferation in the germinative zones, this study utilized a model of postnatal damage induced by NMDA injection in the right sensorimotor cortex at postnatal day 9. Dividing cell populations were labeled with 5-Bromodeoxyuridine (BrdU) in the intact and damaged postnatal brain. Identity of proliferating cells was determined by double immunolabeling with nestin, GFAP, NeuN and tomato lectin (TL). Results: In the control brain, grouped BrdU+ cells were observed in the Rostral Migratory Stream (RMS), SVZ and SGZ. Maximal proliferation was seen at P12, persisted until P23 and diminished by P49. After injury, a striking reduction in the number of BrdU+ cells was observed in the ipsilateral SVZ from 10 hours (58% decrease) until 14 days post-lesion (88% decrease). In contrast, an increase in grouped BrdU+ cells was seen in the striatum adjacent to the depleted SVZ. Significantly reduced numbers of BrdU+ cells were also seen in the RMS until 3 days post-lesion. No changes were noted in the SGZ. Both in controls and lesioned hemispheres, BrdU+ cells located in the germinal zones were mostly nestin positive and negative for GFAP, NeuN, and TL. In the SVZ area lining the ventricle, BrdU+/nestin+ cells were mainly located between TL+ ependyma and parenchymal GFAP+ astrocytes. After excitotoxicity, a decrease in the number and orientation of GFAP/nestin+ prolongations leaving the SVZ to the cortex, corpus callosum and striatum was noted until 5 days post-lesion. Conclusion: Postnatal excitotoxic injury differentially affects proliferating cells in the germinative zones: no change is observed in the dentate gyrus whereas excitotoxicity causes a significant decrease in proliferating cells in the SVZ and RMS. Depletion of BrdU+ cells in the postnatal SVZ and RMS differs from previous studies after adult brain injury and may affect the SVZ-RMS migration and is suggestive of progenitor recruitment to injured areas

ABP integral en histología (teoria i pràctiques), una experiència amb èxit a la Facultat de Medicina

A la nostra Unitat tenim la responsabilitat de dues assignatures de la Llicenciatura de Medicina: (1) Histologia Mèdica (HM), semestral, troncal de 1r curs de 4,5 crèdits (3 crèdits teòrics i 1,5 crèdits pràctics). Al curs 2006-07 es varen matricular 387 estudiants. (2) Estructura Microscòpica d'Aparells I Sistemes Humans (EMASH), anyal, troncal de 2n curs de 9 crèdits (4,5 crèdits teòrics i 4,5 crèdits pràctics. Al curs 2006-07 es varen matricular 298 estudiants.En els darrers anys el nostre objectiu ha sigut migrar des de un mètode docent tradicional de classes magistrals fins a un mètode tipus ABP (Aprenentatge Basat en Problemes) integral (teoria i pràctiques), que a més a més seguís les directius del Protocol de Bolònia per tal d'integrar aquestes assignatures a un nou programa docent de la Llicenciatura a l' EEES (Espai Europeu d'Educació Superior)

Short and Long-Term Analysis and Comparison of Neurodegeneration and Inflammatory Cell Response in the Ipsilateral and Contralateral Hemisphere of the Neonatal Mouse Brain after Hypoxia/Ischemia

Altres ajuts: K. Shrivastava holds an I3 Intensification postdoctoral fellowship from Universitat Autonoma Barcelona. M. Chertoff holds a Marie Curie International Incoming fellowship (2009-IIF-253110). The work is dedicated to Dr Laia Acarin, an outstanding scientist, who deceased during the evaluation of this manuscript, on December 29th, 2011.Understanding the evolution of neonatal hypoxic/ischemic is essential for novel neuroprotective approaches. We describe the neuropathology and glial/inflammatory response, from 3 hours to 100 days, after carotid occlusion and hypoxia (8% O, 55 minutes) to the C57/BL6 P7 mouse. Massive tissue injury and atrophy in the ipsilateral (IL) hippocampus, corpus callosum, and caudate-putamen are consistently shown. Astrogliosis peaks at 14 days, but glial scar is still evident at day 100. Microgliosis peaks at 3-7 days and decreases by day 14. Both glial responses start at 3 hours in the corpus callosum and hippocampal fissure, to progressively cover the degenerating CA field. Neutrophils increase in the ventricles and hippocampal vasculature, showing also parenchymal extravasation at 7 days. Remarkably, delayed milder atrophy is also seen in the contralateral (CL) hippocampus and corpus callosum, areas showing astrogliosis and microgliosis during the first 72 hours. This detailed and long-term cellular response characterization of the ipsilateral and contralateral hemisphere after H/I may help in the design of better therapeutic strategies