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Elche, Spain

The Miguel Hernández University of Elche , is a Spanish Public University, open to the world, offering prestigious education, excellent research, and quality services facilitating the comprehensive development of its students and their insertion into the labor market. It is located in the province of Alicante and was established in 1996. Its name commemorates the Spanish poet Miguel Hernández.The UMH offers Bachelor’s degrees, Master’s and PhD programs adapted to the European Higher Education Area in the fields of the arts, experimental and technical science, engineering, and health and social science at its four university campuses .The UMH is particularly concerned about its students entering the labor market. Here, the University has excelled, achieving excellent results thanks to 6,000 businesses maintaining collaboration agreements with the University. Moreover, the UMH has been confirmed to be an academic institution committed to quality, as it was recently renewed with the European Seal of Excellence Gold level for the third time. The UMH is the only Spanish university to obtain this on three occasions.The UMH has also fostered partnerships with other national and international institutions to promote student mobility and attract foreign students. In its bid for its internationalization, the UMH has set in motion a complete program of activities to facilitate foreign academic stays and to receive students who wish to further their education within our classrooms.Quality research characterizes the UMH, as a study done by the Observatory of Research Activities in Spanish Universities on research productivity by Spanish universities shows. Their study places the UMH in the third position for 2011 in terms of annual scientific production per faculty member and accredited 6-year research periods per faculty member. UMH research activities are strongly related to their socioeconomic surroundings, but many of its laboratories possess levels of excellence recognized nationally as well as internationally. Wikipedia.

Gutierrez L.M.,University Miguel Hernandez
International Review of Cell and Molecular Biology | Year: 2012

The cortical cytoskeleton is a dense network of filamentous actin (F-actin) that participates in the events associated with secretion from neuroendocrine cells. This filamentous web traps secretory vesicles, acting as a retention system that blocks the access of vesicles to secretory sites during the resting state, and it mediates their active directional transport during stimulation. The changes in the cortical cytoskeleton that drive this functional transformation have been well documented, particularly in cultured chromaffin cells. At the biochemical level, alterations in F-actin are governed by the activity of molecular motors like myosins II and V and by other calcium-dependent proteins that influence the polymerization and cross-linking of F-actin structures. In addition to modulating vesicle transport, the F-actin cortical network and its associated motor proteins also influence the late phases of the secretory process, including membrane fusion and the release of active substances through the exocytotic fusion pore. Here, we discuss the potential interactions between the F-actin cortical web and proteins such as SNAREs during secretion. We also discuss the role of the cytoskeleton in organizing the molecular elements required to sustain regulated exocytosis, forming a molecular structure that foments the efficient release of neurotransmitters and hormones. © 2012 Elsevier Inc..

Nieto M.A.,University Miguel Hernandez
Science | Year: 2013

During embryonic development, many cells are born far from their final destination and must travel long distances. To become motile and invasive, embryonic epithelial cells undergo a process of mesenchymal conversion known as epithelial-to-mesenchymal transition (EMT). Likewise, EMT can be seen in cancer cells as they leave the primary tumor and disseminate to other parts of the body to colonize distant organs and form metastases. In addition, through the reverse process (mesenchymal-to-epithelial transition), both normal and carcinoma cells revert to the epithelial phenotype to, respectively, differentiate into organs or form secondary tumors. The parallels in phenotypic plasticity in normal morphogenesis and cancer highlight the importance of studying the embryo to understand tumor progression and to aid in the design of improved therapeutic strategies.

Marin O.,University Miguel Hernandez
Cold Spring Harbor perspectives in biology | Year: 2010

Neuronal migration is, along with axon guidance, one of the fundamental mechanisms underlying the wiring of the brain. As other organs, the nervous system has acquired the ability to grow both in size and complexity by using migration as a strategy to position cell types from different origins into specific coordinates, allowing for the generation of brain circuitries. Guidance of migrating neurons shares many features with axon guidance, from the use of substrates to the specific cues regulating chemotaxis. There are, however, important differences in the cell biology of these two processes. The most evident case is nucleokinesis, which is an essential component of migration that needs to be integrated within the guidance of the cell. Perhaps more surprisingly, the cellular mechanisms underlying the response of the leading process of migrating cells to guidance cues might be different to those involved in growth cone steering, at least for some neuronal populations.

Demyelinating disorders such as leukodystrophies and multiple sclerosis are neurodegenerative diseases characterized by the progressive loss of myelin that may lead toward a chronic demyelination of the brain's white matter, impairing normal axonal conduction velocity and ultimately causing neurodegeneration. Current treatments modifying the pathological mechanisms are capable of ameliorating the disease; however, frequently, these therapies are not sufficient to repress the progressive demyelination into a chronic condition and permanent loss of function. To this end, we analyzed the effect that bone marrow-derived mesenchymal stromal cell (BM-MSC) grafts exert in a chronically demyelinated mouse brain. As a result, oligodendrocyte progenitors were recruited surrounding the graft due to the expression of various trophic signals by the grafted MSCs. Although there was no significant reaction in the non-grafted side, in the grafted regions oligodendrocyte progenitors were detected. These progenitors were derived from the nearby tissue as well as from the neurogenic niches, including the subependymal zone and dentate gyrus. Once near the graft site, the cells matured to myelinating oligodendrocytes. Finally, electrophysiological studies demonstrated that axonal conduction velocity was significantly increased in the grafted side of the fimbria. In conclusion, we demonstrate here that in chronic demyelinated white matter, BM-MSC transplantation activates oligodendrocyte progenitors and induces remyelination in the tissue surrounding the stem cell graft.

Jego P.,University Miguel Hernandez
Journal of Cerebral Blood Flow and Metabolism | Year: 2014

Functional magnetic resonance imaging (fMRI) is a fundamental tool to investigate human brain networks. However, the cellular mechanisms underlying fMRI signals are not fully understood. One hypothetical mechanism is the putative vascular control exerted by cytosolic calcium in perivascular astrocytes. We have performed combined fMRI-electrophysiology experiments in mice lacking the inositol 1,4,5-triphosphate-type-2 receptor, with the primary pathway of cytosolic calcium increase eliminated into astrocytes. Our results show that evoked electrophysiologic activity and fMRI signals acquired during either transient or sustained neuronal activations occur independently of these large calcium signals. This result challenges the suggested intermediary role of astrocytic calcium surges in fMRI-signal generation.Journal of Cerebral Blood Flow and Metabolism advance online publication, 6 August 2014; doi:10.1038/jcbfm.2014.144.

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