Double proximity effect in lateral S-NF-S junctions

We investigate planar Josephson junctions where the intermediate spacer between the two superconductors is an hybrid structure made by a normal metal and a ferromagnet. The different behaviors of the S-N-S junctions with thicknesses of 50 nm in both Cu and Nb layers, and S-N/F-S junctions with 10 nm of Co, 50 nm of Cu and 50 nm of Nb are studied. In this way, we analyze the influence of the ferromagnetic exchange interaction on the proximity effect. A dramatic supression of the josephson critical current of the Nb-(Cu/Co)-Nb junctions is observed. We believe that the reason for this is due to the length scale of the superconducting correlations of the electrons and holes of the weak link is larger than the thickness of Cu/Co bilayer.

Isolation of mineralizing Nestin+ Nkx6.1+ vascular muscular cells from the adult human spinal cord

Background: The adult central nervous system (CNS) contains different populations of immature cells that could possibly be used to repair brain and spinal cord lesions. The diversity and the properties of these cells in the human adult CNS remain to be fully explored. We previously isolated Nestin(+) Sox2(+) neural multipotential cells from the adult human spinal cord using the neurosphere method (i.e. non adherent conditions and defined medium). -- Results: Here we report the isolation and long term propagation of another population of Nestin(+) cells from this tissue using adherent culture conditions and serum. QPCR and immunofluorescence indicated that these cells had mesenchymal features as evidenced by the expression of Snai2 and Twist1 and lack of expression of neural markers such as Sox2, Olig2 or GFAP. Indeed, these cells expressed markers typical of smooth muscle vascular cells such as Calponin, Caldesmone and Acta2 (Smooth muscle actin). These cells could not differentiate into chondrocytes, adipocytes, neuronal and glial cells, however they readily mineralized when placed in osteogenic conditions. Further characterization allowed us to identify the Nkx6.1 transcription factor as a marker for these cells. Nkx6.1 was expressed in vivo by CNS vascular muscular cells located in the parenchyma and the meninges. -- Conclusion: Smooth muscle cells expressing Nestin and Nkx6.1 is the main cell population derived from culturing human spinal cord cells in adherent conditions with serum. Mineralization of these cells in vitro could represent a valuable model for studying calcifications of CNS vessels which are observed in pathological situations or as part of the normal aging. In addition, long term propagation of these cells will allow the study of their interaction with other CNS cells and their implication in scar formation during spinal cord injury.

Early Functional Deficit and Microglial Disturbances in a Mouse Model of Amyotrophic Lateral Sclerosis

11 p.

Energy and information in Hodgkin-Huxley neurons

[EN]The generation of spikes by neurons is energetically a costly process and the evaluation of the metabolic energy required to maintain the signaling activity of neurons a challenge of practical interest. Neuron models are frequently used to represent the dynamics of real neurons but hardly ever to evaluate the electrochemical energy required to maintain that dynamics. This paper discusses the interpretation of a Hodgkin-Huxley circuit as an energy model for real biological neurons and uses it to evaluate the consumption of metabolic energy in the transmission of information between neurons coupled by electrical synapses, i.e., gap junctions. We show that for a single postsynaptic neuron maximum energy efficiency, measured in bits of mutual information per molecule of adenosine triphosphate (ATP) consumed, requires maximum energy consumption. For groups of parallel postsynaptic neurons we determine values of the synaptic conductance at which the energy efficiency of the transmission presents clear maxima at relatively very low values of metabolic energy consumption. Contrary to what could be expected, the best performance occurs at a low energy cost.

Gen LPP : Avances en el conocimiento de uno de los genes candidato de la enfermedad celíaca

[ES] La enfermedad celíaca (EC) es una enteropatía autoinmune de predisposición genética, producida por la ingestión en la dieta de péptidos derivados de cereales como el trigo o la cebada. Aunque se creía que afectaba casi de forma exclusiva a los individuos europeos (1%), actualmente se conocen casos en todo el mundo. El modelo patogénico se centra en los mecanismos de la inmunidad adaptativa dependientes de la estimulación de linfocitos T CD4+ reactivos, pero existe además un efecto tóxico directo del gluten sobre el epitelio intestinal, dependiente de la inmunidad innata. La participación de la Genética en la susceptibilidad a la enfermedad es conocida desde hace tiempo, siendo el locus HLA el que explica aproximadamente el 40% del componente genético de la enfermedad. Para tratar de identificar otros genes con susceptibilidad, se han venido realizando múltiples esfuerzos durante los últimos años. Uno de los últimos, llevado a cabo en 2011, fue el Proyecto Immunochip. En él, se analizaron más de 200.000 variantes y se descubrieron 13 nuevos loci de riesgo para la EC, que junto con los descubiertos en anteriores trabajos y el locus HLA, daban un total de 40 loci de riesgo. Entre ellos, se encontraba la región que ocupa el gen LPP . Localizado en el cromosoma 3, un estudio reciente lo vincula con los procesos de adhesión celular en el intestino. En el presente trabajo, se ha estudiado el efecto de la gliadina sobre la expresión del gen de interés (LPP ) y el posible efecto de un silenciamiento del mismo sobre dos genes relacionados con las uniones celulares (ACTB y TJP1). En el caso de la gliadina, no se halló un cambio significativo en la expresión del gen. Mientras, los resultados del efecto del silenciamiento fueron dispares, no siendo concluyentes para el gen ACTB, pero encontrando una posible asociación entre los genes LPP y TJP1.