The impact of CoRoT on close binary research

The space experiment CoRoT will provide continuous monitoring and high accuracy light curves of about sixty thousand stars. Selected binary systems will be observed in the Additional Program frame as targets of long and continuous pointed observations. Moreover, thousands of new binaries will certainly be detected and hundreds of them will have extremely accurate light curves. This will allow studies of fine effects on the light curves, monitoring of stellar activity and, in combination with ground-based observations, will provide exquisite determination of stellar parameters. Among the new discoveries of interesting systems of special value will be those of low mass binaries.Comment: 6 pages, 2 figures, contribution to "Colse binaries in the 21th century", Syros (Greece), June 2005. To be published by Ap&S

MyDebts : gestió de despeses en grup

A dia d'avuí, al fer coses en grup ens trobem en certs moments on a l'hora de pagar per algun servei grupal, ja sigui el d'un restaurant o les entrades del cinema, hi han problemes per dur a terme la repartició d'aquestes despeses entre els membres del grup. Aquest projecte de final de Grau, el que intenta, és solucionar aquest problema amb una aplicació web on poder introduir el que paga cada membre i que ella s'encarregui de gestionar què és el que deu cadascú i guardar tota la informació per després visualitzar-la a partir de la creació de grups d'usuaris prèviament registrats. MyDebts permet als usuaris registrats crear grups personalitzats, visualitzar l'historial de despeses per grup i contactar amb qualsevol membre via correu electrònic, entre d'altres funcionalitats. Al ser una aplicació web, s'hi pot accedir des de qualsevol dispositiu i s'hi adaptarà amb un disseny responsive. A part de l'aplicació, també es fa un estudi de mercat analitzant la competència i donant els punts clau per la seva introducció al mercat.Nowadays paying our friends for a paid activity we did toghether has led to be a problema, for exemple when paying for a restaurant bill or the cinema tickets, there can be difficulties on the division of these costs among the group membres. The aim of this final degree project is to try to solve this problem using a web application which allows you to enter the exact quantity that each membre has paid and then it manages to calculate what everyone owes to each membre of the group. Then, it saves all the information in order to be shown later to the user's groups who had already registered. MyDebts allows all the registered users to create persnalied groups, to see history expenses and to contact with any member needed via mail, among other facilities. As being a web application, it is accessible form any kind of device thanks to the responsive design. In addition, there is also a market study which analyses the competence of the application and als ogives the key points to the product placement.A día de hoy, al hacer cosas en grupo nos encontramos en ciertos momentos que, en el momento de pagar por algún servicio grupal, ya sea el de un restaurante o las entradas del cine, hay ciertos problemas para llevar a cabo la repartición de estos gastos entre los miembros del grupo. Este proyecto de final de grado, lo que intenta, es solucionar este problema con una aplicación web donde poder introducir lo que paga cada miembro y que ella se encargue de gestionar qué es lo que debe cada uno y guardar toda la información para después visualizarla mediante la creación de grupos de usuarios previamente registrados. MyDebts permite a los usuarios registrados crear grupos personalizados, visualizar el historial de gastos y contactar con cualquier miembro vía correo electrónico, entre otras funcionalidades. Al ser una aplicación web, se puede acceder a ella desde cualquier dispositivo y se adaptará con un diseño responsive. A parte de la aplicación, también se realiza un estudio de mercado analizando la competencia y dando los puntos claves para su lanzamiento al mercado

Disrupting MLC1 and GlialCAM and ClC-2 interactions in leukodystrophy entails glial chloride channel dysfunction

Defects in the astrocytic membrane protein MLC1, the adhesion molecule GlialCAM or the chloride channel ClC-2 underlie human leukoencephalopathies. Whereas GlialCAM binds ClC-2 and MLC1, and modifies ClC-2 currents in vitro, no functional connections between MLC1 and ClC-2 are known. Here we investigate this by generating loss-of-function Glialcam and Mlc1 mouse models manifesting myelin vacuolization. We find that ClC-2 is unnecessary for MLC1 and GlialCAM localization in brain, whereas GlialCAM is important for targeting MLC1 and ClC-2 to specialized glial domains in vivo and for modifying ClC-2's biophysical properties specifically in oligodendrocytes (OLs), the cells chiefly affected by vacuolization. Unexpectedly, MLC1 is crucial for proper localization of GlialCAM and ClC-2, and for changing ClC-2 currents. Our data unmask an unforeseen functional relationship between MLC1 and ClC-2 in vivo, which is probably mediated by GlialCAM, and suggest that ClC-2 participates in the pathogenesis of megalencephalic leukoencephalopathy with subcortical cysts

Detection of a classical Delta Scuti star in the new eclipsing binary system HIP 7666

HIP 7666 is a variable star newly discovered during the Hipparcos mission and classified as of unknown type (ESA 1997). During 23 nights between July 2000 and November 2000, over 2300 CCD observations in the V band were obtained from Hostalets de Pierola and Monegrillo observatories in Spain. These data show that the new variable is a detached eclipsing binary system with an orbital period of 2.37229 days. In addition, one of the components undergoes very short-period oscillations with a main pulsation frequency of 24.46 or 25.47 c/d. HIP 7666 is therefore a new member of the presently very few known detached eclipsing binary systems with a Delta Scuti type component.Comment: 6 pages, 8 Postscript figure

Disrupting MLC1 and GlialCAM and ClC-2interactions in leukodystrophy entails glial chloridechannel dysfunction

Defects in the astrocytic membrane protein MLC1, the adhesion molecule GlialCAM or the chloride channel ClC-2 underlie human leukoencephalopathies. Whereas GlialCAM binds ClC-2 and MLC1, and modifies ClC-2 currents in vitro, no functional connections between MLC1 and ClC-2 are known. Here we investigate this by generating loss-of-function Glialcam and Mlc1 mouse models manifesting myelin vacuolization. We find that ClC-2 is unnecessary for MLC1 and GlialCAM localization in brain, whereas GlialCAM is important for targeting MLC1 and ClC-2 to specialized glial domains in vivo and for modifying ClC-2's biophysical properties specifically in oligodendrocytes (OLs), the cells chiefly affected by vacuolization. Unexpectedly, MLC1 is crucial for proper localization of GlialCAM and ClC-2, and for changing ClC-2 currents. Our data unmask an unforeseen functional relationship between MLC1 and ClC-2 in vivo, which is probably mediated by GlialCAM, and suggest that ClC-2 participates in the pathogenesis of megalencephalic leukoencephalopathy with subcortical cysts

Megalencephalic leukoencephalopathy with subcortical cysts protein 1 regulates glial surface localization of GLIALCAM from fish to humans

Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a leukodystrophy characterized by myelin vacuolization and caused by mutations in MLC1 or GLIALCAM. Patients with recessive mutations in either MLC1 or GLIALCAM show the same clinical phenotype. It has been shown that GLIALCAM is necessary for the correct targeting of MLC1 to the membrane at cell junctions, but its own localization was independent of MLC1 in vitro. However, recent studies in Mlc1−/− mice have shown that GlialCAM is mislocalized in glial cells. In order to investigate whether the relationship between Mlc1 and GlialCAM is species-specific, we first identified MLC-related genes in zebrafish and generated an mlc1−/− zebrafish. We have characterized mlc1−/− zebrafish both functionally and histologically and compared the phenotype with that of the Mlc1−/− mice. In mlc1−/− zebrafish, as in Mlc1−/− mice, Glialcam is mislocalized. Re-examination of a brain biopsy from an MLC patient indicates that GLIALCAM is also mislocalized in Bergmann glia in the cerebellum. In vitro, impaired localization of GlialCAM was observed in astrocyte cultures from Mlc1−/− mouse only in the presence of elevated potassium levels, which mimics neuronal activity. In summary, here we demonstrate an evolutionary conserved role for MLC1 in regulating glial surface levels of GLIALCAM, and this interrelationship explains why patients with mutations in either gene (MLC1 or GLIALCAM) share the same clinical phenotyp

Mitochondrial and sarcoplasmic reticulum abnormalities in cancer cachexia: Altered energetic efficiency?

Background Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass. Methods The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques. Results Using in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca2 +-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content. Conclusions In addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum-mitochondrial assembly that is essential for muscle function and homeostasis. General significance The present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia. Highlights ► Skeletal muscle from cachectic animals showed fiber morphologic alterations. ► These alterations are mitochondrial disruption and dilatation of sarcoplasmic reticulum. ► An overexpression of both sarco/endoplasmic Ca2 +-ATPase (SERCA1) and adenine nucleotide translocator (ANT1) was reported. ► Tumor burden also leads to a marked decreased in muscle ATP content. Previous article in issu

Megalencephalic leukoencephalopathy with subcortical cysts: a personal biochemical retrospective

Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a rare type of leukodystrophy characterized by dysfunction of the role of glial cells in controlling brain fluid and ion homeostasis. Patients affected by MLC present macrocephaly, cysts and white matter vacuolation, which lead to motor and cognitive impairments. To date, there is no treatment for MLC, only supportive care. MLC is caused by mutations in the MLC1 and GLIALCAM genes. MLC1 is a membrane protein with low identity to the Kv1.1 potassium channel and GlialCAM belongs to an adhesion molecule family. Both proteins form a complex with an as-yet-unknown function that is expressed mainly in the astrocytes surrounding the blood-brain barrier and in Bergmann glia. GlialCAM also acts as an auxiliary subunit of the chloride channel ClC-2, thus regulating its localization at cell-cell junctions and modifying its functional properties by affecting the common gate of ClC-2. Recent studies in Mlc1-,GlialCAM-and Clcn2-knockout mice or Mlc1- knockout zebrafish have provided fresh insight into the pathophysiology of MLC and further details about the molecular interactions between these three proteins. Additional studies have shown that GlialCAM/MLC1 also regulates other ion channels (TRPV4, VRAC) or transporters (Na+/K+-ATPase) in a not-understood manner. Furthermore, it has been shown that GlialCAM/ MLC1 may influence signal transduction mechanisms, thereby affecting other proteins not related with transport such as the EGFreceptor. Here, we offer a personal biochemical retrospective of the work that has been performed to gain knowledge of the pathophysiology of MLC, and we discuss future strategies that may be used to identify therapeutic solutions for MLC patients

Outburst activity in comets: II. A multi-band photometric monitoring of comet 29p/Schwassmann-Wachmann 1

We have carried out a continuous multi-band photometric monitoring of the nuclear activity of comet 29P/Schwassmann-Wachmann 1 from 2008 to 2010. Our main aim has been to study the outburst mechanism on the basis of a follow-up of the photometric variations associated with the release of dust. We used a standardized method to obtain the 10 arc-sec nucleus photometry in the V, R, and I filters of the Johnson-Kron-Cousins system, being accurately calibrated with standard Landolt stars. Production of dust in the R and I bands during the 2010 Feb. 3 outburst has been also computed. We conclude that the massive ejection of large (optically-thin) particles from the surface at the time of the outburst is the triggering mechanism to produce the outburst. Ulterior sublimation of these ice-rich dust particles during the following days induces fragmentation, generating micrometer-sized grains that increase the dust spatial density to produce the outburst in the optical range due to scattering of sun light. The material leaving the nucleus adopts a fan-like dust feature, formed by micrometer-sized particles that are decaying in brightness as it evolved outwards. By analyzing the photometric signal measured in a standardized 10-arcsec aperture using the Phase Dispersion Minimization technique we have found a clear periodicity of 50 days. Remarkably, this value is also consistent with an outburst frequency of 7.4 outbursts/year deduced from the number of outbursts noticed during the effective observing time.Comment: 19 pages, 3 Tables, and 6 figure