Aplicació per a un hotel SPA (.NET)

Treball final de carrera que consisteix en un software per a un hotel SPA que ha de gestionar les seves activitats i peticions. El programari està implementat en .NET (WPF i WCF).

Proyecto final carrera ETIG Hotel SPA

El proyecto consiste en desarrollar un software para la gestión de los servicios que ofrece un Hotel Spa.Por un lado, un software con el que los clientes podrán interactuar para la petición de servicios al hotel. Estas peticiones de servicios son: -Peticiones servicios de habitaciones (incidencias, peticiones de material, servicio despertador, servicio limpieza, etc.) -Reservar un recurso (salas de reunión, pistas de deportes, etc.) -Planificar actividades realizadas en el recinto del hotel (gimnasio, masajista, conferencias, audiciones, espectáculos musicales, etc.)Y por otro lado el software necesario para gestionar estas peticiones que estará a la disposición de los encargados del hotel.El nombre de la aplicación es: eHotelSPANet.Para el desarrollo del software se utilizarán las herramientas de Microsoft usando la tecnología .NET, concretamente: -WPF (Windows Presentation Foundation). -WCF (Windows Communications Foundation) SQL Server 2008

Aplicació Microsoft .Net : Hotel Spa

Desenvolupament d'una aplicació amb Microsoft .NET, WCF, WPF, Linq2SQL, d'un Hotel Spa.

TFC .NET- HotelSpa

El projecte se centra en desenvolupar una aplicació per un hotel amb instal·lacions d'esbarjo i relaxació.

A variant in the gene FUT9 is associated with susceptibility to placental malaria infection

Malaria in pregnancy forms a substantial part of the worldwide burden of malaria, with an estimated annual death toll of up to 200,000 infants, as well as increased maternal morbidity and mortality. Studies of genetic susceptibility to malaria have so far focused on infant malaria, with only a few studies investigating the genetic basis of placental malaria, focusing only on a limited number of candidate genes. The aim of this study therefore was to identify novel host genetic factors involved in placental malaria infection. To this end we carried out a nested case-control study on 180 Mozambican pregnant women with placental malaria infection, and 180 controls within an intervention trial of malaria prevention. We genotyped 880 SNPs in a set of 64 functionally related genes involved in glycosylation and innate immunity. A SNP located in the gene FUT9, rs3811070, was significantly associated with placental malaria infection (OR = 2.31, permutation p-value = 0.028). Haplotypic analysis revealed a similarly strong association of a common haplotype of four SNPs including rs3811070. FUT9 codes for a fucosyl-transferase that is catalyzing the last step in the biosynthesis of the Lewis-x antigen, which forms part of the Lewis blood group-related antigens. These results therefore suggest an involvement of this antigen in the pathogenesis of placental malaria infection.

A targeted association study of immunity genes and networks suggests novel associations with placental malaria infection

A large proportion of the death toll associated with malaria is a consequence of malaria infection during pregnancy, causing up to 200,000 infant deaths annually. We previously published the first extensive genetic association study of placental malaria infection, and here we extend this analysis considerably, investigating genetic variation in over 9,000 SNPs in more than 1,000 genes involved in immunity and inflammation for their involvement in susceptibility to placental malaria infection. We applied a new approach incorporating results from both single gene analysis as well as gene-gene interactionson a protein-protein interaction network. We found suggestive associations of variants in the gene KLRK1 in the single geneanalysis, as well as evidence for associations of multiple members of the IL-7/IL-7R signalling cascade in the combined analysis. To our knowledge, this is the first large-scale genetic study on placental malaria infection to date, opening the door for follow-up studies trying to elucidate the genetic basis of this neglected form of malaria.

Sargassum muticum (Yendo) Fensholt, nueva cita para la Peninsula Iberica

Sargassum muticum (Yendo) Fensholt, feofícea originaria de Japón (Pacífico Oeste), está extendiendo rápidamente su área de distribución, asociada a los transportes de ostras japonesas (CRITCHLEY, A. & R. DIJKEMA, Bot. Mar. 27:211-216,1984). Actualmente está citada en el Japón, en la costa Pacífica de América del Norte, en el Atlántico europeo de Inglaterra, Canal de la Mancha y Holanda y en el Mediterráneo francés (CRITCHLEY, A. J. Mar. Biol. Ass. U.K. 63: 617-625, 1983).

Positional bias of general and tissue-specific regulatory motifs in mouse gene promoters

Background: The arrangement of regulatory motifs in gene promoters, or promoterarchitecture, is the result of mutation and selection processes that have operated over manymillions of years. In mammals, tissue-specific transcriptional regulation is related to the presence ofspecific protein-interacting DNA motifs in gene promoters. However, little is known about therelative location and spacing of these motifs. To fill this gap, we have performed a systematic searchfor motifs that show significant bias at specific promoter locations in a large collection ofhousekeeping and tissue-specific genes.Results: We observe that promoters driving housekeeping gene expression are enriched inparticular motifs with strong positional bias, such as YY1, which are of little relevance in promotersdriving tissue-specific expression. We also identify a large number of motifs that show positionalbias in genes expressed in a highly tissue-specific manner. They include well-known tissue-specificmotifs, such as HNF1 and HNF4 motifs in liver, kidney and small intestine, or RFX motifs in testis,as well as many potentially novel regulatory motifs. Based on this analysis, we provide predictionsfor 559 tissue-specific motifs in mouse gene promoters.Conclusion: The study shows that motif positional bias is an important feature of mammalianproximal promoters and that it affects both general and tissue-specific motifs. Motif positionalconstraints define very distinct promoter architectures depending on breadth of expression andtype of tissue.