A new approach for modelling passenger trains evacuation procedures

This paper presents EvacTrain 2.0 a new model to simulate and explore the results of different evacuation strategies in passenger trains. This model is stochastic and can generate several results within a few seconds. This is why it is intended to be used for decision support during emergencies. EvacTrain is compared with another evacuation model and partially validated against a fire drill. Results show that this model can provide an accurate representation of real evacuation process. The general findings suggest a new paradigm for the application of evacuation modelling in passenger trains: their potential use for supporting emergency decisions in real-time.The authors would like to thank to the Spanish Ministry of Economy and Competitiveness for the EVACTRAIN Project grant, Ref.: BIA2011-26738, co-financed by FEDER

Phosphoinositide 3-kinase beta controls replication factor C assembly and function.

Genomic integrity is preserved by the action of protein complexes that control DNA homeostasis. These include the sliding clamps, trimeric protein rings that are arranged around DNA by clamp loaders. Replication factor C (RFC) is the clamp loader for proliferating cell nuclear antigen, which acts on DNA replication. Other processes that require mobile contact of proteins with DNA use alternative RFC complexes that exchange RFC1 for CTF18 or RAD17. Phosphoinositide 3-kinases (PI3K) are lipid kinases that generate 3-poly-phosphorylated-phosphoinositides at the plasma membrane following receptor stimulation. The two ubiquitous isoforms, PI3Kalpha and PI3Kbeta, have been extensively studied due to their involvement in cancer and nuclear PI3Kbeta has been found to regulate DNA replication and repair, processes controlled by molecular clamps. We studied here whether PI3Kbeta directly controls the process of molecular clamps loading. We show that PI3Kbeta associated with RFC1 and RFC1-like subunits. Only when in complex with PI3Kbeta, RFC1 bound to Ran GTPase and localized to the nucleus, suggesting that PI3Kbeta regulates RFC1 nuclear import. PI3Kbeta controlled not only RFC1- and RFC-RAD17 complexes, but also RFC-CTF18, in turn affecting CTF18-mediated chromatid cohesion. PI3Kbeta thus has a general function in genomic stability by controlling the localization and function of RFC complexes

Diagnóstico Territorial del Litoral de Cantabria. Volumen I: Informe.

Estudios de base para la redacción del Plan de Ordenación del Litoral (POL) de Cantabria.Este proyecto de investigación aplicada se ha realizado gracias al Convenio de Colaboración entre el Gobierno de Cantabria y la Universidad de Cantabria titulado “Diagnóstico Territorial del Litoral de Cantabria”

Papel de PI3K IA durante la fase M

Tesis doctoral inédita. Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de lectura: 13-02-201

KNL1-Bubs and RZZ provide two separable pathways for checkpoint activation at human kinetochores

The spindle assembly checkpoint (SAC) ensures the accurate segregation of sister chromatids during mitosis. Activation of the SAC occurs through a series of ordered molecular events that result in recruitment of Mad1:Mad2 complexes to improperly attached kinetochores. The current model involves sequential phospho-dependent recruitment of Bub3:Bub1 to KNL1 followed by binding of Mad1:Mad2 to Bub1. Here, we show in non-transformed diploid human cells that the KNL1-Bub3-Bub1 (KBB) pathway is required during normal mitotic progression when kinetochores are misaligned but is nonessential for SAC activation and Mad2 loading when kinetochores are unattached from microtubules. We provide evidence that the Rod-ZW10-Zwilch (RZZ) complex is necessary to recruit Mad1:Mad2 to, and delay anaphase onset in response to, unattached kinetochores independently of the KBB pathway. These data suggest that the KBB and RZZ complexes provide two distinct kinetochore receptors for Mad1:Mad2 and reveal mechanistic differences between SAC activation by unattached and improperly attached kinetochores

Diagnóstico Territorial del Litoral de Cantabria. Volumen III: Base de Datos de Unidades Territoriales.

Estudios de base para la redacción del Plan de Ordenación del Litoral (POL) de Cantabria.Este proyecto de investigación aplicada se ha realizado gracias al Convenio de Colaboración entre el Gobierno de Cantabria y la Universidad de Cantabria titulado “Diagnóstico Territorial del Litoral de Cantabria”

Diagnóstico Territorial del Litoral de Cantabria. Volumen II: Cartografía de Unidades Territoriales y Red Viaria.

Estudios de base para la redacción del Plan de Ordenación del Litoral (POL) de Cantabria.Este proyecto de investigación aplicada se ha realizado gracias al Convenio de Colaboración entre el Gobierno de Cantabria y la Universidad de Cantabria titulado “Diagnóstico Territorial del Litoral de Cantabria”

SADB phosphorylation of γ-tubulin regulates centrosome duplication

17 pages, 11 figures.-- PMID: 19648910 [PubMed].-- Printed version published Sep 2009.Supporting information available at: http://www.nature.com/ncb/journal/vaop/ncurrent/suppinfo/ncb1921_S1.htmlSymmetrical cell division requires duplication of DNA and protein content to generate two daughter cells. Centrosomes also duplicate during cell division, but the mechanism controlling this process is incompletely understood. We describe an alternative splice form of SadB encoding a short SADB Ser/Thr kinase whose activity fluctuates during the cell cycle, localizes to centrosomes, and controls centrosome duplication. Reduction of endogenous SADB levels diminished centrosome numbers, whereas enhanced SADB expression induced centrosome amplification. SADB exerted this action through phosphorylation of γ-tubulin on Ser 131, as expression of a phosphomimetic Ser 131-to-Asp γ-tubulin mutant alone increased centrosome numbers, whereas non-phosphorylatable Ala 131-γ-tubulin impaired centrosome duplication. We propose that SADB kinase activity controls centrosome homeostasis by regulating phosphorylation of γ-tubulin.This work was supported by the Spanish Ministry of Science and Innovation (SAF200405955, 200763624 to ACC, CSD 2006‑00023 to JMV), the Spanish Association against Cancer, the Spanish Ministry of Health (PI050964), the Royal Physiographic Society in Lund, the Ake Wibergs, Thelma Zoegas, OE och Edla Johanssons and U‑MAS Cancer Research Found, and fellowships from Teggers Fond, EMBO and the Swedish Society for Medical Research.Peer reviewe