Techniques for an image space occlusion culling engine

In this work we present several techniques applied to implement an Image Space Software Occlusion Culling Engine to increase the speed of rendering general dynamic scenes with high depth complexity. This conservative culling method is based on a tiled Occlusion Map that is updated only when needed, deferring and even avoiding the expensive per pixel rasterization process. We show how the tiles become a useful way to increase the speed of visibility tests. Finally we describe how different parts of the engine were parallelized using OpenMP directives and SIMD instructions.Eje: Workshop Computación gráfica, imágenes y visualización (WCGIV)Red de Universidades con Carreras en Informática (RedUNCI

Detección de indicadores de seguridad de pacientes (PSI-Patient Safety Indicators) en un estudio multi-céntrico de carga de enfermedad y resultados de la atención

La calidad/ seguridad de la atención médica se puede estimar analizando los registros de egresos de hospitales generales de agudos (HGA). Se obtuvieron indicadores de seguridad de los pacientes (PSI), que detectan eventos adversos en la atención médica (EAs). En un estudio multi-céntrico se adecuó un método para obtener los PSI en la Argentina basado en codificaciones diagnosticas primarias (Dx1) y secundarias (Dx2) y codificaciones de procedimientos (Px1 y Px 2). La estandarización de los diagnósticos y de los procedimientos permitió realizar la plataforma del estudio Utilización de Servicios, Costos y Resultados en Argentina (USCR-A). Se obtienen los EAs definidos por los PSI #3, #7 y #13. El objetivo de este trabajo es presentar los resultados cuali y cuantitativos de una aplicación de los PSI en el contexto del trabajo y registro del estudio multi-céntrico en Utilización de Servicios, Costos y Resultados en Argentina (USCR-A).Sociedad Argentina de Informática e Investigación Operativ

Implementing software occlusion culling for real-time applications

The visualization of complex virtual scenes can be significantly accelerated by applying Occlusion Culling. In this work we introduce a variant of the Hierarchical Occlusion Map method to be used in Real-Time applications. To avoid using real objects geometry we generate specialized conservative Occluders based on Axis Aligned Bounding Boxes which are converted into coplanar quads and then rasterized in CPU using a downscaled Depth Buffer. We implement this method in a 3D scene using a software occlusion map rasterizer module specifically optimized to rasterize Occluder quads into a Depth Buffer. We demonstrate that this approach effectively increases the number of occluded objects without generating significant runtime overhead.Eje: Workshop Computación gráfica, imágenes y visualización (WCGIV)Red de Universidades con Carreras en Informática (RedUNCI

Techniques for an image space occlusion culling engine

In this work we present several techniques applied to implement an Image Space Software Occlusion Culling Engine to increase the speed of rendering general dynamic scenes with high depth complexity. This conservative culling method is based on a tiled Occlusion Map that is updated only when needed, deferring and even avoiding the expensive per pixel rasterization process. We show how the tiles become a useful way to increase the speed of visibility tests. Finally we describe how different parts of the engine were parallelized using OpenMP directives and SIMD instructions.Eje: Workshop Computación gráfica, imágenes y visualización (WCGIV)Red de Universidades con Carreras en Informática (RedUNCI

HIPK2 and extrachromosomal histone H2B are separately recruited by Aurora-B for cytokinesis

Cytokinesis, the final phase of cell division, is necessary to form two distinct daughter cells with correct distribution of genomic and cytoplasmic materials. Its failure provokes genetically unstable states, such as tetraploidization and polyploidization, which can contribute to tumorigenesis. Aurora-B kinase controls multiple cytokinetic events, from chromosome condensation to abscission when the midbody is severed. We have previously shown that HIPK2, a kinase involved in DNA damage response and development, localizes at the midbody and contributes to abscission by phosphorylating extrachromosomal histone H2B at Ser14. Of relevance, HIPK2-defective cells do not phosphorylate H2B and do not successfully complete cytokinesis leading to accumulation of binucleated cells, chromosomal instability, and increased tumorigenicity. However, how HIPK2 and H2B are recruited to the midbody during cytokinesis is still unknown. Here, we show that regardless of their direct (H2B) and indirect (HIPK2) binding of chromosomal DNA, both H2B and HIPK2 localize at the midbody independently of nucleic acids. Instead, by using mitotic kinase-specific inhibitors in a spatio-temporal regulated manner, we found that Aurora-B kinase activity is required to recruit both HIPK2 and H2B to the midbody. Molecular characterization showed that Aurora-B directly binds and phosphorylates H2B at Ser32 while indirectly recruits HIPK2 through the central spindle components MgcRacGAP and PRC1. Thus, among different cytokinetic functions, Aurora-B separately recruits HIPK2 and H2B to the midbody and these activities contribute to faithful cytokinesis

Cytokinesis in bloodstream stage Trypanosoma brucei requires a family of katanins and spastin

Microtubule severing enzymes regulate microtubule dynamics in a wide range of organisms and are implicated in important cell cycle processes such as mitotic spindle assembly and disassembly, chromosome movement and cytokinesis. Here we explore the function of several microtubule severing enzyme homologues, the katanins (KAT80, KAT60a, KAT60b and KAT60c), spastin (SPA) and fidgetin (FID) in the bloodstream stage of the African trypanosome parasite, Trypanosoma brucei. The trypanosome cytoskeleton is microtubule based and remains assembled throughout the cell cycle, necessitating its remodelling during cytokinesis. Using RNA interference to deplete individual proteins, we show that the trypanosome katanin and spastin homologues are non-redundant and essential for bloodstream form proliferation. Further, cell cycle analysis revealed that these proteins play essential but discrete roles in cytokinesis. The KAT60 proteins each appear to be important during the early stages of cytokinesis, while downregulation of KAT80 specifically inhibited furrow ingression and SPA depletion prevented completion of abscission. In contrast, RNA interference of FID did not result in any discernible effects. We propose that the stable microtubule cytoskeleton of T. brucei necessitates the coordinated action of a family of katanins and spastin to bring about the cytoskeletal remodelling necessary to complete cell divisio

Thiolutin is a zinc chelator that inhibits the Rpn11 and other JAMM metalloproteases

Thiolutin is a disulfide-containing antibiotic and anti-angiogenic compound produced by Streptomyces. Its biological targets are not known. We show that reduced thiolutin is a zinc chelator that inhibits the JAB1/MPN/Mov34 (JAMM) domain–containing metalloprotease Rpn11, a deubiquitinating enzyme of the 19S proteasome. Thiolutin also inhibits the JAMM metalloproteases Csn5, the deneddylase of the COP9 signalosome; AMSH, which regulates ubiquitin-dependent sorting of cell-surface receptors; and BRCC36, a K63-specific deubiquitinase of the BRCC36-containing isopeptidase complex and the BRCA1–BRCA2-containing complex. We provide evidence that other dithiolopyrrolones also function as inhibitors of JAMM metalloproteases

Defects in ER–endosome contacts impact lysosome function in hereditary spastic paraplegia

Contacts between endosomes and the endoplasmic reticulum (ER) promote endosomal tubule fission, but the mechanisms involved and consequences of tubule fission failure are incompletely understood. We found that interaction between the microtubule-severing enzyme spastin and the ESCRT protein IST1 at ER–endosome contacts drives endosomal tubule fission. Failure of fission caused defective sorting of mannose 6-phosphate receptor, with consequently disrupted lysosomal enzyme trafficking and abnormal lysosomal morphology, including in mouse primary neurons and human stem cell–derived neurons. Consistent with a role for ER-mediated endosomal tubule fission in lysosome function, similar lysosomal abnormalities were seen in cellular models lacking the WASH complex component strumpellin or the ER morphogen REEP1. Mutations in spastin, strumpellin, or REEP1 cause hereditary spastic paraplegia (HSP), a disease characterized by axonal degeneration. Our results implicate failure of the ER–endosome contact process in axonopathy and suggest that coupling of ER-mediated endosomal tubule fission to lysosome function links different classes of HSP proteins, previously considered functionally distinct, into a unifying pathway for axonal degeneration.This work was supported by grants to E. Reid: UK Medical Research Council Project Grant (MR/M00046X/1), Wellcome Trust Senior Research Fellowship in Clinical Science (082381), Project Grant from United States Spastic Paraplegia Foundation, Project Grant from Tom Wahlig Stiftung, and Project Grant form UK HSP Family Group. J.R. Edgar is supported by the Wellcome Trust (grant 086598). T. Newton and G. Pearson are supported by the Medical Research Council PhD studentships (G0800117 and MR/K50127X/1). F. Berner was supported by the National Institute for Health Research Biomedical Research Centre at Addenbrooke's Hospital. B. Winner is supported by the Tom Wahlig Advanced Fellowship, the German Federal Ministry of Education and Research (01GQ113), the Bavarian Ministry of Education and Culture, Sciences and Arts in the framework of the Bavarian Molecular Biosystems Research Network and ForIPS, and the Interdisciplinary Centre for Clinical Research (University Hospital of Erlangen, N3 and F3). Cambridge Institute for Medical Research is supported by a Wellcome Trust Strategic Award (100140) and Equipment Grant (093026)