GPU Accelerated Particle Visualization with Splotch

Splotch is a rendering algorithm for exploration and visual discovery in particle-based datasets coming from astronomical observations or numerical simulations. The strengths of the approach are production of high quality imagery and support for very large-scale datasets through an effective mix of the OpenMP and MPI parallel programming paradigms. This article reports our experiences in re-designing Splotch for exploiting emerging HPC architectures nowadays increasingly populated with GPUs. A performance model is introduced for data transfers, computations and memory access, to guide our re-factoring of Splotch. A number of parallelization issues are discussed, in particular relating to race conditions and workload balancing, towards achieving optimal performances. Our implementation was accomplished by using the CUDA programming paradigm. Our strategy is founded on novel schemes achieving optimized data organisation and classification of particles. We deploy a reference simulation to present performance results on acceleration gains and scalability. We finally outline our vision for future work developments including possibilities for further optimisations and exploitation of emerging technologies.Comment: 25 pages, 9 figures. Astronomy and Computing (2014

VisIVOWeb: A WWW Environment for Large-Scale Astrophysical Visualization

This article presents a newly developed Web portal called VisIVOWeb that aims to provide the astrophysical community with powerful visualization tools for large-scale data sets in the context of Web 2.0. VisIVOWeb can effectively handle modern numerical simulations and real-world observations. Our open-source software is based on established visualization toolkits offering high-quality rendering algorithms. The underlying data management is discussed with the supported visualization interfaces and movie-making functionality. We introduce VisIVOWeb Network, a robust network of customized Web portals for visual discovery, and VisIVOWeb Connect, a lightweight and efficient solution for seamlessly connecting to existing astrophysical archives. A significant effort has been devoted for ensuring interoperability with existing tools by adhering to IVOA standards. We conclude with a summary of our work and a discussion on future developments

VisIVO - Integrated Tools and Services for Large-Scale Astrophysical Visualization

VisIVO is an integrated suite of tools and services specifically designed for the Virtual Observatory. This suite constitutes a software framework for effective visual discovery in currently available (and next-generation) very large-scale astrophysical datasets. VisIVO consists of VisiVO Desktop - a stand alone application for interactive visualization on standard PCs, VisIVO Server - a grid-enabled platform for high performance visualization and VisIVO Web - a custom designed web portal supporting services based on the VisIVO Server functionality. The main characteristic of VisIVO is support for high-performance, multidimensional visualization of very large-scale astrophysical datasets. Users can obtain meaningful visualizations rapidly while preserving full and intuitive control of the relevant visualization parameters. This paper focuses on newly developed integrated tools in VisIVO Server allowing intuitive visual discovery with 3D views being created from data tables. VisIVO Server can be installed easily on any web server with a database repository. We discuss briefly aspects of our implementation of VisiVO Server on a computational grid and also outline the functionality of the services offered by VisIVO Web. Finally we conclude with a summary of our work and pointers to future developments

Redefining the Genetic Hierarchies Controlling Skeletal Myogenesis: Pax-3 and Myf-5 Act Upstream of MyoD

AbstractWe analyzed Pax-3 (splotch)Myf-5 (targeted with nlacZ), and splotch/Myf-5 homozygous mutant mice to investigate the roles that these genes play in programming skeletal myogenesis. In splotch and Myf-5 homozygous embryos, myogenic progenitor cell perturbations and early muscle defects are distinct. Remarkablysplotch/Myf-5 double homozygotes have a dramatic phenotype not seen in the individual mutants: body muscles are absent. MyoD does not rescue this double mutant phenotype since activation of this gene proves to be dependent on either Pax-3 or Myf-5. ThereforePax-3 and Myf-5 define two distinct myogenic pathways, and MyoD acts genetically downstream of these genes for myogenesis in the body. This genetic hierarchy does not appear to operate for head muscle formation

Genetics of human neural tube defects

Neural tube defects (NTDs) are common, severe congenital malformations whose causation involves multiple genes and environmental factors. Although more than 200 genes are known to cause NTDs in mice, there has been rather limited progress in delineating the molecular basis underlying most human NTDs. Numerous genetic studies have been carried out to investigate candidate genes in cohorts of patients, with particular reference to those that participate in folate one-carbon metabolism. Although the homocysteine remethylation gene MTHFR has emerged as a risk factor in some human populations, few other consistent findings have resulted from this approach. Similarly, attention focused on the human homologues of mouse NTD genes has contributed only limited positive findings to date, although an emerging association between genes of the non-canonical Wnt (planar cell polarity) pathway and NTDs provides candidates for future studies. Priorities for the next phase of this research include: (i) larger studies that are sufficiently powered to detect significant associations with relatively minor risk factors; (ii) analysis of multiple candidate genes in groups of well-genotyped individuals to detect possible gene–gene interactions; (iii) use of high throughput genomic technology to evaluate the role of copy number variants and to detect ‘private’ and regulatory mutations, neither of which have been studied to date; (iv) detailed analysis of patient samples stratified by phenotype to enable, for example, hypothesis-driven testing of candidates genes in groups of NTDs with specific defects of folate metabolism, or in groups of fetuses with well-defined phenotypes such as craniorachischisis

Development and prevention of neural tube defects in the mouse embryo

The morphogenetic process of cranial neural tube closure was studied in normal and mutant splotch mouse embryos to identify factors contributing to the development of the neural tube defect (NTD), exencephaly. The study noted sex differences in the timing of the neurulation process and strain differences in the initiation of cranial neural tube closure, at the site termed closure 2. Splotch embryos exhibit closure 2 at a rostral level, within the forebrain region, and exencephaly results from failure of elevation of the midbrain neural folds in a proportion of homozygotes. Backcrossing the splotch mutation onto the DBA/2 background caused a caudal shift in the position of closure 2, to the midbrain region, and a reduction in the incidence of exencephaly, suggesting that altering the position of closure 2 may aid midbrain fold elevation and prevent the development of exencephaly. Whole-mount in situ hybridisation revealed that expression patterns of Pax2, Pax5 and Fgf8 remained constant within the forebrain- midbrain region, regardless of variation in the position of closure 2 in different strains. NTD in humans can be prevented by periconceptional supplementation with folic acid, although the mechanism of action of folate is unknown. The deoxyuridine (dU) suppression test was adapted for use in whole embryo culture and several genetic models of NTD were screened for defects of folate metabolism. The splotch mutant showed an abnormal dU suppression test, with excessive incorporation of 3H-thymidine. Administration of thymidine or folic acid prevented the NTD in splotch homozygotes, both in vitro and in vivo. Folic acid also ameliorated the excessive incorporation of 3H-thymidine and prevented the neural crest defects in homozygous embryos. The splotch mutant therefore appears to provide a model for folate-preventable NTD in humans

Neural tube-ectoderm interactions are required for trigeminal placode formation

Cranial sensory ganglia in vertebrates develop from the ectodermal placodes, the neural crest, or both. Although much is known about the neural crest contribution to cranial ganglia, relatively little is known about how placode cells form, invaginate and migrate to their targets. Here, we identify Pax-3 as a molecular marker for placode cells that contribute to the ophthalmic branch of the trigeminal ganglion and use it, in conjunction with DiI labeling of the surface ectoderm, to analyze some of the mechanisms underlying placode development. Pax-3 expression in the ophthalmic placode is observed as early as the 4-somite stage in a narrow band of ectoderm contiguous to the midbrain neural folds. Its expression broadens to a patch of ectoderm adjacent to the midbrain and the rostral hindbrain at the 8- to 10-somite stage. Invagination of the first Pax-3-positive cells begins at the 13-somite stage. Placodal invagination continues through the 35-somite stage, by which time condensation of the trigeminal ganglion has begun. To challenge the normal tissue interactions leading to placode formation, we ablated the cranial neural crest cells or implanted barriers between the neural tube and the ectoderm. Our results demonstrate that, although the presence of neural crest cells is not mandatory for Pax-3 expression in the forming placode, a diffusible signal from the neuroectoderm is required for induction and/or maintenance of the ophthalmic placode

Spina bifida-predisposing heterozygous mutations in Planar Cell Polarity genes and Zic2 reduce bone mass in young mice

Fractures are a common comorbidity in children with the neural tube defect (NTD) spina bifida. Mutations in the Wnt/planar cell polarity (PCP) pathway contribute to NTDs in humans and mice, but whether this pathway independently determines bone mass is poorly understood. Here, we first confirmed that core Wnt/PCP components are expressed in osteoblasts and osteoclasts in vitro. In vivo, we performed detailed µCT comparisons of bone structure in tibiae from young male mice heterozygous for NTD-associated mutations versus WT littermates. PCP signalling disruption caused by Vangl2 (Vangl2Lp/+) or Celsr1 (Celsr1Crsh/+) mutations significantly reduced trabecular bone mass and distal tibial cortical thickness. NTD-associated mutations in non-PCP transcription factors were also investigated. Pax3 mutation (Pax3Sp2H/+) had minimal effects on bone mass. Zic2 mutation (Zic2Ku/+) significantly altered the position of the tibia/fibula junction and diminished cortical bone in the proximal tibia. Beyond these genes, we bioinformatically documented the known extent of shared genetic networks between NTDs and bone properties. 46 genes involved in neural tube closure are annotated with bone-related ontologies. These findings document shared genetic networks between spina bifida risk and bone structure, including PCP components and Zic2. Genetic variants which predispose to spina bifida may therefore independently diminish bone mass