1,232 research outputs found

    Development of FTK architecture: a fast hardware track trigger for the ATLAS detector

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    The Fast Tracker (FTK) is a proposed upgrade to the ATLAS trigger system that will operate at full Level-1 output rates and provide high quality tracks reconstructed over the entire detector by the start of processing in Level-2. FTK solves the combinatorial challenge inherent to tracking by exploiting the massive parallelism of Associative Memories (AM) that can compare inner detector hits to millions of pre-calculated patterns simultaneously. The tracking problem within matched patterns is further simplified by using pre-computed linearized fitting constants and leveraging fast DSP's in modern commercial FPGA's. Overall, FTK is able to compute the helix parameters for all tracks in an event and apply quality cuts in approximately one millisecond. By employing a pipelined architecture, FTK is able to continuously operate at Level-1 rates without deadtime. The system design is defined and studied using ATLAS full simulation. Reconstruction quality is evaluated for single muon events with zero pileup, as well as WH events at the LHC design luminosity. FTK results are compared with the tracking capability of an offline algorithm.Comment: To be published in the proceedings of DPF-2009, Detroit, MI, July 2009, eConf C09072

    The Evolution of FTK, a Real-Time Tracker for Hadron Collider Experiments

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    We describe the architecture evolution of the highly-parallel dedicated processor FTK, which is driven by the simulation of LHC events at high luminosity (1034 cm-2 s-1). FTK is able to provide precise on-line track reconstruction for future hadronic collider experiments. The processor, organized in a two-tiered pipelined architecture, execute very fast algorithms based on the use of a large bank of pre-stored patterns of trajectory points (first tier) in combination with full resolution track fitting to refine pattern recognition and to determine off-line quality track parameters. We describe here how the high luminosity simulation results have produced a new organization of the hardware inside the FTK processor core.Comment: 11th ICATPP conferenc

    The Agricultural Genome to Phenome Initiative (AG2PI): creating a shared vision across crop and livestock research communities

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    Predicting phenotype from genotype is a central challenge in biology. By understanding genomic information to predict and improve traits, scientists can address the challenges and opportunities of achieving sustainable genetic improvement of complex, economically important traits in agriculturally relevant species. Converting the enormous, recent technical advances in all areas of genomics and phenomics into sustained and ecologically responsible improvements in food and fuel production is complex. It will require engaging agricultural genome to phenome (G2P) experts, drawing from a broad community, including crop and livestock scientists and essential integrative disciplines (e.g., engineers, economists, data and social scientists). To achieve this vision, the USDA NIFA-funded project inaugurating the Agricultural Genome to Phenome Initiative (AG2PI) is working to: Develop a cohesive vision for agricultural G2P research by identifying research gaps and opportunities; advancing community solutions to these challenges and gaps; and rapidly disseminating findings to the broader community. Towards these ends, this AG2PI project is organizing virtual field days, conferences, training workshops, and awarding seed grants to conceive new insights (details at www.ag2pi.org). Since October 2020, more than 10,000 unique participants from every inhabited continent have engaged in these activities. To illustrate AG2PI’s scope, we present survey results on agricultural G2P research needs and opportunities, highlighting opinions and suggestions for the future. We invite stakeholders interested in this complex but critical effort to help create an optimal, sustainable food supply for society and challenge the community to add to our vision for future accomplishments by a fully actualized AG2PI enterprise

    Development of New Placental and Fetal Expressed Sequence Tags (EST) for Gene Discovery in Pig Reproduction

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    One major problem that has high economic impact on pig reproduction is the unexplained loss of potential porcine conceptuses during the first month of gestation. To better understand when and how these losses occur, it is imperative to investigate the underlying genetic regulatory mechanisms. We have recently initiated a large-scale cDNA sequencing project to provide molecular information regarding the genes expressed in female reproductive tissues. cDNA libraries are planned for ovary, hypothalamus, pituitary, placenta, uterus, and several stages of embryonic development. Sequence information will also be highly useful in developing sequence-tagged sites for physical mapping and developing comparative links between the human, mouse, and pig genome maps. We have previously reported the creation of two cDNA libraries, porcine fetal (day 20), and conceptus (day 17). Sequencing of these libraries produced 220 Expressed Sequence Tags (ESTs), with 180 sequences analyzed by clustering algorithms, and 139 clusters identified within these sequences. We now report the creation of two more libraries from porcine fetal (day 45) and placental tissues. The day 45 fetal library has 971,150 independent clones (average insert: 1.4 kb), whereas the placental library has 1,320,000 independent clones. Initial sequencing of the fetal library has produced 119 ESTs (81 clusters), whereas we have obtained 1411 ESTs (1056 clusters) from the placental library. After clustering all sequences thus far obtained, we have identified 1,233 unique clusters. Sequences obtained in this project will be deposited into Genbank dbEST, and all comparative homolog

    Addition of Thirteen Genes to the Porcine Comparative Gene Map Reveals New Regions of Conserved Synteny

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    Thirteen genes were mapped to the porcine genome by using either linkage mapping of the PiGMaP families (eight genes) or typing of a porcine somatic cell hybrid panel (12 genes). The genes were chosen from interesting locations in the human genome. The physical gene assignments to pig chromosomes (SSC) with corresponding human chromosome (HSA) locations include the following: FGF7 (HSA15), MADH4 (HSA18), and MC4R (HSA18) to SSC1, RXRB (HSA6), and SSTR1 (HSA14) to SSC7, UCP1 (HSA4) to SSC8, PGR (HSA11) to SSC9, TTN (HSA2) and ANT1 (HSA4) to SSC15, GRIA1 (HSA5) to SSC16, AR (HSA-X), and GRIA3 (HSA-X) to SSC-X. Additionally, CD59 (HSA11) was linkage mapped to SSC2. The majority of the assignments confirm results from bidirectional chromosome painting (4). A rearrangement in gene order was detected within the region of correspondence between SSC1 and HSA15. Two assignments were made that were not expected from the painting results (MC4R and GRIA1) and one assignment of a gene from a region where the painting study was not informative (ANT1)

    The transcriptional response to Salmonella infection in swine

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    The porcine response to infection with Salmonella is the result of differential expression of host-specific genes. To characterize these alterations in gene expression, functional genomic analyses were performed on swine tissues following experimental inoculation of the pigs with Salmonella enterica serovars Choleraesuis and Typhimurium. Suppression subtractive hybridization and quantitative real-time RT-PCR revealed that the transcriptional profiles of the porcine response to the swine-adapted strain (Choleraesuis) and the non-host-adapted strain (Typhimurium) exhibit unique differences

    Gene expression in intestinal mucosal biopsy specimens obtained from dogs with chronic enteropathy

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    Objective—To characterize mucosal gene expression in dogs with chronic enteropathy (CE). Animals—18 dogs with CE and 6 healthy control dogs. Procedures—Small intestinal mucosal biopsy specimens were endoscopically obtained from dogs. Disease severity in dogs with CE was determined via inflammatory bowel index scores and histologic grading of biopsy specimens. Total RNA was extracted from biopsy specimens and microchip array analysis (approx 43,000 probe sets) and quantitative reverse transcriptase PCR assays were performed. Results—1,875 genes were differentially expressed between dogs with CE and healthy control dogs; 1,582 (85%) genes were downregulated in dogs with CE, including neurotensin, fatty acid–binding protein 6, fatty acid synthase, aldehyde dehydrogenase 1 family member B1, metallothionein, and claudin 8, whereas few genes were upregulated in dogs with CE, including genes encoding products involved in extracellular matrix degradation (matrix metallopeptidases 1, 3, and 13), inflammation (tumor necrosis factor, interleukin-8, peroxisome proliferator–activated receptor γ, and S100 calcium-binding protein G), iron transport (solute carrier family 40 member 1), and immunity (CD96 and carcinoembryonic antigen–related cell adhesion molecule [CEACAM] 18). Dogs with CE and protein-losing enteropathy had the greatest number of differentially expressed genes. Results of quantitative reverse transcriptase PCR assay for select genes were similar to those for microchip array analysis. Conclusions and Clinical Relevance—Expression of genes encoding products regulating mucosal inflammation was altered in dogs with CE and varied with disease severity. Impact for Human Medicine—Molecular pathogenesis of CE in dogs may be similar to that in humans with inflammatory bowel disease

    Gene expression in intestinal mucosal biopsy specimens obtained from dogs with chronic enteropathy

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    Objective—To characterize mucosal gene expression in dogs with chronic enteropathy (CE). Animals—18 dogs with CE and 6 healthy control dogs. Procedures—Small intestinal mucosal biopsy specimens were endoscopically obtained from dogs. Disease severity in dogs with CE was determined via inflammatory bowel index scores and histologic grading of biopsy specimens. Total RNA was extracted from biopsy specimens and microchip array analysis (approx 43,000 probe sets) and quantitative reverse transcriptase PCR assays were performed. Results—1,875 genes were differentially expressed between dogs with CE and healthy control dogs; 1,582 (85%) genes were downregulated in dogs with CE, including neurotensin, fatty acid–binding protein 6, fatty acid synthase, aldehyde dehydrogenase 1 family member B1, metallothionein, and claudin 8, whereas few genes were upregulated in dogs with CE, including genes encoding products involved in extracellular matrix degradation (matrix metallopeptidases 1, 3, and 13), inflammation (tumor necrosis factor, interleukin-8, peroxisome proliferator–activated receptor γ, and S100 calcium-binding protein G), iron transport (solute carrier family 40 member 1), and immunity (CD96 and carcinoembryonic antigen–related cell adhesion molecule [CEACAM] 18). Dogs with CE and protein-losing enteropathy had the greatest number of differentially expressed genes. Results of quantitative reverse transcriptase PCR assay for select genes were similar to those for microchip array analysis. Conclusions and Clinical Relevance—Expression of genes encoding products regulating mucosal inflammation was altered in dogs with CE and varied with disease severity. Impact for Human Medicine—Molecular pathogenesis of CE in dogs may be similar to that in humans with inflammatory bowel disease
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