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

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

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

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

The transcriptional response to Salmonella infection in swine

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

Value-creating boards: diversity and evolved processes

This qualitative study is based on 47 interviews with board members of UK listed companies and reveals that value-creating boards have two main characteristics: a diversity of perspective and evolved board processes. The findings of the study show that the critical attributes of boardroom diversity are members’ culture/nationality, functional background, and gender diversity. Value-creating boards also have evolved processes, such as an objective nomination process, periodic evaluations of the board and its members, and their ability to work as a team. The paper contributes to the Strategic Leadership theory, and other role-effectiveness theories. It makes a significant contribution to existing literature on board diversity and value creation by suggesting that board diversity needs a broader definition – more than mere demographic attributes of directors, and board processes, – to improve boards’ ability to create value for organizations. The paper also contributes to praxis by presenting evidence of the impact of board diversity on value creations and suggesting the most critical aspects of value-creating boards. The findings may also guide the formulation of legislation for improving corporate governance by defining diversity more broadly

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

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

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

Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection

Citation: Koltes, J. E., Fritz-Waters, E., Eisley, C. J., Choi, I., Bao, H., Kommadath, A., . . . Reecy, J. M. (2015). Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection. Bmc Genomics, 16, 13. doi:10.1186/s12864-015-1635-9Background: Previously, we identified a major quantitative trait locus (QTL) for host response to Porcine Respiratory and Reproductive Syndrome virus (PRRSV) infection in high linkage disequilibrium (LD) with SNP rs80800372 on Sus scrofa chromosome 4 (SSC4). Results: Within this QTL, guanylate binding protein 5 (GBP5) was differentially expressed (DE) (p < 0.05) in blood from AA versus AB rs80800372 genotyped pigs at 7,11, and 14 days post PRRSV infection. All variants within the GBP5 transcript in LD with rs80800372 exhibited allele specific expression (ASE) in AB individuals (p < 0.0001). A transcript re-assembly revealed three alternatively spliced transcripts for GBP5. An intronic SNP in GBP5, rs340943904, introduces a splice acceptor site that inserts five nucleotides into the transcript. Individuals homozygous for the unfavorable AA genotype predominantly produced this transcript, with a shifted reading frame and early stop codon that truncates the 88 C-terminal amino acids of the protein. RNA-seq analysis confirmed this SNP was associated with differential splicing by QTL genotype (p < 0.0001) and this was validated by quantitative capillary electrophoresis (p < 0.0001). The wild-type transcript was expressed at a higher level in AB versus AA individuals, whereas the five-nucleotide insertion transcript was the dominant form in AA individuals. Splicing and ASE results are consistent with the observed dominant nature of the favorable QTL allele. The rs340943904 SNP was also 100 % concordant with rs80800372 in a validation population that possessed an alternate form of the favorable B QTL haplotype. Conclusions: GBP5 is known to play a role in inflammasome assembly during immune response. However, the role of GBP5 host genetic variation in viral immunity is novel. These findings demonstrate that rs340943904 is a strong candidate causal mutation for the SSC4 QTL that controls variation in host response to PRRSV.Additional Authors: Lunney, J. K.;Liu, P.;Carpenter, S.;Rowland, R. R. R.;Dekkers, J. C. M.;Reecy, J. M