b tagging in ATLAS and CMS

Many physics signals presently studied at the high energy collision experiments lead to final states with jets originating from heavy flavor quarks. This report reviews the algorithms for heavy flavor jets identification developed by the ATLAS and CMS Collaborations in view of the Run2 data taking period at the Large Hadron Collider. The improvements of the algorithms used in 2015 and 2016 data analyses with respect to previous data taking periods are discussed, as well as the ongoing developments in view of the next years of data taking. The measurements of the performance of the algorithms on data as well as the dedicated techniques for the identification of heavy flavor jets in events with boosted topologies are also presented. Finally, the effectiveness of heavy flavor jet identification in the complex environment expected during the high luminosity LHC phase is discussed.Comment: 6 pages, Proceeding for the Fifth Annual Large Hadron Collider Physics (LHCP2017) conferenc

Whole genome assembly of a natto production strain Bacillus subtilis natto from very short read data

<p>Abstract</p> <p>Background</p> <p><it>Bacillus subtilis </it>natto is closely related to the laboratory standard strain <it>B. subtilis </it>Marburg 168, and functions as a starter for the production of the traditional Japanese food "natto" made from soybeans. Although re-sequencing whole genomes of several laboratory domesticated <it>B. subtilis </it>168 derivatives has already been attempted using short read sequencing data, the assembly of the whole genome sequence of a closely related strain, <it>B. subtilis </it>natto, from very short read data is more challenging, particularly with our aim to assemble one fully connected scaffold from short reads around 35 bp in length.</p> <p>Results</p> <p>We applied a comparative genome assembly method, which combines <it>de novo </it>assembly and reference guided assembly, to one of the <it>B. subtilis </it>natto strains. We successfully assembled 28 scaffolds and managed to avoid substantial fragmentation. Completion of the assembly through long PCR experiments resulted in one connected scaffold for <it>B. subtilis </it>natto. Based on the assembled genome sequence, our orthologous gene analysis between natto BEST195 and Marburg 168 revealed that 82.4% of 4375 predicted genes in BEST195 are one-to-one orthologous to genes in 168, with two genes in-paralog, 3.2% are deleted in 168, 14.3% are inserted in BEST195, and 5.9% of genes present in 168 are deleted in BEST195. The natto genome contains the same alleles in the promoter region of <it>degQ </it>and the coding region of <it>swrAA </it>as the wild strain, RO-FF-1.</p> <p>These are specific for γ-PGA production ability, which is related to natto production. Further, the <it>B. subtilis </it>natto strain completely lacked a polyketide synthesis operon, disrupted the plipastatin production operon, and possesses previously unidentified transposases.</p> <p>Conclusions</p> <p>The determination of the whole genome sequence of <it>Bacillus subtilis </it>natto provided detailed analyses of a set of genes related to natto production, demonstrating the number and locations of insertion sequences that <it>B. subtilis </it>natto harbors but <it>B. subtilis </it>168 lacks. Multiple genome-level comparisons among five closely related <it>Bacillus </it>species were also carried out. The determined genome sequence of <it>B. subtilis </it>natto and gene annotations are available from the Natto genome browser <url>http://natto-genome.org/</url>.</p

ヒドウジョウミャク オ オンゾン シタ ヒオンゾン ビソクスイ セツジョジュツ ショウカカン ニュウセン シュジュツゴ ノ ヒゾウ ノ タイセキ ヘンカ

Aim: There is a paucity of information about changes in splenic volume after surgery. The aim of this study was to investigate postoperative changes in splenic volume（SV）and the factors influencing SV after spleen-preserving distal pancreatectomy（SPDP）with conservation of the splenic artery and vein （CSAV）, and after surgery of the digestive tract and breast.Methods: We investigated 113 patients who underwent SPDP with CSAV（n=7）, breast surgery （n=24）, colorectal surgery（n=45）, distal gastrectomy（n=27）and total gastrectomy（n=10）. SV changes were determined for three years after surgery using volumetry based on computed tomographic imaging, and splenic vein diameter changes after SPDP with CSAV were also determined.Results: Splenic vein diameter after SPDP with CSAV did not change during 3 years. SV did not change significantly during 3 years after SPDP with CSAV and distal gastrectomy. After breast and colorectal surgery, and total gastrectomy, SV was decreased.Conclusions: Postoperative SV changes differed according to the type of surgery. SV did not change significantly during 3 years after SPDP with CSAV

Murasaki: A Fast, Parallelizable Algorithm to Find Anchors from Multiple Genomes

BACKGROUND: With the number of available genome sequences increasing rapidly, the magnitude of sequence data required for multiple-genome analyses is a challenging problem. When large-scale rearrangements break the collinearity of gene orders among genomes, genome comparison algorithms must first identify sets of short well-conserved sequences present in each genome, termed anchors. Previously, anchor identification among multiple genomes has been achieved using pairwise alignment tools like BLASTZ through progressive alignment tools like TBA, but the computational requirements for sequence comparisons of multiple genomes quickly becomes a limiting factor as the number and scale of genomes grows. METHODOLOGY/PRINCIPAL FINDINGS: Our algorithm, named Murasaki, makes it possible to identify anchors within multiple large sequences on the scale of several hundred megabases in few minutes using a single CPU. Two advanced features of Murasaki are (1) adaptive hash function generation, which enables efficient use of arbitrary mismatch patterns (spaced seeds) and therefore the comparison of multiple mammalian genomes in a practical amount of computation time, and (2) parallelizable execution that decreases the required wall-clock and CPU times. Murasaki can perform a sensitive anchoring of eight mammalian genomes (human, chimp, rhesus, orangutan, mouse, rat, dog, and cow) in 21 hours CPU time (42 minutes wall time). This is the first single-pass in-core anchoring of multiple mammalian genomes. We evaluated Murasaki by comparing it with the genome alignment programs BLASTZ and TBA. We show that Murasaki can anchor multiple genomes in near linear time, compared to the quadratic time requirements of BLASTZ and TBA, while improving overall accuracy. CONCLUSIONS/SIGNIFICANCE: Murasaki provides an open source platform to take advantage of long patterns, cluster computing, and novel hash algorithms to produce accurate anchors across multiple genomes with computational efficiency significantly greater than existing methods. Murasaki is available under GPL at http://murasaki.sourceforge.net

ABCA1 gene-physical activity interaction for HDL-C

Few studies have investigated the interactions between HDL-C-related SNPs identified by genome-wide association (GWA) study and physical activity (PA) on HDL-C. First, we conducted a sex-stratified GWA study in a discovery sample (2,231 men and 2,431 women) and replication sample (2,599 men and 3,109 women) to identify SNPs influencing log-transformed HDL-C in Japanese participants in the baseline survey of the Japan Multi-Institutional Collaborative Cohort Study. We also replicated previously reported HDL-C-related SNPs in a combined (discovery plus replication) sample (4,830 men and 5,540 women). We then analyzed the interactions of the HDL-C-related SNPs with PA on HDL-C. The sex-stratified GWA analyses identified 11 and 10 HDL-C-related SNPs in men and women as targets for an interaction analysis. Among these, only one interaction of ABCA1 rs1883025 with PA was statistically significant in men, after Bonferroni correction [P-interaction = 0.001 (α = 0.05/21 = 0.002)]. The per-major-allele (C allele) increase in log-transformed HDL-C was lost in men with low PA (β = 0.008) compared with those with medium (β = 0.032) or high PA (β = 0.034). These findings suggest that the benefit of carrying a C allele of ABCA1 rs1883025 on enhancing HDL-C may be attenuated in inactive men

Body mass index and colorectal cancer risk : A Mendelian randomization study

Traditional observational studies have reported a positive association between higher body mass index (BMI) and the risk of colorectal cancer (CRC). However, evidence from other approaches to pursue the causal relationship between BMI and CRC is sparse. A two-sample Mendelian randomization (MR) study was undertaken using 68 single nucleotide polymorphisms (SNPs) from the Japanese genome-wide association study (GWAS) and 654 SNPs from the GWAS catalogue for BMI as sets of instrumental variables. For the analysis of SNP-BMI associations, we undertook a meta-analysis with 36 303 participants in the Japanese Consortium of Genetic Epidemiology studies (J-CGE), comprising normal populations. For the analysis of SNP-CRC associations, we utilized 7636 CRC cases and 37 141 controls from five studies in Japan, and undertook a meta-analysis. Mendelian randomization analysis of inverse-variance weighted method indicated that a one-unit (kg/m2) increase in genetically predicted BMI was associated with an odds ratio of 1.13 (95% confidence interval, 1.06-1.20; P value <.001) for CRC using the set of 68 SNPs, and an odds ratio of 1.07 (1.03-1.11, 0.001) for CRC using the set of 654 SNPs. Sensitivity analyses robustly showed increased odds ratios for CRC for every one-unit increase in genetically predicted BMI. Our MR analyses strongly support the evidence that higher BMI influences the risk of CRC. Although Asians are generally leaner than Europeans and North Americans, avoiding higher BMI seems to be important for the prevention of CRC in Asian populations

Stroke genetics informs drug discovery and risk prediction across ancestries

Daniel Strbian työryhmän jäsenenä Correction; Early Access DOI: 10.1038/s41586-022-05492-5 Early Access: NOV 2022Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.Peer reviewe

Tumour resistance in induced pluripotent stem cells derived from naked mole-rats

The naked mole-rat (NMR, Heterocephalus glaber), which is the longest-lived rodent species, exhibits extraordinary resistance to cancer. Here we report that NMR somatic cells exhibit a unique tumour-suppressor response to reprogramming induction. In this study, we generate NMR-induced pluripotent stem cells (NMR-iPSCs) and find that NMR-iPSCs do not exhibit teratoma-forming tumorigenicity due to the species-specific activation of tumour-suppressor alternative reading frame (ARF) and a disruption mutation of the oncogene ES cell-expressed Ras (ERAS). The forced expression of Arf in mouse iPSCs markedly reduces tumorigenicity. Furthermore, we identify an NMR-specific tumour-suppression phenotype—ARF suppression-induced senescence (ASIS)—that may protect iPSCs and somatic cells from ARF suppression and, as a consequence, tumorigenicity. Thus, NMR-specific ARF regulation and the disruption of ERAS regulate tumour resistance in NMR-iPSCs. Our findings obtained from studies of NMR-iPSCs provide new insight into the mechanisms of tumorigenicity in iPSCs and cancer resistance in the NMR