dataesr/scientific-paragraphs-categorization huggingface dataset:
As stated previously, the Laser system emits light pulses also during physics runs. Since all calorimeter channels are exposed to Laser light at the same time, the statistics is sufficient to determine the reconstructed time to a precision of about 1 ns. Because the Laser is not synchronised with the LHC clock, the reconstructed time in each channel must be corrected for the Laser phase using the Laser TDC information t TDC. In addition, the time of arrival of the Laser pulses to the TileCal PMTs is different from the signal time for particles from collisions, due to the path followed by the Laser light. Therefore, in a channel perfectly timed-in for physics, the Laser pulse arrives at a different time  12   for each channel as a function of the luminosity block. Since this time is supposed to be close to zero, the monitoring program searches for differences from this baseline.
Impact of the timing jumps on the calorimeter time performance The overall impact of the timing jump corrections on the reconstructed time was studied with jet collision data using a sub-set of the 2012 data representing 1. 3 fb -1 of collected physics data. To reduce the impact of the time dependence on the reconstructed energy, the channel energy was required E channel > 4 GeV, but still read out with high gain. 13 he results are displayed in figure  20 , where the reconstructed time is shown for all calorimeter channels with and without the timing jump corrections. While the Gaussian core, corresponding to channels (and events) not affected by timing jumps, remains basically unchanged, the timing jump corrections significantly reduce the number of events in the tails. The overall RMS is improved by 9 % (from 0.
Conclusions The Laser system is one of the three calibration systems of the ATLAS Tile Calorimeter. It is a key component for monitoring and calibrating the 9852 TileCal photomultipliers and their associated readout electronics. The Laser calibration constant f Las applied on each channel has been regularly measured, with a statistical uncertainty at the level of 0. 3 %, and is one ingredient in the TileCal cell energy reconstruction. Comparing these correction factors with the ones derived with the Cesium calibration system, a good compatibility between them was found and the systematic uncertainty on the Laser calibration constants is estimated to be 0. 2 % for the long barrel modules and 0. 5 % for the extended barrel modules. The Laser system has also been used to monitor the timing of the TileCal front-end electronics during physics runs, allowing to correct for timing jumps provoked by mis-configuration resulting from power supplies trips.
During a median follow-up of 8. 9 years (range 6 months to 29 years), 167 patients metastasised. Ten specimens of adjacent normal breast tissue from breast cancer patients or normal breast tissue from women undergoing cosmetic breast surgery were used as sources of normal RNA. For immunofluorescence, samples were obtained from patients who had undergone a mastectomy without preliminary therapy, at the N. N. Blokhin Russian Cancer Research Center. The Institutional Review Board of N. N. Blokhin Russian Cancer Research Center approved the project and all patients, who were involved in the study, gave written informed consents that their samples could be used for investigational purposes. Data were analysed anonymously. All potential participants who declined to participate or otherwise did not participate were eligible for treatment (if applicable) and were not disadvantaged in any other way by not participating in the study.
Untreated human samples from colorectal adenomas (n ¼ 43), primary colorectal carcinomas (n ¼ 67), liver metastasis (n ¼ 27) and matched normal adjacent colorectal tissues (n ¼ 103) were collected and analysed at the Institut Curie. The origin of breast cell lines and conditions for their culture were described previously  (Maire et al, 2013). qRT-PCR. Total RNA was extracted from normal and malignant breast samples using the acid-phenol guanidium protocol. RNA quality was determined by electrophoresis through agarose gels. The gene-specific primers were chosen with the assistance of the Oligo 6. 0 programme (National Biosciences, Colorado Springs, CO, USA). dbEST and nr databases were scanned to confirm the specificity of the nucleotide sequences chosen for the primers and the absence of single-nucleotide polymorphisms.
ACKNOWLEDGEMENTS We thank  Caroline Lecerf  and  Celine Baldeyron  for performing RPPA experiments,  Vera Dugina  for advice on immunofluorescence of biopsies,  Virginie Maire  for providing protein extracts from the breast cell lines,  Nadia Kurochkina  for help with western blots and  Dominique Lallemand  for critically reading the manuscript. This work was supported by  ANR-11-BSV8-0010-02  to A. G. ,  Institut National du Cancer  ( INCA_6521 ) to A. G. and I. B. ,  Fondation ARC pour la Recherche sur le Cancer  ( PGA120140200831 ) to A. G. and I. B. , the  Comitedepartemental des Hauts-de-Seine de la Ligue Nationale Contre le Cancer  to I. B. , an educational fellowship  SP-6587. 2013. 4  to M. E. L. and RFBR grant  14-04-91056CNRC_a  to A. Y. A. The RPPA platform is supported by  Canceropole Ile-de-France.
cells undergoing adipogenesis. The data show the genes that were coexpressed with FBN1, including genes coding for other connective tissue proteins and the proteases that modify them and for the transcription factors that control their expression. Data analysed were derived from datasets available in the public domain and the analysis highlights the utility of such datasets for ongoing analysis and hence reduction in the use of experimental animals. & 2016 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons. org/licenses/by/4. 0/). The mouse analysis used data from a previous study  [3]  in which RNA was extracted from epididymal adipose tissue from 28 inbred mouse strains. Mice were 25 weeks of age. RNA from two to four mice per strain was pooled The human analysis used data from the FANTOM5 project  [4].
Acknowledgements The  Roslin Institute  (MRD and KMS) is supported by  Institute Strategic Programme Grants  from the  Biotechnology and Biological Resources Council (BBSRC)  of the United Kindgom, grant numbers  BB/J004235/1  and  BB/J004316/1. EA was supported by a  Research Grant  from  MEXT  to the  RIKEN Center for Life Science Technologies. PA and ID receive support from the  Swedish Research Council.
M ycobacteriophages are viruses that specifically infect a my- cobacterial host. Mycobacterium smegmatis is currently a host to Ͼ6,900 phages  (1). Phage populations are numerous and diverse: it is estimated that 10 31 different particles exist  (2, 3). Based on shared gene content, these phages are divided into 26 clusters, with singletons that do not belong to any clusters. The genomes in this report establish cluster S, one of the smaller clusters, making up 0. 2% of current known phages and currently containing no subclusters  (1, 2). Marvin was the first discovered cluster S phage and remained a singleton until the discovery of two similar phages: MosMoris and Gattaca (see GenBank nucleotide sequence accession numbers in Table  1 ). One of the phages, Marvin, was isolated in Radnor, PA; the other two, MosMoris and Gattaca, were isolated in Milbridge, ME  (1) , from soil samples in different years by direct plating.
Once isolated, the phages form plaques on a lawn of M. smegmatis mc 2 155. Plaques were picked, purified, and amplified, and the DNA was extracted. Marvin, MosMoris, and Gattaca were sequenced at the Joint Genome Institute (Sanger sequencing) and the Pittsburgh Bacteriophage Institute (Ion Torrent and Illumina sequencing), respectively. After sequencing, reads were assembled using Newbler and Consed. The DNA Master software (http://cobamide2. bio. pitt. edu) was used to annotate the genomes with an integrated approach using Glimmer, GeneMark, BLAST, and Shine-Dalgarno positioned weight scores. Phamerator (4) and HHpred (5) were used to predict the function of hypothetical proteins. These cluster S mycobacteriophages display a morphotype of Siphoviridae and have an average GϩC content of 64.
The genes are syntenic and tightly packed, except for the region where the direction of transcription changes. MosMoris and Gattaca both contain insertions of an HNH endonuclease in the minor tail genes that is absent in Marvin. In addition, Marvin has a putative insertion with low coding potential near 9,500 bp that is not seen in the other two cluster members. The S cluster's closest relationships by nucleotide similarity map are two singletons, Wildcat and Sparky (2), two phages with low similarity to other phages. The closest clusters to the S cluster are the M and T clusters. Accession number(s). The whole-genome sequences have been deposited at GenBank under the accession numbers listed in Table  1.
ACKNOWLEDGMENTS We declare that there is no conflict of interest regarding the publication of this paper. Payton Pedersen  contributed to the annotation of MosMoris but could not be reached upon finalization of the manuscript. This research was conducted under the  Howard Hughes Medical Institute Science Education Alliance Phage Hunters   Advancing Genomics and Evolutionary Science (SEA-PHAGES) program. In-kind support was provided by The  University of Maine at Machias. Information technology and server support were provided by the  University of Maine at Machias IT , and grant administration was kindly provided by the  Mount Desert Island Biological Laboratory  and by  Sherrie Sprangers  and  Thomas Potter  at  U. Maine Machias.
Columns were eluted with 0. 1 M LiNO 3 at 0. 5 mL/min. Solvent was filtered through 0. 1 lm filter unit (Millipore, Billerica, MA). A dn/dC value of 0. 155 mL/g was used. The sample (0. 5 g/L) (200 lL) was injected after filtration on 0. 45 lm unit filter (Millipore, Billerica, MA). The collected data were analyzed using the ASTRA 6. 0. 6. 13 software package from Wyatt Technology (Goleta, CA).
DPPH and NO scavenging activity Several data suggest that HA is able to scavenge free radical in solution. The explanation of the antiradical activity of HA may be due to the presence of carboxylic groups, which may interact with the free radicals  (Campo et al. 2004 ). The DPPH scavenging capacity of LMWHA was higher than HA (Figure  4(A) ). The highest inhibition rate was 39. 02, 58. 28 and 93. 06% for HA, LMWHA and AA, respectively, at the concentration of 1 mg/mL. Scavenging activity of HA and LMWHA against NO was presented in Figure  4 (B). At a concentration of 1 mg/mL, the scavenging ability was 41. 05, 56. 98 and 85. 75% for HA, LMWHA and AA, respectively. Also the IC 50 of HA and LMWHA were determined from the plot of inhibition percentage. LMWHA exhibited stronger radical scavenging activity and the IC 50 value of HA and LWMHA was 1.
Formation of the contractile myofibril of the skeletal muscle is a complex process which when perturbed leads to muscular dystrophy. Herein, we provide a mRNAseq dataset on three different zebrafish mutants affecting muscle organization during embryogenesis. These comprise the myosin folding chaperone unc45b (unc45bÀ /À ), heat shock protein 90aa1. 1 (hsp90aa1. 1À /À ) and the acetylcholine esterase (acheÀ /À ) gene. The transcriptome analysis was performed in duplicate experiments at 72 h post-fertilization (hpf) for all three mutants, with two additional times of development (24 hpf and 48 hpf) for unc45bÀ /À. A total of 20 samples were analyzed by hierarchical clustering for differential gene expression. The data from this study support the observation made in  Etard et al. (2015)  [1] (http://dx.
Data source location Institute of Toxicology and Genetics, Karlsruhe Institute of Technology, Campus Nord, Eggenstein-Leopoldshafen, Germany Data accessibility Data are available with this article, and via NCBI's GEO accession number GEO: GSE74202 (through the direct link http://www. ncbi. nlm. nih. gov/geo/query/ acc. cgi?acc ¼GSE74202).
Value of the data This dataset comprises the transcriptome analysis of the zebrafish mutants unc45b À / À, hsp90aa1. 1 À / À and ache À / À during embryonic development. It provides the list of regulated genes and associated Gene Ontology analysis of skeletal muscle cells under cellular stress and defective chaperoning activity. It is anticipated that this dataset can serve as a reference point for other analysis on myopathies. hsp90a À / À 1 hsp90a À / À 72 hpf Mutant hsp90a À / À at 72 hpf , replicate 1 hsp90a À / À 2 hsp90a À / À 72 hpf Mutant hsp90a À / À at 72 hpf , replicate 2 unc45b À / À 1_24 hpf unc45b À / À 24 hpf Mutant unc45b À / À at 24 hpf, replicate 1 unc45b À / À 1_48 hpf unc45b À / À 48 hpf Mutant unc45b À / À at 48 hpf, replicate 1 unc45b À / À 1_72 hpf unc45b À / À 72 hpf Mutant unc45b À / À at 72 hpf, replicate 1 unc45b À / À 2_24 hpf unc45b À / À 24 hpf Mutant unc45b À / À at unc45b þ / À ; unc45b þ / þ 24 hpf Wild type siblings of unc45b À / À at 24 hpf, replicate 1 unc45b WT 1_48 hpf unc45b þ / À ; unc45b þ / þ 48 hpf Wild type siblings of unc45b À / À at 48 hpf, replicate 1 unc45b WT 1_72 hpf unc45b þ / À ; unc45b þ / þ 72 hpf Wild type siblings of unc45b À / À at 72 hpf, replicate 1 unc45b WT 2_24 hpf unc45b þ / À ; unc45b þ / þ 24 hpf Wild type siblings of unc45b À / À at 24 hpf, replicate 2 unc45b WT 2_48 hpf unc45b þ / À ; unc45b þ / þ 48 hpf Wild type siblings of unc45b À / À at 48 hpf, replicate 2 unc45b WT 2_72 hpf unc45b þ / À ; unc45b þ / þ 72 hpf Wild type siblings of unc45b À / À at 72 hpf, replicate 2.
Data This data consists of 20 high-throughput sequencing samples of unc45b À / À at 24 hpf, 48 hpf and 72 hpf, as well as acheÀ / À and hsp90aa1. 1 À / À and their respective siblings at 72 hpf (n ¼2 for each genotype and stage) generated on an Illumina HiSeq 1000  [1]. The data are deposited under the Gene Expression Omnibus (GEO) number GEO: GSE74202 at http://www. ncbi. nlm. nih. gov/geo/query/acc. cgi?acc ¼GSE74202.
Expression data were normalized using the regularized log transformation method from DESeq2. 200 mL Trizol (Thermo Fisher) after removing fish water with a pipette. The extraction of total RNA was performed as described in the manufacturer's protocol, with the modification that an additional extraction with chloroform was performed before precipitation with isopropanol. Total RNA pellets were resuspended in 50 ml RNase-free water (Ambion). RNA integrity was checked by loading about 100 ng total RNA on a RNA6000 Nanochip using an Agilent 2100 Bioanalyser (Agilent Technologies). Samples showed no sign of degradation (RNA index number49). The list of genotypes and stages of samples collected in the study are provided in Table  1.
Library preparation, quality control and data analysis Sequencing libraries were prepared with the TruSeq RNA Library Prep kit v2 (Illumina), following manufacturer's protocol. Briefly, total RNA (1 mg) for each sample was used for poly(A) RNA selection hsp90a-/-2 using poly-dT coated magnetic beads followed by fragmentation. First strand cDNA synthesis was performed with the Superscript II (Thermo Fisher) using random hexamer primers. The cDNA fragments were subjected to end-repair and dA-tailing, and finally ligated to specific double stranded barcoded adapters. Libraries were amplified by 12 cycles of PCR. The quality and concentration of the resulting sequencing libraries were determined on a DNA1000 chip using an Agilent 2100 Bioanalyser (Agilent Technologies). The mRNASeq libraries were sequenced at 7 pM on a HiSeq1000 device (Illumina) to generate 50 bp paired-end reads.
2 ). The hierarchical clustering of 24 selected genes involved in various biological processes such muscle development and neurogenesis shows specific patterns of expression depending on the genotype (Fig. 3 ). The differential gene expression of the binary comparisons between the mutant and the respective controls were made with the R package DESeq2. A MA plot for the analysis of the differential gene expression between control and unc45b À / À embryos at 72 hpf is shown (Fig. 4 ). For each gene, the mean expression was plotted against the logarithm of the fold change. Genes with significant deregulation are shown in red (adjusted p-value o0. 01). Zebrafish genes up-regulated or down-regulated in the comparative analysis between the unc45bÀ /À and control larvae at 72 hpf (adjusted p-valueo0.
01) were subjected to pathway enrichment analysis. 1 were obtained from Ensembl Compara  [8]  via Biomart (release 75)  [9]. Then unique Ensembl human or zebrafish identifiers were used to obtain their associated Gene Ontology terms using the R package biomaRt  [10]. Finally, enrichment of GO terms was assessed by computing p-values from a Fisher's exacttest (gene universe set to 18,000). A comparison between the top enriched GO terms with human and zebrafish genes up-regulated in the unc45bÀ /À compared to control at 72 hpf is given in Tables  2  and 3. The data show that pathways involved in muscle physiology and hypoxia are enriched in the set of genes up-regulated in unc45bÀ /À compared to the control at 72 hpf.
48-0. 84; P=0. 001). There was no heterogeneity in the effects of cangrelor on MI based on index diagnosis (Table  II  in the online-only Data Supplement). The distribution of peak biomarkers in patients treated with cangrelor and clopidogrel is shown in Figure  I  in the online-only Data Supplement. Patients randomized in CHAMPION PHOENIX who had an MI as defined with the definition in the original protocol that was based on the second universal definition of MI were at increased risk of death at 30 days even after adjustment for potential confounders (adjusted OR, 4. 60; 95% CI, 2. 49-8. 51; P<0. 001; Figure  3 ). MI also was associated with increased risk of death at 30 days when using the SCAI definition (adjusted OR, 8. 85; 95% CI, 4. 29-18. 25; P<0. 001) and when considering only MI that resulted in a peak CK-MB ≥10 times the ULN (adjusted OR, 9.
Because the majority of ischemic events that occurred during the first 48 hours of CHAMPION PHOENIX were type 4a MIs related to PCI, these data highlight the need for adequate and effective antithrombotic therapies. 8 0] [11]  The oral P2Y 12 inhibitors currently used in practice have a delayed onset of action and do not result in antiplatelet effects for ≈60 to 120 minutes. 12, 13 The delay in the onset of antiplatelet effect is a particular problem in patients such as those treated with ad hoc PCI after elective coronary angiography or in patients undergoing PCI for acute coronary syndrome in whom little antiplatelet effect may be present during the actual PCI. Furthermore, some medications such as those used during moderate sedation may delay the onset of antiplatelet effects. 14 ntravenous glycoprotein IIb/IIIa inhibitors are available and can be used in patients undergoing PCI who are not pretreated with an oral P2Y 12 inhibitor.
These data should be considered in light of some limitations. First, these analyses are post hoc analyses that were not prespecified. As a result, they represent sensitivity analyses that supplement the findings from the predefined, primary results of the trial. Accordingly, the MI definition based on the SCAI criteria was not prospectively adjudicated and was obtained retrospectively. This trial assessed MI using the universal definition that was available at that time the trial was designed and did not use the third universal definition that is now available. In addition, CK-MB was systematically collected in the CHAMPION PHOENIX trial, whereas the second and third universal definitions of MI prefer cardiac troponin. Bleeding was investigator reported and was not adjudicated,   ORIGINAL RESEARCH ARTICLE 731 although post hoc adjudication did not qualitatively change the safety profile.
Testing in first-degree relatives unaffected by cancer of an individual with a very suggestive family history of HBOC was also proposed if it was impossible to test the relatives affected with cancer. Patients had not undergone specific BRCA testing before the multigene panel analysis. For each patient, informed consent for genetic analysis was obtained. General information was entered into the Oncogene database, an in-house database generated via Clinsight, used for the management of Oncogenetic consultations and is registered with the Commission Nationale Information et Liberté (CNIL). This database includes demographic data, self-identified personal and family histories of cancer, and follow-up for patients with a pathogenic or probably pathogenic mutation in a gene predisposing for HBOC.
Variant classification Sequence variants and large insertions and deletions were classified according to the American College of Medical Genetics (ACMG) guidelines for variant interpretation  [49]. Variants were classified as pathogenic or probably pathogenic if they conferred a truncating, initiation codon or splice donor/acceptor effect, if functional data demonstrated an effect on protein function relevant to a disease phenotype, or if pathogenicity was otherwise demonstrated in the published literature. If no functional data were available, missense, silent, and intronic variants were classified as variants of uncertain significance (VUS), benign or probably benign based on allele frequency in dbSNP or the Exome Variant Server [see URL]. In the genes other than BRCA, a variant was considered for review it was classified as pathogenic, probably pathogenic or discordant according to ClinVar.
Data analysis The incidence of pathogenic and probably pathogenic mutations was calculated for each gene, and the clinical presentations were discussed based on demographic information and clinical history. Genes were grouped in four categories: highly penetrant genes (BRCA1, BRCA2, STK11, MLH1, MSH2, MSH6, EPCAM, PMS2, CDH1, TP53, PTEN), moderately penetrant/HR pathway (BARD1, CHEK2, RAD51C, BRIP1, RAD50, MRE11A, PALB2, ATM), one candidate gene for HBOC (PIK3CA) and other cancer-spectrum predisposing genes (APC, MUTYH, PTCH1, PTCH2, SUFU). Pathogenic mutations in the latter category, in the absence of cancer within the disease spectrum known for these genes in the patient or family members, were considered incidental findings. The impact of having two predisposing genes was particularly studied.
Rationale and objective: Lung cancer is the most commonly diagnosed cancer and the leading cause of cancer death in the world. In Central and South America lung cancer is now one of most frequent cancers and the leading cause of cancer-related death in both sexes. We describe patterns and trends in lung cancer incidence and mortality in Central and South America and give a brief overview of the current status of tobacco control measures based on the most recent MPOWER report. Methods: We obtained regional and national-level incidence data from 48 population-based cancer registries in 13 countries and cancer deaths from the WHO mortality database for 18 countries. We estimated world population age-standardized incidence and mortality rates per 100,000 person-years. Incidence of lung cancer by histological subtype were only available from high-quality population-based cancer registries for the period 2003-2007.
Material and methods In the present analysis lung cancer was coded as C33-34 according to 10th edition of the International Classification of Diseases (ICD-10). Until the year 1991, the underlying cause of death was categorized according to the ICD 9th revision however all data were converted to the ICD 10th revision. The data sources and methods are described in detail in an earlier article in this issue. In brief, we obtained regional and national-level incidence data from 48 population-based cancer registries in 13 countries and cancer deaths from the World Health Organization mortality database for 18 countries. We estimated age-standardized incidence (ASR) and mortality (ASMR) rates per 100,000 person-years using the direct method and the World standard population, as proposed by Doll et al.