dataesr/scientific-paragraphs-categorization huggingface dataset:
Resolution in the Orbitrap was set to r ϭ 60,000. In the scan range of m/z 300 -1800, the 10 most intense peptide ions with charge states Ն2 were sequentially isolated and fragmented by higher-energy collisional dissociation (normalized collision energy of 40%). Dynamic exclusion was activated during 30 s with a repeat count of 1. Polydimethyl-cyclosiloxane (m/z of 445. 1200025) ions were used for internal calibration. Raw data files were converted with Proteome Discoverer software (version 1. 3; Thermo Fischer Scientific). Precursor mass range of 350 -5000 Da and signal-tonoise ratio of 1. 5 were the criteria used for generation of peak lists. To characterize the glycosylated peptides, the data obtained were matched automatically against a locally maintained house database with sequences of interest and contaminants (516 sequences).
MS/MS ion searches were performed using MASCOT software as described above. The tolerance of the ions was set to 5 ppm for parent and 0. 1 Da for fragment ion matches, and the instrument setting was specified as "ESI-Fourier transform ion cyclotron resonance mass spectrometry. " Peptide hits were validated when an expected score was Ͻ 0. 05. Enzymatic Assays-Assays were carried out in 96-well microplates using a Tecan Infinite M200 microplate reader (Tecan France, Lyon, France). Antitrypsin activity of OVAX was assessed by incubating trypsin (5 nM), OVAX (0 -500 nM) with or without heparin (10, 100 g/ml final concentration), or ␣1-antitrypsin (0 -500 nM) in 50 mM Hepes, 0. 1 M NaCl, pH 8, for 1 h at 37 °C prior to addition of tosyl-GPR-pNA substrate (0. 3 mM). The slope obtained after a 20 min was compared with that of the control consisting of trypsin (5 nM) and tosyl-GPR-pNA (0.
1 mg/ml. Each spectrum represents the average of three scans, with the buffer subtracted. The estimation of secondary structure content from circular dichroism measurements was performed using the CDPro software package (reference protein set selected, SPD48). Regarding thermal denaturation, the unfolding transitions curves were obtained by measuring the ellipticity at 222 nm every 0. 2 °C in a 1-mm cell. The temperature was raised from 20 to 90 °C with a 2 °C/min gradient. The denaturation temperature of unfolding (mid-transition temperature) was determined assuming that the unfolding equilibrium followed a two-state mechanism. OVAX Homology Modeling-Automated homology modeling was performed by using the SWISS-MODEL workspace  (20). All of the modeling parameters were set to the default. The OVAX three-dimensional model was built based on the 1.
95 Å resolution structure of chicken uncleaved ovalbumin (Protein Data Bank code 1OVA) as a specific template. 12 )) were investigated against Listeria monocytogenes EGD strain (L. monocytogenes), Salmonella enterica sv. Enteritidis ATCC 13076 (S. enterica sv. Enteritidis), Escherichia coli ATCC 25922 (E. coli), and Staphylococcus aureus ATCC 29740 (S. aureus) as described previously  (12). Antimicrobial activities of avian ␤-defensin 11 (10 -100 g/ml, 9271. 56 Da (  12 )), ovalbumin (0. 5-2. 2 mg/ml, 42. 9 kDa), and OVAX (0. 5-2. 2 mg/ml, 45,430 kDa) were assessed using radial diffusion assay  (12, 21). The minimum active concentration  (22)  of each molecule was calculated by linear regression to determine the minimal concentration of molecules required to observe a measurable clear zone (0.
PCR Amplification of OVAX Transcript-To further confirm the predicted sequence published by NCBI, we amplified OVAX transcript from magnum tissue. Sequencing of the PCR product of OVAX transcript revealed the presence of additional nucleotides GTACAGAAACCTAAG corresponding to a VQKPK residues (Fig. 3 ). Although some ambiguities were detected on three of the corresponding 15 nucleotides (illustrated by asterisks on Fig. 3 ), T/G, A/C, T/C/G, after six runs of sequencing, the sequence GTACAGAAACCTAAG was found to be present in the OVAX gene (gi:358485510). Interestingly, the prediction of OVAX protein sequence performed using the GeneMark tool as opposed to Gnomon (NCBI) using the gene sequence available at the NCBI server (GeneID 420898, NC_00689. 3, released on February 27, 2012) also gives this additional VQKPK peptide (supplemental Fig.
9 and 71. 2 °C, respectively (Fig. 7B ). Three-dimensional Model of OVAX-A three-dimensional structure of OVAX was modeled by homology to the x-ray structure of uncleaved ovalbumin (Protein Data Bank code 1OVA). As amino-terminal residues of OVAX (MFFYNTDFR) were not present in the ovalbumin sequence, their modeling by homology was not possible. Therefore, the resulting model of OVAX corresponds to residues 11 to 402. Fig. 8  illustrates the ovalbumin structure (Fig. 8A , left panel, purple) containing the Cys 73 -Cys 120 disulfide bond compared with the resulting OVAX model (Fig. 8B , left panel, green), including the pentapeptide VQKPK highlighted in red. The distribution of positive charges (blue) and negative charges (red) on the molecular surface of ovalbumin (Fig. 8A , right panel) and OVAX (Fig.
This pattern of expression is consistent with its preferred localization in egg white, similar to ovalbumin  (24, 30, 31). However, OVAX is believed to be a 100 times less concentrated than ovalbumin in egg white based on expression (4). The differential responsiveness of OVAX and OVAY genes compared with ovalbumin gene is supposed to contribute to their differential transcription rates and to the markedly different steady-state levels of their respective gene transcripts (4). It has been shown that the synthesis of egg white proteins depends on levels and types of steroid hormones but also on the combination of the two  (32). Assuming that the concentration of ovalbumin is ϳ50 mg/ml egg white, we estimated the concentration of OVAX to be 0. 5 mg/ml in egg white. The yield of purification of OVAX using heparin-Sepharose followed by gel filtration and biotin-Sepharose gave a concentration of ϳ0.
Considering that ovalbumin and OVAX have similar content in secondary structures and that they are highly similar in sequence, we modeled OVAX based on the three-dimensional structure of uncleaved ovalbumin. We showed that OVAX, in contrast to ovalbumin, displays a specific exposed domain with a high content of positive residues grouped together at the surface of the molecule. This domain includes the pentapeptide VQKPK, which was not predicted in the various public sequences but that we could prove by PCR amplification of the corresponding transcript and by internal Edman sequencing (data not shown). Additional studies will be initiated in future to investigate the three-dimensional structure of OVAX and to further identify the precise sequence of its heparin-binding site(s). There is increasing evidence in literature that heparin-binding proteins and peptides participate in host defense against pathogens  (11) (12) (13) (14).
Acknowledgments-We are grateful to  Maryse Mills  for excellent technical assistance. We thank  INRA ,  UE PEAT 609 , and in particular  Jean-Didier Terlot-Bryssine  ( Nouzilly, France ) for providing eggs. We thank  Dr. Anne-Christine Lalmanach  ( INRA, UMR1282 Infectiologie et Santé Publique, Nouzilly, France ) for assistance regarding antimicrobial assays. We thank  Prof. Maxwell Hincke  ( Department of Cellular & Molecular Medicine, University of Ottawa, Ottawa, Canada ) for critical reading of the manuscript and constructive remarks.
* This work was supported by the  National French Agency (OVO-mining ,  ANR-09-BLAN-0136-01 ) and the  European Commission  (" Reducing Egg Susceptibility to Contamination in Avian Production in Europe , " FOOD-CT-2006-036018 ). Author's Choice-Final version full access. □ S This article contains supplemental Figs. 1 and 2.
Statistical Analyses Transfection data are expressed as the mean 6 S. E. Paired comparisons were made using student's t-test. Data were considered statistically significant at p,0. 05. All graphical data and statistical analyses were generated with GraphPAD Prism software (Version 3. 0). Densitometric analyses were performed using computerized densitometry and Quantity OneH software (Biorad). Densitometric values for both protein band (immunoblot) and promoter CFTR amplicons (ChIP) were determined in areas of equal size and were reported in normalized arbitrary units relative to either expression of LaminA/C protein or input (nonimmunoprecipitated chromatin), respectively.
As a negative control for the C/EBPb antibody, ChIP analysis was performed on another region of the CFTR gene devoid of any C/EBPb binding motif (data not shown). To measure the functional contribution of C/EBPb towards promoter activity, reporter gene assays were performed with a CFTR promoter fused to a luciferase-coding cDNA in Beas2B cells. Overexpression of the C/EBPb-LAP construct resulted in a 3. 7 fold increase promoter activity (Figure  1B , upper panel). As expected, the truncated C/EBPb-LIP form did not activate the CFTR promoter and the observed decrease in promoter activity supported a dominant negative influence of the LIP isoform as previously reported  [2]. The functional role of C/EBPb was corroborated by the almost complete abolishment of CFTR gene promoter activation following transient co-transfections of the dominant-negative (A-C/EBP), reported to dimerize with C/ EBPb thus blocking its DNA binding (Figure  1B , upper panel).
Mutation of a C/EBPb Binding Motif Reduces the CFTR Transcriptional Activity In silico analyses (TFsearch http://www. cbrc. jp/research/db/ TFSEARCH. html, and Consite software http://asp. ii. uib. no:8090/cgi-bin/CONSITE/consite/) were performed to identify putative binding sites for the transcription factor C/EBPb. The results indicated that the CFTR minimal promoter region contains different binding motifs for C/EBPb as depicted in Figure  2A. To address whether C/EBPb influences the CFTR promoter directly or exerts its effects through an indirect activation of other proteins that do directly influence CFTR, mutagenesis reactions of the core sequence (TTNNNCAATNNN) of each C/EBPb binding site in the reporter construct were performed. As shown in Figure  2B , the construction containing a nucleotide substitution (b3M) within the consensus core of the C/EBPb motif located at the position 2111/2100, named C/EBPb3, induced a significant 80% reduction in the transcriptional activity compared to the wild-type construct.
C/EBPb Transactivation is in Part Due to Interaction between USF2 and YY1 Considering the observed cooperation between C/EBPb and USF2 and the antagonism between C/EBPb and YY1, we wondered whether YY1 had any effect on the cooperativity between C/EBPb and USF2. We firstly tested whether enforced YY1 expression antagonizes USF2 transactivation. Surprisingly, YY1 overexpression had no considerable effect on the CFTR promoter transactivation induced by USF overexpression (Figure  5A , left panel). To evaluate the effect of a combined YY1 and USF2 overexpression on the endogenous CFTR mRNA level, RT-qPCR assays were conducted. The results confirm the data obtained by gene reporter assays (Figure  5A , right panel). To explain the functional cooperation between C/EBPb and USF2, we next explored whether USF might block the action of YY1 through USF2/YY1 interaction.
We next examined the role of phosphatase inhibitor on the C/ EBPb-mediated CFTR transactivation. As observed in Figure  5B , at 10 mM NAF significantly promoted CFTR activation induced by over-expression of C/EBPb in Beas2B cells. In contrast, NAF treatment did not modify USF2 transactivation on the CFTR promoter (data not shown). Western blot assays were carried out to assess the protein expression levels under the indicated treatments. Immunoblotting with a specific anti-phospho-C/EBPb antibody showed that treatment with NAF increased the level of phosphorylated C/EBPb (Figure  6B , upper panel, left panel). Interestingly, immunoblotting also revealed that the level of endogenous CFTR protein increased after C/EBPb overexpression, reaching its maximum level upon NAF (Figure  6B , middle and left panel).
RT-qPCR assays were then performed to evaluate the effect of C/EBPb phosphorylation on the mRNA level of endogenous CFTR. The results confirmed the data obtained by gene reporter assays (Figure  6B , lower panels). Interestingly, overexpression of hLAPT235A vector induced a decrease in CFTR mRNA level. These results indicate for the first time that C/EBPb phosphorylation is involved in CFTR transcriptional activation. Phosphorylation Affects Both C/EBPb and YY1 DNA Binding Abilities and Favours YY1/USF2 Interaction Considering that C/EBPb appears to undergo phosphorylation in correlation with the acquisition of DNA-binding activity  [2] , we used ChIP assays to address the C/EBPb activity in terms of its phosphorylation status. NAF induced-phosphorylated C/EBPb was associated with both an increased C/EBPb DNA binding activity and a decrease in YY1 DNA binding in vivo (Figure  7A , left and right panels, respectively).
These data show that phosphorylation of C/EBPb increases its DNA binding ability and disrupts the YY1 occupancy of its DNA cognition site. Consequently, we investigated whether this latter effect is mediated by interactions between YY1 and USF2. Co-immunoprecipitation assays demonstrated that NAF treatment does indeed favour the interaction between YY1 and USF2 (Figure  7B ). As a positive control, immunoblotting was performed using an anti-YY1 antibody. The data presented above suggest that phosphorylation plays an important role in C/EBPb binding to DNA. These findings also demonstrate that the phosphorylation status also influences the DNA binding properties of the YY1 factor and increases the USF2/YY1 interaction.
Detector and dataset The measurements described in this paper are performed with data, corresponding to an integrated luminosity of 1. 0 fb -1 , from 7 TeV centre-of-mass pp collisions, collected with the LHCb detector during 2011. Samples of simulated events are used to estimate the efficiency of the selection requirements, to investigate possible sources of background contributions, and to model the event distributions in the likelihood fit. In the simulation, pp collisions are generated using Pythia 6. 4  [19]  with a specific LHCb configuration  [20]. Decays of hadronic particles are described by EvtGen  [21] , in which final state radiation is generated using Photos  [22]. The interaction of the generated particles with the detector and its response are implemented using the Geant4 toolkit  [23, 24]  as described in ref.
Simulated events are reweighted by these data-driven calibration curves in order to extract the hadron trigger efficiency for each mode, propagating properly the calibration-related uncertainties. Finally, the ageing of the calorimeters during the data taking period when the data sample analysed was recorded induced changes in the absolute scale of the trigger efficiencies. While this was mostly mitigated by periodic recalibration, relative variations occurred of order 10%. Since the kinematics vary marginally from one mode to the other, a systematic effect on the ratio of efficiencies arises. It is fully absorbed by increasing the trigger efficiency systematic uncertainty by 10%.
Results and conclusion The 2011 LHCb dataset, corresponding to an integrated luminosity of 1. 0 fb -1 recorded at a centre-of-mass energy of 7 TeV, has been analysed to search for the decays B 0 (s) → K 0 S h + h -. The decays B 0 s → K 0 S K ± π ∓ and B 0 s → K 0 S π + π -are observed for the first time. The former is unambiguous, while for the latter the significance of the observation is 5. 9 standard deviations, including statistical and systematic uncertainties. The decay mode B 0 → K 0 S K ± π ∓ , previously observed by the BaBar experiment  [17] , is confirmed. The efficiency-corrected Dalitz-plot distributions of the three decay modes B 0 s → K 0 S π + π -, JHEP10(2013)143 Downstream Fit Selection Trigger PID Total f s /f d B B 0 → K 0 S K ± π ∓ / B B 0 → K 0 S π + π - 5 6 3 1 8 - B B 0 → K 0 S K + K -/ B B 0 → K 0 S π + π - 1 5 3 1 6 - B B 0 s → K 0 S π + π -/ B B 0 → K 0 S π + π - 8 16 2 1 18 8 B B 0 s → K 0 S K ± π ∓ / B B 0 → K 0 S π + π - 2 5 1 1 6 8 B B 0 s → K 0 S K + K -/ B B 0 → K 0 S π + π - 1 18 3 1 18 8 Long B B 0 → K 0 S K ± π ∓ / B B 0 → K 0 S π + π - 5 10 1 1 14 - B B 0 → K 0 S K + K -/ B B 0 → K 0 S π + π - 3 20 1 1 20 - B B 0 s → K 0 S π + π -/ B B 0 → K 0 S π + π - 5 10 1 1 11 8 B B 0 s → K 0 S K ± π ∓ / B B 0 → K 0 S π + π - 3 12 2 1 13 8 B B 0 s → K 0 S K + K -/ B B 0 → K 0 S π + π - 2 22 1 1 22 8 Table  2.
Acknowledgments We express our gratitude to our colleagues in the CERN accelerator departments for the excellent performance of the LHC. We thank the technical and administrative staff at the LHCb institutes. We acknowledge support from  CERN  and from the national agencies:  CAPES ,  CNPq ,  FAPERJ  and  FINEP (Brazil) ;  NSFC (China) ;  CNRS/IN2P3  and  Region Auvergne (France) ;  BMBF ,  DFG ,  HGF  and  MPG (Germany) ;  SFI (Ireland) ;  INFN (Italy) ;  FOM  and  NWO  (The Netherlands); SCSR (Poland);  MEN/IFA (Romania) ;  MinES, Rosatom ,  RFBR  and  NRC "Kurchatov Institute" (Russia) ;  MinECo, XuntaGal and GEN-CAT (Spain) ;  SNSF  and  SER (Switzerland) ;  NAS Ukraine (Ukraine) ;  STFC (U. K. ) ;  NSF (U. S. A. ). We also acknowledge the support received from the  ERC  under  FP7. The Tier1 computing centres are supported by  IN2P3 (France) ,  KIT  and  BMBF (Germany) ,  INFN (Italy) ,  NWO  and SURF (The Netherlands),  PIC (Spain) ,  GridPP (U.
Plasmids For the transfection of MDCK with E1 genes, pCI-neo plasmid backbone containing CAV-2 E1A gene under the CMV promoter control and CAV-2 E1B gene under the control of its own promoter was used and named pCI-NeoK9  [16, 20]. E1 region corresponds to the sequence 354-3609 bp available in GenBank accession no. J04368  [20]. Additionally, pCI-NeoK9 confers neomycin resistance allowing the selection of cells after transfection. Cre recombinase expression was obtained with pZeoCre plasmid  [23]  conferring Zeocin resistance and in which Cre was cloned under the control of SV40 promoter.
Vectors CAVGFP, JBD5 and HD CAVGFP are vectors derived from CAV-2 strain Toronto A 26/61, GenBank U77082. CAVGFP  [20]  and HD CAVGFP  [25]  are E1-deleted (DE1) and HD vectors, respectively, and contain an eGFP expression cassette. JBD5 is a helper vector containing loxP flanking the packaging domains and a RSV-lacZ expression cassette  [25]. For CAVGFP and JBD5 viral stocks preparation, 150 cm 2 T-flasks with DKZeo cells at a confluency of 80-90% were infected with a MOI of 5 infectious particles (I. P. ) per cell with medium exchange at the time of infection. 40 hours post infection (hpi) cells were collected and lysed with 0. 1% (v/v) Triton 100 (Sigma-Aldrich, Steinhein, Germany) in Tris-HCl 10 mM, pH 8. The lysate was clarified by centrifugation at 3000 g during 10 min at 4uC and purified by CsCl gradients as described previously  [20].
4 mL MgCl 2 (3 mM), 2 mL forward and reverse primer (0. 3 mM), and 9. 6 mL PCR grade water. LightCycler master mix was distributed into the LightCycler capillaries (18 mL each) and either 2 mL of pCI-neoE1K9, pGAPDH (standard curves for E1 and GAPDH gene) or cDNA was added. The following LightCycler run protocol was used: denaturation program (95uC, 10 minutes); amplification and quantification program repeated 40 times (95uC for 10 seconds; 60uC (E1A gene) and 55uC (E1B 19 kDa, E1B 55 kDa) for 10 seconds; 72uC for 9 seconds); melting curve program (95uC 0 seconds; 65uC for 15 seconds; 95uC 0 seconds); and finally a cooling step to 40uC. The results obtained were analyzed with LightCycler software 4. 1 (Roche Diagnostics).
Oxidative Stress Induction and Cell Viability Assessment The susceptibility to oxidative stress injury was assessed by analyzing tert-butyl hydroperoxide induced death rates. Briefly, cells were inoculated at 0. 8610 4 cells/cm 2 in 24 well plates. At the 2 nd day of culture, when cells reached approximately 90% of confluence, tert-butyl hydroperoxide (Sigma) was added in increasing concentrations ranging from 1. 3 to 608. 4 mM. Cell viability was quantified 18 h later by negative propidium iodide (Sigma) staining and IC 50 values calculated by non-linear fitting with a 95% confidence interval using Graphpad Prism (Graphpad Software, Inc. , La Jolla, CA, USA) and same approach as the one previously described  [28].
Cre Expression in MDCK-E1 and HD CAV-2 Amplification To amplify helper-dependent (HD) CAV-2 vectors, and avoid helper-vector (HV) contamination, MDCK-E1 cells have to express Cre-recombinase. MDCK-E1#106, being the clone with the highest CAV-2 productivity (Figures  2a  and 3 ), was stably transfected with Cre recombinase gene and several clones were obtained. Cre activity was determined indirectly by infecting the subclones with AdMA19  [27] , which when cleaved in the loxP site expresses luciferase (see materials and methods section), and compared with DKCre cells (Figure  5 ). In comparison to DKCre cells, 25% presented either equal or higher Cre activity. The subclones with higher Cre activity presented lower cell growth (data not shown). To determine if high productivities are maintained after Cre expression, CAVGFP production was evaluated in five subclones with different Cre activities: Cre#2, Cre#10, Cre#19, Cre#16 and Cre#30.
This work was supported by the Fundaca ˜o para a Ciencia e a Tecnologia (FCT) -Portugal (through the projects  PTDC/BIO/69452/2006  and  PTDC/EBB-BIO/118615/2010 ) and by the  European Community 's  Seventh Framework programme  ( FP7/2007-2013)  under grant agreement nu  222992 -BrainCAV. Paulo Fernandes ,  Ana F. Rodrigues  and Helio Tomas are recipients of Ph. D. grants from  FCT  ( SFRH/BD/70810/2010 ,  SFRH/BD/48393/2008  and  SFRH/BD/79022/2011 , respectively). Eric J. Kremer  is an  Institut National de la Santeet de la Recherche Medicale (Inserm)  fellow. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
This paper shows that the problem of web services representation is crucial and analyzes the various factors that influence on it. It presents the traditional representation of web services considering traditional textual descriptions based on the information contained in WSDL files. Unfortunately, textual web services descriptions are dirty and need significant cleaning to keep only useful information. To deal with this problem, we introduce rules based text tagging method, which allows filtering web service description to keep only significant information. A new representation based on such filtered data is then introduced. Many web services have empty descriptions. Also, we consider web services representations based on the WSDL file structure (types, attributes, etc. ). Alternatively, we introduce a new representation called symbolic reputation, which is computed from relationships between web services.
Moreover, the number of host that offer available web services, through specific engines like Axis 2 , is significantly increasing. Consequently, the WSDL files describing services can be crawled and parsed automatically. Such files contain different kind of information like textual descriptions, simple and/or complex types, attributes, etc. (see Section 3 for more details). Contrary to simulation based approaches, real world services inherit the complexity of the real world. With the increasing number of published Web services providing similar functionalities, it's very tedious for a service consumer to make decision to select the appropriate one according to her/his needs. Therefore mechanisms and techniques are required to help consumers to make the best choice. In addition, web services use natural language descriptions (ambiguity of sentences), they are multi-languages and cross-domains.