dataesr/scientific-paragraphs-categorization huggingface dataset:
Statistical analysis Database management and statistical analyses were carried out using SPSS (Statistical Package for the Sociological Sciences), version 21. 0. Results are presented as means ± SD, or percentages. Means were compared using Student test. The significance threshold was set at 5 % (p < 0. 05). The impact of the mutated alleles and genotypes was identified by a Chui square test. Our study escapes from Hardy-Weinberg model for two major reasons: The first is that our sampling is a selective sampling (patients with genetic risk factor and healthy controls unexposed to genetic cardiovascular factors). The second is the dominance of the consanguinity (union between first cousins) in the Tunisian population.
Acknowledgments We thank so much  Dr. Mohamed AYED ,  Dr. Lamjed BOUSLAMA , and  Mrs. M'birika BEN ALI  (English teacher) for their help to do this work. We thank also the staff of the  Biochemistry Laboratory  and the  Cardiology Department of Farhat Hached Hospital of Sousse  and the members of the platform of the  Biotechnology Center of Borj Cedria, Tunisia  for their valuable contribution in this work.
(2000)  recommendations. Furthermore, its DNA was extracted and partial sequencing of the rrs (16s rRNA) and secY (pre-protein translocase SecY protein) was proceeded employing the primers F (5′-ATGCCGAT-CATTTTTGCTTC-3′) and R (5′-CGTCCCTTAATTTTAGACTTCTTC-3′)  (Ahmed et al. 2006) , and LA (5′-GGCGGCGCGTCTTAAACATG-3′) and LB (5′-TTCCCCCCATTGAGCAAGATT-3′)  (Merien et al. 1992). Sequencing was performed at the Genotyping of Pathogens and Public Health Platform (Institut Pasteur, Paris, France). All molecular epidemiological data were stored and analyzed with Bionumerics software (Version 6. 5; Applied-Maths, Belgium). Genotyping was also performed by multiple-locus variable-number tandem repeat analysis (MLVA) using the loci VNTR4, VNTR7, and VNTR10 as described by  Salaün et al. (2003). Based on the partial sequencing of gene secY, PFGE was conducted using Not I restriction enzyme  (Herrmann et al.
RESULTS AND DISCUSSION Nine out of the fifteen (60 %) tested sera were reactive, five of them against serogroup Australis (sv. Bratislava) with titres of 400. Four were reactive against serogroup Icterohaemorrhagiae (sv. Copenhageni) with titres of 100. PCR was able to detect leptospiral DNA in the urine of 7/15 (46. 7 %) swine, being four seroreactive and three seronegative. One urine sample, from a 4 year-old male, yielded pure culture of leptospires, named SU5 (GenBank KP263059). SU5 was serogrouped as Australis (titre 1,600), and partial sequencing of secY and rrs genes characterized it as Leptospira interrogans genomospecies. Based on secY nucleotide sequences (Fig. 1 ), this isolate showed similarity to reference strain Balico (sv Australis) isolated from humans in Australia, and to reference strain Jez_Bratislava (sv Bratislava), isolated from a hedgehog in Slovakia, as well as to strain 200801323 (sv Bratislava) isolated from human in Martinique.
Patients will be stratified by region, previous therapy and ECOG status. The primary endpoint is overall survival (OS). Assuming proportional hazards, a two-tailed level of significance of 0. 05 and 80% power will be applied. Additionally this design assumes an exponential survival distribution to detect a HR = 0. 792 in favor of the DCVAC/PCA group. Registration number NCT02111577, EudraCT number 2012-002814-38.
Stained cells were analyzed on a MACSQuant cytometer (Miltenyi). The data files were analyzed using FlowJo (Tree Star, Inc. ). MPO activity. Myeloperoxidase (MPO), a marker of polymorphonuclear neutrophil primary granules, was determined in colonic tissues, according to a modified method of Bradley et al. (27). Segments of colon were homogenized in potassium phosphate buffer (KPB; 50 mM, pH 6. 0). Endogenous catalases were inhibited by three cycles of freezing and thawing. Cell pellets were resuspended in the detergent hexadecyltrimethylammonium bromide buffer (0. 5% in KPB; Sigma) to release MPO from the primary granules. After sonication on ice, suspensions were centrifuged at 13,000 rpm for 15 min at 4°C, and supernatants were assayed spectrophotometrically for MPO activity and protein content.
(28). Each of three histological parameters was scored from 0 to 4, based on the severity of inflammation, the extent of inflammation, and epithelium damage, and correlated to the percentage of tissue involved. The histological score was the sum of these parameters. Statistical analyses. Statistical evaluation of differences between the experimental groups was determined by using one-way analysis of variance, followed by a Bonferroni post test (which allows comparison of all pairs of groups). All tests were performed with GraphPad Prism 5. 03 (GraphPad Software, Inc. , San Diego, CA). All data are presented as means Ϯ the standard errors of the mean (SEM). A P value of Ͻ0. 05 was considered significant.
ACKNOWLEDGMENTS We sincerely thank research team members for helpful discussions and suggestions,  Ambre Riba  ( V. Theodorou 's team) for technical assistance, and the members of the  Platform of Experimental Histopathology (INSERM/UPS US006 CREFRE) at Toulouse Purpan, France. This work was supported by research grant  ANR-13-BSV1-0028-01  from the  Agence Nationale de la Recherche  and the platform Aninfimip, an  EquipEx ('Equipement d'Excellence')  supported by the  French government  through the  Investments for the Future program  ( ANR-11-EQPX-0003 ). T. S. was supported by the  Agence Nationale de la Recherche (ANR-.
For the 3 samples that were positive by MZN staining but negative by nested PCR, the presence of inhibitors was confirmed using a PCR inhibition test. The overall prevalence of Cryptosporidium spp. infection obtained by MZN and/or nested PCR was 11% (Table  1 ), and children <5 years old showed a higher rate of Cryptosporidium spp. infection of 44. 5%  (8/18). The characteristic clinical data of Cryptosporidium spp. infected patients is shown in Table  1. The PCR products of the 15 positive samples were successfully sequenced on both strands. The sequences obtained showed over 99% identity with the reference sequences. Among the isolates, 10 (66. 7%) were identified as C. hominis, while the remaining 5 (33. 3%) were identified as C. parvum. Cryptosporidium spp. other than C. parvum and C. hominis were not found.
gov/ BLAST/) using the basic local alignment search tool (BLAST) program. Specimens genotyped as C. parvum or C. hominis were further subtyped using a second nested PCR, which amplifies a fragment of the 60 kDa glycoprotein (gp60) gene, as described previously [21]. The amplified DNA fragments were purified, sequenced, and analyzed by alignment of gp60 sequences with reference sequences retrieved from GenBank using the program ClustalX (http://www. clustal. org/). C. parvum and C. hominis gp60 subtypes were named by counting the number of trinucleotide repeats of TCA (A), TCG (G), and TCT (T) and the ACATCA repeat (R) after the trinucleotide repeats [11]. The nucleotide sequences obtained in this study were deposited in GenBank under accession numbers KM215739 to KM215766.
ACKNOWLEDGMENTS We thank  Jean-ReneHuynh ,  S. Baumgartner ,  H. Ashe , and  I. Ando  for reagents and stocks and  R. Delanoue  and  C. Geminard  for critical reading of the manuscript. Work in S. N. laboratory is supported by the '' Centre National de la Recherche Scientifique,'' the ''Ministere de la Recherche et de l'Enseignement Superieur,'' the ''Agence Nationale de la Recherche '' (program  ANR-09-BLAN-0113 ), the '' Association Francaise contre les Myopathies ,'' and LABEX SIGNALIFE (no. ANR-11-LABX-0028-01 ).
These data indicate that SiO 2 NPs increase alveolar-capillary barrier with minor alterations of the vascular endothelium. Labelled or unlabelled 15 nm SiO2 NPs were characterised in different media. The hydrodynamic size of agglomerates and polydispersity index (PdI) of suspensions were determined by DLS and their charge by measuring the zeta-potential (Z-pot). Endotoxin detection was performed by the Limulus amebocyte Assay (LAL) method following manufacturer's instructions. Detection limit of the assay was 0. 1 EU/ml and concentration of NPs in the assay was 0. 4 mg/ml. Pre-exposure to silica NPs enhances mice mortality during P. a-induced pneumonia Considering that SiO 2 NPs interact with AM and AEC, two cell types driving lung defence against P. a, we studied the consequences of NP exposure in a mouse model of P.
In contrast to our study, Cu NPs and carbon nanotubes induced significant inflammation 'per se' , which may have impair bacterial clearance by mechanisms independent of AM phagocytic activity. In addition Shvedova and co-workers have shown that pre-exposure of AMs to carbon nanotubes reduces their phagocytic/killing capacity toward L. monocytogenes  [19]. By contrast, we show here that pre-exposure of AM to SiO 2 NPs did not modify P. a killing nor P. a-mediated cytokine release by AM. Discrepancies between our data and others could be due to the composition of NPs, size, shape, concentration, exposure times or the cell type used  [15, 17, 19, 31]. In line with our data, Witasp and co-workers showed that internalisation of mesoporous silica particles (>100 nm of diameter) 18 h after infection, number of neutrophils and concentration of cytokines (A), IgM and albumin (B) were measured in BALs (2 ml).
Bioluminescence measurements Photon emission of the luminescent bacteria in the lungs of infected mice was measured using the IVIS 100 system (Xenogen Corp. , Alameda, CA) as previously described  [29]. To achieve detection in C57BL/6 J mice, chest hair was removed with a depilatory agent. 15 h after infection, the mice were anesthetized under 2. 5 % isoflurane inhalation and photon emission is acquired by a charge couple device (CCD) camera. A digital falsecolor photon emission image was generated. The analysis was then performed with the Living Image software (Xenogen Corp. , Alameda, CA), by defining a constant region of interested ( ROI) corresponding to the surface of the chest encompassing the whole lung region. The results are expressed as number of photons/sec/ROI. Co-exposure of alveolar macrophages to SiO 2 NPs and P.
Flow cytometry BAL fluids from FITC-SiO 2 NPs treated mice (5 mg/kg) were recovered 5 h post NP instillation and cells were centrifuged at 4°C (2000 rpm, 10 min). Cells were washed in 1% BSA-PBS buffer and incubated with monoclonal anti-mouse CD16/32 antibody (BD Biosciences) for 15 min on ice to block Fc receptors. Cells were then stained with a rat anti-mouse F4/80 antibody coupled to eFluor450 (clone: BM8, eBioscience) and a hamster anti-mouse CD11c antibody coupled to APC (clone: HL3, BD Biosciences) (30 min, at 4°C in 1% BSA-PBS). After washing, fluorescence associated with cells was acquired in a CyAn ADP cytometer (Beckman Coulter). Analysis of data was performed using FlowJo program. FITC positive cells were only found in the macrophage gate (named R1 in FSC/SSC dot plot). To detect FITC positive cells from negative cells, BAL fluids from non-treated mice were obtained and treated in parallel to determine the autofluorescence signal (characteristic of AM) from R1 population.
Acknowledgments We thank investigators from the platform of ' Imagerie Dynamique' at Institut Pasteur  for their support in the bioluminiscence studies and the Apotome microscopy (special thanks go to Emmanuelle Perret). We also thank  Professor Ruben Ramphal  for providing us the bioluminescent P. a PAK strain. This work was supported by the  INSERM ,  Université Paris 7 Diderot  and  ANSES EST 2010/2/79  project.
Acknowledgments We would like to thank  Helena Kulikova  and  Lenka Zitkova  for excellent administrative support and  Martin Kindl  for help with graphical images. We are grateful to  Tatiana Kostalova  for the valuable advices and help with dissection of salivary glands and thank  Claire Garros  for valuable comments and discussion. Culicoides nubeculosus were supplied from a National Capability grant by the  Biotechnology and Biological Sciences Research Council  to The  Pirbright Institute. This study was partially funded by the  COST (European Cooperation in Science and Technology) Action TD1303 EurNegVec  and  COST-CZ LD14076  and by the  EU  project  FP7-HEALTH-2010-261504  EDENext. This paper is catalogued by the EDENext Steering Committee as EDENext358 (http://www. edenext. eu).
In different murine disease models, including asthma  [33, 34] , arthritis  [35] [36] [37] , myocarditis  [38] , pathogen clearance  [39] , tumor immunity  [40, 41] , and IBD  [42] [43] [44] , absence of CD69 expression deeply affected the disease course by exacerbating the disease severity in most cases. Because CD69 is highly expressed by memory T cells and regulatory T cells in the gut, which play an essential role (i) in eliminating pathogens and (ii) in regulating potential harmful immune responses in the gut, we consider CD69 not as a simple activation marker but as a molecule involved in the regulation of immune responses at mucosal sites. We searched http://www. ncbi. nlm. nih. gov/pubmed database (search terms CD69 or inflammation or inflammatory bowel disease) for the studies on CD69 and intestinal inflammation.
Microarray data analysis Microarray data have been obtained as described  (Regnault et al. , 2009). Briefly six E-IAA negative and three E-IAA positive animals at 5 weeks of age have been used for isolation of PLN. One E-IAA negative sample (A36. 4) was grouped according to its gene expression profiles together with the E-IAA positive group of animals, by clustering analysis. Therefore the final number of positive samples analyzed together contained four samples and the negative control group five samples. The MG_U74A_version 2 arrays (Affymetrix, Santa Clara, Ca) were used containing 12,486 probe sets. All the initial data, from which we extracted this novel analysis, were deposited in NCBI's Gene Expression Omnibus  (Edgar et al. , 2002)  with the GEO series accession number GSE15582 (http://www.
ncbi. nlm. nih. gov/geo/query/acc. cgi?acc= GSE15582). Data were processed as previously described  (Regnault et al. , 2009). Briefly, raw data were preprocessed using the Robust Multiarray Averaging (RMA) normalization method for individual probe values and for summary values for each probe set. Statistical analysis of samples was performed using the Local Pool Error (LPE) test, an algorithm dedicated to small number of samples  (Jain et al. , 2003)  and the P values adjusted by the Benjamini-Hochberg multiple testing correction. The dChip software was used for hierarchical clustering with Euclidean distance and average as a linkage method  (Li and Wong, 2001). Heatmap was constructed by taking into consideration the gene expression patterns  (Pelizzola et al. , 2006). Functional and cellular localization annotations were evaluated by using the DAVID NIAID/NIH online annotation tool (http://david.
niaid. nih. gov/david/), the Panther classification system (http://www. pantherdb. org/) and the KEGG database (http://www. genome. jp/ kegg/). Annotation terms were obtained taking into consideration the significance of P values for GO terms  (Dennis et al. , 2003). The GO Browser tool of NetAffx was used to confirm independently the GO annotations. Further evaluations of functional annotations and pathways were performed using the Ingenuity Pathway Analysis software (Ingenuity Systems) and the iReport data mining system (http://www. ingenuity. com/products/ireport). For functional predictions of gene networks and gene co-expression search the GeneMANIA Cytoscape plug-in online tool (http://www. genemania. org/) has been used  (Warde-Farley et al. , 2010).
Chromosomal enrichment Chromosomal enrichment was performed using the DAVID NIAID/ NIH online annotation tool (http://david. niaid. nih. gov/david/) for chromosome localization. P-values for each chromosome output were calculated according to the number of E-IAA differentially expressed transcripts attributed to each chromosome versus i) the number of unique genes found to be expressed to all nine PLN samples with known chromosome localizations (P calls, gene n°= 560; 529 genes on chromosomes) (Table  S3 ), considered to be PLN expressed at least in our conditions and ii) the total number of genes present on the MG_U74A_version 2 arrays (10,913 unique genes, 10,417 genes with known chromosome localizations). Chromosomal loci for insulin dependent diabetes identified by genetic analysis in mouse (Idd), in rat (Iddm) and in human (IDDM) were retrieved by search of the literature and from the T1D Database (http://www.
Immunostaining for flow cytometry After trypsinization, living cells were incubated for 1 h at 4°C with anti-ICAM-1 primary antibody (clone 2D5 produced locally as previously described)  (20). After centrifugation, pellets were re-suspended in 50 µl of RPMI 1640 containing the secondary antibody coupled with FITC (goat anti-mouse-FITC purchased from Jackson ImmunoResearch, Philadelphia, PA, USA) and left to incubate for 30 min at 4°C. After centrifugation, cells were re-suspended in 500 µl of RPMI 1640 + 10% FBS and fluorescence was measured with a FACSCAN flow cytometer (Becton Dickinson, Le Pont-De-Claix, France). Results were analyzed using WinMDI software.
Nuclei were labeled with Hoechst 33342. Cells were observed with an epi-fluorescence microscope (Carl Zeiss AxioImager) with the pseudo-confocal module APOTOME. Images were analyzed with ImageJ software (ImageJ, NIH, USA). For co-localization experiments, the Pearson's correlation coefficient (Rr) and the Mander's overlap coefficient (R) were calculated using the ImageJ co-localization plugin after background subtraction.
Western blotting After reaching confluence, HCMEC/D3 cells were trypsinized and lysed for 30 min on ice with a Tris-HCl 50 mM, pH 7. 5, NaCl 150 mM buffer containing 1% NP40 or 0. 1% SDS (as mentioned in each case) and a protease inhibitor cocktail (Sigma-Aldrich). Whole cell extracts were submitted to SDS-PAGE (10% acrylamide gels), blotted onto polyvinylidene difluoride membranes and stained with a rabbit polyclonal primary antibody raised against TLR4 (Santa Cruz) or actin (Sigma-Aldrich) and a secondary goat anti-rabbit antibody coupled with peroxidase (Invitrogen). Bands were quantified with BioRad Image Lab software.
This molecule targets GAL1 as does Anginex at a site away from the CBS and attenuates lactose binding to the lectin by a threefold  43  illustrating that a threefold difference in affinity can be relevant to an in vivo situation. This process is not an on/off switch of GAL1 carbohydrate specificity; rather, we conclude that there is a fine tuning of the affinity of these interactions depending on the cell needs. This is an original and unforeseen way for a cell to modify the equilibria of the GAL1/glycan lattice besides changes in protein glycosylation or lectin expression. To shed light on the in vivo situation, modulation of GAL1 binding at the surface of OP9 stromal cells in presence or in absence of l5-UR has been investigated by flow cytometry. No significant variations have been observed (data not shown).
Protein concentration was calculated by measuring the absorbance at 280 nm using a nanodrop ND1000 (Thermoscientific) and titrations were carried out on a MicroCal ITC200 microcalorimeter (GE Healthcare). Each experiment was designed using a titrant concentration (carbohydrate molecule in the syringe) set 10 to 15 times the analyte concentration (protein in the cell) and generally using 17 injections of 2. 3 ml at 25 °C (see Supplementary Table  1  for details). A first small injection (generally 0. 2 ml) was included in the titration protocol to remove air bubble trapped in the syringe prior titration. l5-UR or l5-UR  peptide was added to the same concentration in both cell and syringe samples for tripartite titration experiments. Integrated raw ITC data were fitted to a one-site non-linear least squares fit model using the MicroCal Origin plugin as implemented in Origin 9.
The c rbohydrate-binding activity of GAL1 has been determined by recording 2D 1 H,  15  N HSQC spectra of  15  N-labelled GAL1 free or bound to l5-UR  after addition of increasing amount of carbohydrate (0. 1, 0. 2, 0. 3, 0. 4, 0. 8 and 2 mM). The CSPs for each resonance were calculated using the equation: Dd obs ¼ [Dd HN 2 þ (Dd N 2 /25)] 1/2 , where DdHN and DdN are, respectively, the proton and nitrogen chemical shifts variation of each residue  51. STD NMR experiments. 1 H and  13  C NMR resonances assignment of LNnT have been performed using 2D 1 H,  13  C HSQC, 2D 1 H,  13  C HSQC-TOCSY, 2D 1 H, 1 H-TOCSY and 2D 1 H, 1 H-COSY experiments. The 1D STD (128 scans, 32 K data points) and the 2D STD TOCSY experiments (mixing time 60 ms with 512 increments of 128 scans each) were performed using a 100:1 LNnT/GAL1 and a 100:1:3 LNnT/GAL1/l5-UR  molar ratio samples, with a 1 mM concentration of LNnT.
Slides were scanned in a GenePix 4300A scanner under normal acquisition mode using GenePix Pro 7. 2. The background-subtracted median fluorescence for the three spots per lectin were averaged and log 2 transformed. Signal averages less than 1,000 for both channels were excluded. Lectins with a signal-to-noise ratio o5 for more than 30% of the total data were also excluded. This left 67 of the 107 lectins printed on the array. Each channel was then median normalized per array and the log 2 ratio of sample over reference was calculated.
Acknowledgements We would like to thank the  Consortium for Functional Glycomics  for providing the Glycan Arrays and the  Core H at Emory University  for the screenings. The raw glycan array data are posted on the CFG website (www. functionalglycomics. org). We thank  Annie Boned  for her help in cell cultures. This work was supported by the  Centre National de la Recherche Scientifique (CNRS) -PEPS 2010 Grant to L. E. L. K. M. acknowledges support from the  Margaret and Herman Faculty Award Fund.
Patients HIV-1-infected individuals receiving ART at Bamrasnaradura Infectious Diseases Institute, Nonthaburi, Thailand were recruited in this study. 10 All participants signed an informed consent form. Most of these HIV patients received a combination of d4T, 3TC, and nevirapine. LA was defined as the presence of fat loss at any site of the body (face, arms, legs, or buttocks). To qualify, the alteration had to be recognized by both the patient and the physician. 11 Aliquots of whole blood were collected from each patient and stored at -20°C until DNA extraction. Serum cholesterol and triglyceride (TG) data were obtained from the patients' records of serum biochemical tests. The study was approved by the institutional ethical committees at the Bamrasnaradura Infectious Diseases Institute and Department of Disease Control, Ministry of Public Health, Thailand.
GWAS The study enrolled 49 HIV patients who developed LA within 2 years of treatment, along with 92 patients who did not develop fat loss at any site of the body (face, arms, legs, or buttocks) (non-LA) even after at least 4 years of treatment (Table  1 ). The DNA samples from these patients were genotyped with Illumina Human660W-Quad v1 Beadarrays testing for 578,525 raw autosomal SNPs. All genotypes were determined using BeadStudio software (version 3. 2. 23) following the manufacturer's standard recommendations. From these SNPs, 458,071 passed the quality control (QC) criteria of genotyping rate >95%, with minor allele frequency >0. 01, and with a Hardy-Weinberg p-value > 10 -5. Individuals with genotyping success rates below 80%, with gender discrepancy (based on the genotyped sex chromosomes using PLINK  12  ) and genetic outliers [using a principal components approach (PCA) calculated by  EIGENSTRAT 13  ] were excluded.