dataesr/scientific-paragraphs-categorization huggingface dataset:
supported by the European Union's Seventh Framework Programme (EU FP7); STOPPAM contract number: 200889. STOPPAM I (Benin) and STOPPAM II (Tanzania). The FSP/MISAME study (Burkina Faso) was funded by Nutrition Third World, The Belgium Ministry of Development, Flemish Interuniversity Council, and French Ministry of Development. The ECHO study (Democratic Republic of the Congo) was funded by the Department of Epidemiology, University of North Carolina Chapel Hill, UNC Gillings School of Global Public Health. The iLiNS-DYAD (Ghana) trial was funded by a grant to the University of California, Davis from the Bill & Melinda Gates Foundation. EMEP was partly supported by the Malaria in Pregnancy (MiP) Consortium, which is funded through a grant from the Bill & Melinda Gates Foundation to the Liverpool School of Tropical Medicine, UK and partly by the US Centers for Disease Control and Prevention (CDC), Division of Parasitic Diseases and Malaria through a cooperative agreement with Kenya Medical Research Institute (KEMRI), Center for Global Health Research (CGHR), Kisumu, Kenya.
The IPTp-MON study (Kenya) was partly supported by the MiP Consortium, which is funded through a grant from the Bill & Melinda Gates Foundation to the Liverpool School of Tropical Medicine, UK and partly supported by the CDC. The ITN project (Kenya) was funded by the US Agency for International Development. The Special Health Support Fund from the Royal Netherlands Embassy (Nairobi, Kenya) provided additional support for the study of the impact of ITN in pregnancy. The Kisumu study (Kenya) was funded by US Agency for International Development (grants AOT0483-PH1-2171 and HRN-A-00-04-00010-02) and the Netherlands Foundation for the Advancement of Tropical Research. The STOPMIP study (Kenya) was funded by the Malaria in Pregnancy (MiP) Consortium, which is funded through a grant from the Bill & Melinda Gates Foundation to the Liverpool School of Tropical Medicine, UK.
The ISTp study (Malawi) was partly supported by the Malaria in Pregnancy (MiP) Consortium, which is funded through a grant from the Bill & Melinda Gates Foundation to the Liverpool School of Tropical Medicine, UK and partly funded by the European and Developing Countries Clinical Trials Partnership (EDCTP). The LAIS study was supported by grants from the Academy of Finland (grants 79787 and 207010), the Foundation for Pediatric Research in Finland, and the Medical Research Fund of Tampere University Hospital. Azithromycin and its placebo were provided free of charge by Pfizer Inc (New York, New York), which also provided funding for.
the polymerase chain reaction testing of the sexually transmitted infections. The IPTp study (Papua New Guinea [PNG]) was funded by the MiP Consortium, through a grant from the Bill & Melinda Gates Foundation (46099); the Pregvax Consortium, through a grant from the EU FP7-2007-HEALTH (PREGVAX 201588) and the Spanish Government (EUROSALUD 2008 Programme); and Pfizer Inc. , through an investigator-initiated research grant (WS394663.
Flow cytometry Cells were resuspended in PBS-2% FBS, transferred to a 96 roundbottom well plate (10 6 cells/well) and labeled with indicated combinations of antibodies (Table  S1  in Supplementary Material) or matched isotype control antibodies (Table  S2  in Supplementary Material) for 30 min at 4°C. Cells were washed twice in PBS-2% FBS and fixed with Cytofix/Cytoperm solution (BD Biosciences) for 15 min at room temperature. Data were acquired, with an LSRII cytometer (Becton-Dickinson, Cochin CYBIO platform) and analyzed with Kaluza Software (Beckman-Coulter). As shown on Figure  1 , penile lymphocytes were identified based on their forward and side scatter, after a cell-doublet exclusion step. Next, lymphocytes were identified as CD45 + cells, and immune cell populations were defined according to their phenotypic characteristics, namely, CD3 -CD19 + for B cells, CD3 + CD4 + for CD4 + T cells, CD3 + CD8 + for CD8 + T cells, and CD3 -CD56 + or CD3 + CD56 + for NK and NKT cells, respectively.
intracellular cytokine staining Penile cells were plated in 500 µl culture medium (RPMI medium containing 10% FBS) for 5 h at 37°C in the presence of Brefeldin A (5 µg/ml, Sigma). Cells were washed twice in PBS-2% FBS and labeled with anti-CD4, anti-CD8 and anti-CD56 antibodies or matched isotype control antibodies for 30 min at 4°C. Cells were washed twice in PBS-2% FBS and fixed with Cytofix/Cytoperm solution (BD Biosciences) for 15 min at room temperature. Cells were washed with PermWash buffer (BD Biosciences) and stained for intracellular IL-2, IFN-γ, TNF-α, IL-4, IL-5, IL-17, and IL-22 for 30 min at 4°C using appropriate antibodies (Table  S1  in Supplementary Material) or corresponding isotype control antibodies (Table  S2  in Supplementary Material), diluted in PermWash buffer. Data were acquired with an LSRII cytometer (Becton-Dickinson, Cochin CYBIO platform) and analyzed following the gating strategy shown in Figure  1  with Kaluza Software (Beckman-Coulter) as indicated before.
immunohistochemistry Urethra, fossa, and glans tissue pieces were fixed with PBS-4% paraformaldehyde, embedded in paraffin and serially sectioned at 4 µm. Immunohistochemistry was performed as we previously described (7, 10) using appropriate antibodies (Table  S3  in Supplementary Material), and the LSAB2 System HRP (Abcam) labeling kit, and visualized with diaminobenzidine (Dako) or histogreen (Abcys) peroxidase substrates according to the manufacturer's recommendations. Image acquisition was performed with an OlympusBX63F microscope (Cochin IMAG'IC platform), and images were analyzed using the open-access GNU Image Manipulation Program (The GIMP Team).
9% [39. 5-48. 2] and 47. 5%  [45] [46] [47] [48] [49] [50]  of CD3 + cells for fossa and glans, respectively) (Figures  3B, D ). Tissue distribution of CD4 + and CD8 + T cells was also evaluated by immunohistochemistry following co-labeling with anti-CD3 (blue staining) and anti-CD8 (brown staining) antibodies. Hence, CD8 + T cells co-express CD3 and CD8 (blue/ brown staining), whereas CD4 + T cells expressed CD3 but not CD8 (blue staining only) (Figure  3E ). Matched isotypes served as negative control (data not shown). In the urethra, fossa, and glans, both CD4 + and CD8 + T cells localized in the lamina propria, close to the mucosal epithelium, whereas the majority of cells within the epithelial compartment were CD8 + T cells. However, it cannot be excluded that some of the cells detected by this technique also express T cell markers on their surface such as NKT cells.
Statistical analyses Data were analyzed with IBM SPSS Statistics software version 20 (IBM Corp, Armonk, NY). Descriptive analyses were used to report cohort characteristics. Differences between viremic and nonviremic recipients and viremic recipients with or without BKPyVAN were assessed using the chi-square test, Fisher exact test, Student t-test or Mann-Whitney U test, as appropriate. To indicate onset of recipient BKPyV viremia, separate Kaplan-Meier curves were generated according to donor and recipient BKPyV seroreactivity groups measured before transplantation. Association between baseline donor and recipient BKPyV seroreactivity groups and the combination of both with onset of posttransplantation recipient BKPyV viremia was determined by Cox regression. Uni-and multivariate Cox regressions were performed to determine which additional baseline covariates affected development of BKPyV viremia and BKPyVAN.
sequence analysis Nucleotide and protein sequences were analyzed using the Bioinformatics Research Portal (ExPasy) of the Swiss Institute of Bioinformatics (http://www. expasy. org), to analyze the translation, molecular weight, and other parameters by the ProtParam tool. The position of the mutation was visualized using PyMol on the structure of the C3b in complex with FH1-4 (PDB ID 2WII)  (51).
Therefore, this cross sectional study aims to assess the health needs of the elderly in order to deliver solid data for providing future geriatric services that can improve the quality of life. Information was gathered from several facilities in Dubai, UAE. People who lived in the UAE and were 65 years old or above were included. Overall, the total elderly population in Dubai is estimated to be 32,000 people. With a margin of error of 5% and a confidence level of 90%, the recommended sample size turned out to be 269 people. Therefore, 300 individuals were included. The interRAI organization's community health assessment instrument (interRAI CHA) was used as a tool for gathering information. After filling in all the questionnaires, the data was entered into the SPSS Statistics program for analysis.
Detailed descriptions of study design, patient eligibility, dose modifications, interruptions, and discontinuations were previously reported  9  and flow cytometry and MRD analyses (flow cytometry and polymerase chain reaction (PCR)) are summarized in the Supplementary Methods. Briefly, a panel of 29 (patients #1-4) or 20 (patient #5) markers were used for flow cytometry analysis, as detailed in the Supplementary Methods. Samples were measured on cytometers (BD TM LSR II (BD Biosciences, San Jose, CA, USA) or Dako CyAn TM (DakoCytomation, Glostrup, Denmark)), and analyses were performed using the FlowJo ® software, version 8. 5. 3 or 7 (FlowJo, LLC, Ashland, CA, USA). The study completion date was 24 May 2016. Baseline characteristics of patients with either CD19-positive or CD19-negative relapse (Table  1 ) were consistent with those of the entire patient population  9.
Acknowledgements We thank  Cornelia Eckert, PhD  ( Charité Campus Virchow, Berlin, Germany ), for PCR methodology development;  Cathy Tuglus, PhD  ( Amgen ), for statistical support; and  Janice Y Ahn, PhD  (Amgen), and  Alan Saltzman, PhD  ( Fishawack Communications, Conshohocken, PA ), whose work was funded by  Amgen , for medical writing support.
(A) PLTP deficiency increased mortality. Age-matched WT and Pltp-/-male mice underwent CLP. Data were analyzed using the Kaplan-Meier method, with statistical significance determined using the log rank test (n = 18-20 mice per group). (B) PLTP deficiency induced hyperglycaemia post-CLP. Blood glucose concentration was determined with a glucose meter before and at 2 h, 4 h, 6 h, 8 h and 24 h following CLP (n = 5 mice per group, t test). (C) PLTP deficiency increased the production of the inflammatory cytokines IL-6, MCP-1, and IL-1β and decreased that of IFN-γ. Plasma samples, harvested from WT and Pltp-/-mice before CLP, and 8 h and 24 h after CLP, were assayed using a Milliplex mouse cytokine panel (n = 5 mice per group, Mann Whitney test). (D) PLTP expression prevented sepsis by decreasing bacterial burden.
Construction of a transgenesis vector containing the sequence encoding human PLTP. cDNA cloning of PLTP in an intermediate vector. A retrotranslated sequence of synthetic cDNA encoding the human PLTP precursor (UniProtKB/Swiss-Prot P55058), bordered at the 5′-position by a Kozak consensus sequence and a unique MluI restriction site and, at the position 3′, by two stop codons and an NheI restriction site, was synthesized and cloned into an intermediate vector, derived from the pBluescript plasmid, containing the ampicillin resistance gene as well as the Col E1 bacterial replication origin. Transgenesis Vector. The transgenesis vector used for the cloning was derived from the plasmid pPolylII, having an ampicillin resistance gene as well as the Col E1 bacterial replication origin. The vector contains an expression cassette that includes from 5′to 3′: a dimer of the 5′HS4 insulator sequence of the chicken beta-globin gene (Genbank U78775)  38  , upstream of the 6.
3 kbp rabbit WAP promoter (whey acidic protein; Genbank X52564)  39  , the second intron of the rabbit beta-globin gene (Genbank V00882) containing a transcription enhancer; a second transcription enhancer (SUR 1. 2. 3) containing the 5′UTR sequence of the SV40 early gene fused with the R region and the start of the HTLV-1 U5 region  40  ; a third transcription enhancer (Igμ2), derived from mu region of the mouse IgG heavy chain (Genbank J00440)  41  and finally the human growth hormone transcription terminator (Genbank Ml3438). This cassette contains an MluI site and an NheI site located between the second and third transcription enhancer; it is flanked on either side by NotI sites allowing the excision of sequences of the plasmid pPolyIII. The DNA insert encoding PLTP, recovered by MluI/NheI digestion from the intermediate vector, was inserted between the MluI and NheI sites of the expression cassette.
Measurements of plasma concentrations of cytokines. Plasma concentrations of IL-6, TNFα, MCP-1, IL-1β, IFN-γ, IL-10 were quantified using a Milliplex MAP Mouse Cytokine/Chemokine Panel (# MCYTOMAG-70K, Millipore, Billerica, MA). The assays were performed according to the manufacturer's instructions. Standards and samples were analyzed on a LuminexR ® apparatus (Bio-Plex 200, BioRad, München, Germany) using the BioPlex Manager Software (Version 5, BioRad, Hercules, CA). LAL assay. The biological activity of LPS was quantified by the endpoint chromogenic LAL assay (QCL-1000 kit; Lonza, Walkersville, MD USA), which gives a magenta colour when positive. Briefly, 50 µl of diluted plasma (1:20), or diluted lipoprotein fraction or lipoprotein-free fraction (1:10) in endotoxin-free water were dispensed in each well of a 96-well plate.
The grids were contrasted with uranyl acetate and lead citrate and observed on a Hitachi H7500 TEM (Hitachi Scientific Instruments Co. , Tokyo, Japan) operating at 80 kV and equipped with an AMT camera driven by AMT software (AMT, Danvers, USA). Histological Examination. Liver, and kidney segments were fixed in 10% (v/v) phosphate-buffered formalin (pH 7. 4) for 48 h and then embedded in paraffin. Five-µm-thick sections were stained with hematoxylin and eosin (HE) and viewed with a digital slide scanner (NanoZoomer, Hamamatsu, Japan) at x400 magnification. All tissue sections were evaluated blindly by a pathologist. Statistics. Data are presented as the mean ± sem. All data were analyzed using GraphPad Prism 7 software (GraphPad Software Inc. ). The differences in survival rates were analyzed by Kaplan-Meier plot and the statistical significance was determined using log-rank test or χ 2 test as indicated.
Acknowledgements This work was supported by the  INSERM (Institut National de la Santé et de la Recherche Médicale) , the  Regional Council of Bourgogne , the  European Regional Development Fund  and a  French government  grant managed by the  French National Research Agency (ANR)  under the  program ''Investissements d' Avenir "with reference  ANR-11-LABX-0021-01-LipSTIC LabEx. The authors gratefully acknowledge:  A. Hamman  and  S. Monier  from the platform of Cytometry,  E. Charron ,  H. Choubley  and  V. Bergas  from the Lipidomic platform,  G. Lucchi  from the  Clinical Innovation Proteomic Platform ,  A. Chlémaire  and  A. Geissler  from the platform of histology,  A-L. Rérole  and  M. Xolin  from  INSERM LNC UMR1231  for expert technical assistance,  G. Tarris  for histological data.
| Design In this secondary analyses, data from a community-based, doubleblind, randomized, placebo-controlled trial  (Taneja et al. , 2009)  of 2,052 hospital-born term infants with birthweight ≤2,500 g were analysed. The primary objective of the trial was to examine the effect of daily zinc supplementation on infant morbidity and growth (ClinicalTrials. gov NCT00272142). The study participants were from urban neighbourhoods in New Delhi, India, and largely belonged to low and middle socioeconomic status. The study infants were randomized to receive either elemental zinc (n = 1,026) or placebo (n = 1,026). Data were collected between January 2005 and August 2007.
Second, our data were limited to hospital-born term LBW babies >37 weeks gestation. Due to unavailability of reliable data on gestational age, analyses of infant growth patterns based on the weeks of gestation could not be performed. Further research to compare the effect of maternal stature on growth trajectories of preterm, small-for-gestational age, and normal birthweight babies would be interesting. Third, the data on breastfeeding practices were limited. Data on breastfeeding practices at enrolment were included in the analyses, but those on later time points were not available. Published literature is suggestive of the fact that breastfeeding has a profound effect on survival and infection prevention in the first 6 months of life  (Sankar et al. , 2015)  but has somewhat a limited role on child linear growth  (Giugliani, Horta, Loret de Mola, Lisboa, & Victora, 2015).
For each time point, the diagnosis was the highest out of the past and current CRS-R evaluations. In other words, if the patient was diagnosed as UWS/VS at the first CRS-R assessment, MCS 1 at the second and UWS/VS at the third, the concluding diagnosis after three CRS-R examinations was MCS 1. The highest diagnosis obtained using six CRS-R evaluations was here considered the reference diagnosis. For the first aim of the study, which was to evaluate the effect of the number of assessments on clinical diagnosis accuracy, we used Friedman's analysis of variance ANOVA as a nonparametric test for repeated measurements because our data were not normally distributed. To test for any influence of the etiology, we assessed separately TBI and non-TBI patients. We also tested a subgroup of patients whose best diagnosis has been observed at least twice, to eliminate the possibility of false positives biasing the results.
Acknowledgment The study was supported by the  University and University Hospital of Lie  `ge, the  French Speaking Community Concerted Research Action  ( ARC-12/17-01 ), the  Belgian National Funds for Scientific Research (FRS-FNRS) ,  Human Brain Project  ( EU-H2020 -fetflagship-hbp-sga1-ga720270),  Luminous  project ( EU-H2020-fetopen-ga686764 ), the  Wallonie-Bruxelles International , the  James McDonnell Foundation ,  Mind Science Foundation ,  IAP  research network  P7/06  of the  Belgian Government (Belgian Science Policy) , the  European Commission , the  Public Utility Foundation 'Universit e Europ eenne du Travail', "Fondazione Europea di Ricerca Biomedica ", and the  Bial Foundation. L. H. , O. B. , and C. M. are research fellows, V. C. V. , A. T. , A. D. , and O. G. are postdoctoral fellows, and S.
Moreover, calcipotriol (MC903), an agonist of VDR, induced VDR to inhibit poly(I:C)-induced IL-36g production in NHEKs  (Figure 3d, 3e). As a transcriptional factor, VDR regulates the transcription of target genes by binding to their promoters. To confirm that VDR exerted its regulatory activity by binding to the promoter of the IL-36g gene, we first used the JASPAR database (http:// jaspar. genereg. net/) to predict VDR binding sites and found five possible binding sites in IL-36g promoter. We then performed chromatin immunoprecipitation assay and confirmed that VDR bound to two of the predicted VDR binding sites (BP1: e1637 to e1623, BP3: e972 to e958) in IL-36g promoter (Figure  3f ). To further identify the functional binding site of VDR in IL-36g promoter, we constructed firefly luciferase reporters containing IL-36g promoter, IL-36g promoter lacking BP1 or BP3, or IL-36g promoter with point mutations in BP1 or BP3, respectively.
, 2006; Schauber et al. , 2007)  and the activation of VDR directly by 1a,25-dihydroxyvitamin D3 exhibits potent antiproliferative activity in keratinocytes  (Lu et al. , 2005) , whether VDR could function as a repressor in the regulation of IL-36g gene transcription remains unknown. Here we found five possible VDR binding sites in IL-36g promoter by using the JASPAR database and confirmed that only BP3 (e972 to e958) is the functional binding site of VDR in IL-36g promoter by chromatin immunoprecipitation and luciferase assays. Furthermore, SLUG has been reported to directly bind to VDR promoter and inhibit the activity of VDR in human breast cancer cells  (Mittal et al. , 2008) , and the knockout of SLUG in mice resulted in an impaired reepithelialization in excisional wounds  (Hudson et al.
ACKNOWLEDGMENTS This work was supported by  National Natural Science Foundation of China  ( 31670925  and  31470878 );  National Key Research and Development Program of China  ( 2016YFC0906200 );  National Program for Support of Top-Notch Young Professionals  to YL;  Henry Fok Educational Foundation  ( 141017 ); and le  Centre National de la Recherche Scientifique , the  University of Orleans and la Region Centre  ( 2003-00085470 ).
One possible solution is to consider the move from uninfected to infected as a continuum such that an individual can be partially infected, perhaps based on a spectrum of immune responses  21. This is not entirely satisfactory, however, and a more intuitive approach is to consider that state may be discrete but our certainty about it is not. Hence, a probability is associated with an individual's infection status at any given point in time, depending on prior and current knowledge. In the present study we use data from a longitudinal field study of wild badgers in south-west England to explore the challenges described above. Empirical data from this cryptic population includes the results of three different imperfect diagnostic tests for M. bovis infection, accumulated during sequential captures of individually-marked badgers over many years.
Within this dataset it is not uncommon to find test-positive individuals subsequently testing negative (using the same diagnostic test) at the next sampling event  19. Graham et al. 22  incorporated prior test result information from these animals using multi-state capture-recapture models  15  , although they did not account for imperfect diagnosis arising from the combined use of a serological and a culture test  19. In the current study, we use a multi-event capture-recapture approach  23  to model imperfect observations of true epidemiological states. Our objective is to estimate the probability that any individual badger is truly infected using information from the whole of its capture history and any combination of previous diagnostic test results. Of course, we do not usually know an individual's true infection status: rather, we have a set of diagnostic test results and from these we wish to infer the probability of an individual being infected.
Discussion In this study we used a unique long-term empirical dataset of badger capture and testing histories to estimate the probability of infection with M. bovis, for each individual badger, given any combination of results from three imperfect diagnostic tests, and accounting for each animal's capture and test result history. In doing so, we reduced the impact of bias associated with imperfect diagnostic test performance and cross-sectional sampling, by expressing the likelihood of infection at an individual level rather than categorising an animal as either infected or uninfected. Although such an approach does not remove the need for interpretation in order to make decisions on how to manage infection in an individual (or population), it does create opportunities to vary the level of confidence associated with such decisions depending on the circumstances.
Methods Ethics statement. Badger capture and sampling was carried out in accordance with licences from Natural England and the UK Home Office. The protocols were approved by local ethical review within the Food and Environment Research Agency and the Animal Health and Veterinary Laboratories Agency (now the Animal and Plant Health Agency). Study area and data collection. Data originated from fieldwork undertaken from July 2006 to October 2013 at Woodchester Park, Gloucestershire, UK (51° 43′ N, 2° 16 W). This 7 km 2 study area is home to a population of wild badgers that has been the subject of long-term research into badger ecology and TB epidemiology  26. For trapping purposes, the study area was divided into three zones of approximately equal size, each of which was usually subject to four seasonal trapping sessions per year (Supplementary Table  S2 ).