dataesr/scientific-paragraphs-categorization huggingface dataset:
A blocking antibody against C5aR (IPH5401) was recently developed and entered phase 1 clinical trial in combination with PD-L1 blockade for lung cancer patients (NSCLC) and head and neck patients (HCC) (NCT03665129). Recent evidence suggests that not only macrophages but also neutrophils express high level of C5aR  (193). Moreover, the authors showed that IPH5401 selectively inhibited C5a-induced activation and migration of human blood neutrophils, suggesting that neutrophils may account as therapeutic target of C5aR blocking antibody.
FUNDING Our work was supported by grant from  INCa-Fondation ARC-Ligue  contre le cancer PAIR SEIN n •  2014-093 , by grants  INCa  PLBio n • 2017-158, by grants Ligue contre le cancer CCAURA by grant  FRM  n  • SPF20160936218 ,  French Government PhD Fellowship  ( 2016-2019 ), and 1-year extension Ph. D. Fellowship from  Ligue Nationale  contre le cancer ( 2019/2020 ). We also want to thank the  Plan Cancer (INCa-ITMO Cancer) , the  LABEX DEVweCAN  ( ANR-10-LABX-0061 ) of the  University of Lyon  and the  RHU MyPROBE  ( ANR-17-RHUS-0008 ), both within the  program Investissements d'Avenir  organized by the  French National Research Agency (ANR) , and the  LYRICAN  (grant  INCa -DGOS-Inserm_12563 ).
We obtained p-values that were adjusted according to the Benjamini and Hochberg procedure to control the false discovery rate at 5% 64. To compare the between inter-goup and intra-group variance we calculated the F-statistic using one-way ANOVA with Welch correction (v2. 4-2). For t-sne analyses  65  gene expression values (Log2EX, SR and cART groups) of all genes and samples were used. For additional statistical tests, Graphpad Prism software (GraphPad Software, Inc. ) was used. Non parametric Mann-Whitney test was used to compare metabolite uptake and mitochondria mass and to compare the ratio between HIV-specific CD8+ T-cell TNFα responses in medium without and with glucose, between HIV controllers and cART individuals. A non-parametric Wilcoxon paired test was used to compare HIV-specific CD8+ T-cell responses in different conditions.
The following antibodies were used: CD107a -V450 (clone H4A3, BD), CD3 -AF700 (clone SP34-2, BD), CD4 -PerCP Cy5. 5 (clone L200, BD), CD8a -APC-Cy7 (clone RPA-T8, BD), IFNg -PE-Cy7 (clone B27, BD), IL-2 -PE (clone MQ1-17H12, BD), TNFa -PE-CF594 (clone Mab11, BD) and Perforin -FITC (clone Pf-344, Mabtech). Flow cytometry was performed with an LSRII instrument (BD Biosciences), and data were analyzed with FlowJo V. 10 software (TreeStar Inc. ).
ACKNOWLEDGEMENTS The authors wish to thank  A Tadesse ,  S Hendou ,  A Essat ,  C Jung  and  K Bourdic  for help with inclusion of HIV-infected individuals. The authors wish to thank  D Desjardin  and  N Bosquet  for help with the macaque studies. The authors especially thank the investigators, clinical personal and HIV-infected individuals participating in the  ANRS CO6 PRIMO  and the  ANRS CO21  cohorts for their cooperation. The authors thank the Cytometry and  Biomarkers UTechS  plate-form at  Institut Pasteur  and the personnel from the  "Infectious Disease Models and Innovative Therapies (IDMIT)  plate-form for technical support. D Young , a medical English editor supported with funds from  AS-C laboratory , provided English editorial assistance to the authors during preparation of this manuscript.
This study was conducted with funds from the  French National Agency for Research on AIDS and Viral Hepatitis (ANRS) ,  MSDAVENIR  and from the  European Union (EU) 's  Horizon 2020 research and innovation programme  under the  Marie Sklodowska-Curie  grant agreement No  706871. MA received support from  EU  (grant  706871 ) and complementary support from  Sidaction. CP received support from  ANRS. JCV-C received support from  Institut Pasteur  through the  Roux-Cantarini program. The  ANRS CO6  and  CO21  cohorts are sponsored and funded by the  ANRS. IDMIT infrastructure was supported by the  French government  " Programme d'Investissements d'Avenir" (PIA)  under Grant  ANR-11-INBS-0008.
Distinct domains of BST2 are involved in ILT7 activation were washed in PBS and stained with the specific primary antibody (anti-BST2 rabbit serum, anti-HA, or anti-Myc) for 45 min at 4 °C. Cells were then washed and stained using appropriate Alexa Fluor-coupled secondary Abs for 30 min at 4 °C. After an additional wash, cells were analyzed for cell-surface BST2 expression by flow cytometry. Cells from co-cultures between transfected HEK-293T and ILT7 ϩ NFAT-GFP reporter cells were collected, washed in PBS, and stained with anti-ILT7_alexa647 antibodies for 45 min at 4 °C. Cells were then washed and analyzed for cell-surface ILT7 and GFP expression by flow cytometry. Fluorescence intensities were acquired using a Cyan ADP flow cytometer and data were analyzed using the FlowJo software (Treestar).
Acknowledgments-We thank  E. Massicotte  and  J. Lord-Grignon  for assistance with flow cytometry; the  IRCM clinic  staff, and all volunteers for providing blood samples. The plasmids encoding the BST2 ectodomain with the nonoverlapping quadruple alanine mutations were a kind gift from  Dr. Paul Spearman  ( University of Cincinnati ). The ILT7 reporter cell lines were a generous gift from  Dr. Y-J. Liu. We also thank  Caroline Mas  ( ISBG, Biophysical Platform Manager ) and  Pierre Soule  ( Application specialist, Nanotemper society ) for expert help with the analyses of the Microscale Thermophoresis experiments.
Edited by This work was supported by  Canadian Institutes of Health Research (CIHR)  Grants  PJT148686  and  FDN 154324  and an  IRCM-UdeM Chair of Excellence in HIV research  (to É. A. C. ),  ANRS  Grant  073744  (to W. W. ), the  Institute Universitaire de France (IUF) and Grenoble Partnership for Structural Biology platforms (ISBG)   UMS 3518 CNRS-CEA-UJF-EMBL  funded by  FRISBI  ( ANR-10-INSB-05-02 ) and  GRAL  ( ANR-10-LABX-49-01 ). This work was also supported by a Ph. D. fellowship from the  Fond National de la Recherche Luxembourg  (to N. A. ). The authors declare that they have no conflicts of interest with the contents of this article. This article contains Tables  S1-S2  and Figs. S1-S5.
Study Design This study is a retrospective multicenter study analyzing EBMT registry data. Additional information was collected using a specific questionnaire. The study was approved by the ADWP and participating EBMT centers reported data from patients affected by ADs (hematological and non-hematological ADs), including those with autoinflammatory and genetic components, who had been treated with allogeneic HSCT from the first registration in 1997 to the end of 2014. Patients with a previous allogeneic HSCT for a conventional hematological indication have been included. Patients transplanted for a malignant hematological disease with a concomitant AD were excluded from the analysis. All EBMT teams are required to obtain signed informed consent for transfer of anonymized data via standardized minimal essential data forms in accordance with data protection regulations.
The following variables were analyzed from the EBMT database: patient gender, patient age at transplantation, disease classification at time of diagnosis according to primary disease established criteria, conditioning regimen, graft characteristics, incidence of acute, and chronic GvHD. In addition, long-term side effects (secondary autoimmune disease or malignancy, viral reactivations), previous and posttransplant treatments, and disease status at last follow-up were analyzed in the subgroup of 64 patients with completed questionnaires. Disease characteristics (severity, refractoriness to standard treatments, revision and reclassification of all diagnoses in view of the spectrum of pediatric ADs, including those with autoinflammatory and overlap with other genetic diseases and inborn errors) were assessed by local physician.
Background: Data on whether T-cell dose of allogeneic peripheral blood stem cell (PBSC) product influences transplant outcome are conflicting. Methods: Using CIBMTR database, we identified 2,736 adult patients who underwent first allogeneic peripheral blood stem cell (PBSC) transplant for acute leukemia (AML, ALL) or myelodysplastic syndrome (MDS) between 2008-2014 using an HLA-matched sibling donor (MSD) or 8/8-matched unrelated donor (MUD). We excluded ex-vivo and in-vivo T-cell depleted transplants. Correlative analysis was performed between CD3+ T-cell dose and risk of graftversus-host-disease (GVHD), relapse, non-relapse mortality (NRM), disease free survival (DFS) and overall survival (OS). Results: Using maximum likelihood estimation method, we identified CD3+ T-cell cell dose cutoff that separated risk of acute GVHD (aGVHD) grade II-IV in both MSD and MUD groups.
A C C E P T E D M A N U S C R I P T 8 Interactions between T-cell dose and the adjusted clinical variables were examined and no significant interactions were detected. Center effect was adjusted as a random factor for all outcomes. 25 The significance level of 0. 01 was used for the overall effects of factors followed by Bonferroni adjustment for pairwise comparisons to account for multiple testing. All statistical analyses were performed using SAS version 9. 4 (SAS Institute, Cary, NC).
Results of the ongoing phase II clinical trial using standardized CD3+ T cell dose with HLA-matched related PBSC transplant is awaited (NCT00959140). Additionally, in the current era of post-transplant cyclophosphamide (PTCy) for prevention of GVHD, it may be imperative to assess the impact of these T-cell subsets in Horowitz MM, Gale RP, Sondel PM, Goldman JM, Kersey J, Kolb.
Data are the average of four independent experiments (n = 4). b Circadian infection protocol. Synchronised Huh-7 were inoculated with HCVpp or HCVcc particles for 1 h and infectivity determined by luciferase assay or measuring the frequency of viral NS5A expressing cells 24 h later. c HCV entry shows a circadian pattern. Synchronised Huh-7 cells were inoculated with HCVpp at defined CTs and particle entry measured 24 h later and data expressed relative to CT0; mean ± S. E. M. , n = 8, Kruskal-Wallis ANOVA with Dunn's test. d HCV infection shows a circadian pattern. Synchronised Huh-7 were inoculated with HCVcc SA13/ JFH-1 or J6/JFH-1 at defined CTs and the frequency of infected cells quantified 24 h later and data expressed relative to CT0; mean ± S. E. M. , n = 4; Kruskal-Wallis ANOVA with Dunn's test.
e Circadian pattern of HCV receptors. Synchronised Huh-7 were lysed every 8 h, total RNA extracted and CD81, claudin-1 and occludin mRNA levels together with the housekeeping GAPDH assessed by qPCR. Individual receptor transcripts were normalised to CT0. Representative of three independent experiments; n = 3, mean ± S. E. M. f BMAL1 regulates HCV entry receptors. Parental (WT) or Bmal1 KO Huh-7 lysates were assessed for BMAL1 and viral receptors CD81, claudin-1 and occludin expression together with housekeeping GAPDH by western blotting. Total RNA from parental or Bmal1 KO Huh-7 were extracted and mRNA of CD81, claudin-1, occludin and GAPDH measured by qRT-PCR. Data are expressed relative to parental cells (mean ± S. E. M. , n = 3, Mann-Whitney test). g BMAL1 regulates HCV entry and infection.
WT or Bmal1 KO Huh-7 were inoculated for 1 h with HCVpp or HCVcc SA13/JFH-1 and infection assessed after 24 h. Data are expressed relative to WT cells (mean ± S. E. M. , n = 5, Mann-Whitney test). h BMAL1 regulates DENV and ZIKV infection. WT or Bmal1 KO Huh-7 were inoculated for 1 h with DENV or ZIKV and infection assessed after 24 h. Data are expressed relative to WT (mean ± S. E. M. , n = 6 for DENV; n = 9 for ZIKV, Mann-Whitney test) Supplementing the culture media with oleic acid had a negligible effect on HCV replication (Supplementary Figure  7 ) but reduced the anti-viral activity of SR9009 and control SCD inhibitor (Fig. 5f ). Furthermore, CRISPR knock-down (KD) of SCD in HCV replicon cells inhibits viral replication and reduced the anti-viral activity of SR9009 and SCDi (Fig. 5g ), demonstrating that REV-ERB perturbation of SCD expression contributes to its anti-viral activity.
Analysis of published ChIPseq datasets  35, 36  from murine liver failed to identify BMAL1 binding to CD81 or claudin-1 promoter regions. However, claudin-1 and occludin mRNAs show a rhythmic expression in murine liver  37  and claudin-1 was reported to be among the top upregulated genes in Rev-erba KO mice  18. Du et al. reported that CD81 transcription was rhythmic in murine liver in phase consistent with REV-ERB target, but this did not result in rhythmic mRNA accumulation possibly due to high stability of the transcript  38. Recent reports demonstrating a role for CD81 in the assembly and budding of human immunodeficiency virus and influenza A viruses  39, 40  highlight the wider implications of our observation that CD81 is circadian regulated for other human pathogens. Our observation that inhibiting miR-122 reduced the anti-viral activity of REV-ERB agonists for HCV suggests that circadian regulation of HCV replication is in part miR-122 dependent.
Microarray and ChIP-seq analyses. Microarray datasets for SR9009 treated Huh-7 cells (20 µM, 24 h treatment, n = 3) were obtained from Oxford Gene Technology, UK. Differentially expressed genes were filtered using the following parameters: p-value < 0. 05, log 2 FC > 0. 5 or log 2 FC < -0. 5. KEGG profiling  60  was used to perform pathway mapping and determine significantly enriched pathways using hypergeometric tests. Metabolic-related pathways were extracted and represented as bar charts with the colour of each bar indicative of its p-value. ChIP-seq datasets for murine REV-ERBα and REV-ERBβ were obtained from Gene Expression Omnibus where peak detection was performed using the HOMER tool. BedGraphs are visualised using the Integrative Genomics Viewer (IGV) tool  61  overlaying the mouse genome (mm10).
Data were analysed using Lipid Data Analyzer (2. 6. 0-2) software. Proteomic analysis. Three biological replicates of control and SR9009-treated Huh-7 cells were lysed in RIPA buffer and proteins separated using NuPAGE 4-12% bis-tris gels (Invitrogen). Peptides obtained from selected proteins (CD81, claudin-1, occludin, SR-BI, occluding, SCD) using in-gel trypsin digestion (tryptic digestion kit, Thermo) were detected and quantified using Liquid chromatography tandem mass spectrometry (LC-MS/MS) methods. Peptides were desalted using an online C18 trap column (PepMap 100, 5 µm particle size, 300 µm i. d. × 5 mm, Thermo Fisher Scientific) at a flow rate of 10 µL/min for 4 min. The nano LC system Dionex Ultimate 3000 (RSLC nano system) and a nano analytical C18 reversed phase column (PepMap), dimensions 75 µm × 50 cm, 2 µm particle size (Thermo Fisher Scientific) were used, with a flow rate of 250 nL/min at 45 o C ( ± 2 o C).
6 m/z; normalised collision energy (NCE): 27; spectrum type: profile. The MS tune file for nano flow rate at 250 nL/min was used with the following settings: scan type: full MS-SIM, scan range: 350-2000 m/z, fragmentation: none, resolution: 70,000, polarity: positive, microscan: 1, AGC target: 1e  6  , maximum IT: 100, sheath gas flow: 0, aux gas flow: 0, sweep gas flow: 0, spray voltage: 2. 3 kV, capillary temperature: 320 o C, S-lens RF level: 50. Data acquired using DDA were processed using the Mascot search engine against human Uniprot protein database. Mascot search results were uploaded to Skyline (version 4. 1. 0. 18169, 64-bit, Seattle, USA) to create a reference library. PRM data were processed using Skyline to quantify peptides in different samples. Statistical analysis. Statistical analyses were performed in Graph Pad Prism 7 (GraphPad, USA) using Mann-Whitney's test or Kruskal-Wallis one-way analysis of variance (ANOVA) with Dunn's test (for multiple comparisons), except where stated otherwise, with a p-value of < 0.
Acknowledgements We would like to thank  Koichi Watashi  ( National Institute of Infectious Diseases, Tokyo, Japan ) for sharing their SCD promoter construct;  Charles Rice  ( Rockefeller University, US ) for HCV WT and m15 viruses and miR122 KO Huh-7 cells;  Andrew Davidson  ( University of Bristol, UK ) for DENV reporter replicon;  Stuart Ray  ( Johns Hopkins University, US ) for HCV E1E2 expression vectors;  E. Gould  ( Centre for Ecology and Hydrology, Oxford, UK ) for DENV2 strain 1668;  Rick Randall  ( University of St Andrews, UK ) for the A549/BVDV-Npro cell line and  Benedetto Grimaldi  for lenti-shRev-erbα construct ( Department of Drug Discovery and Development, Genoa, Italy). We acknowledge technical assistance of  Jiaqi Chen ,  Greg West ,  Aimee L. Parsons  and  Claudia Orbegozo Rubio.
Work  in the J. A. M. laboratory is funded by:  EU 2020 Research and Innovation Programme Consortia HEP-CAR  under grant agreement No. 667273  and  Wellcome Trust   IA 200838/Z/16/Z. A. K. was funded by the  UK MRC  ( MC-UU-12014 ,  MR/N017552/1 ). Work by M. H. , A. K. and N. Z. are supported by the  Oxford Glycobiology Endowment. D. R. and A. L. are Wellcome Trust investigators  107849/Z/15/Z. M. W. lab is supported by the  EU2020 HEP-CAR grant  and by the  BBSRC  ( BB/PO13384/1 ).
Data availability The metabolomics data have been deposited to the EMBL-EBI MetaboLights database (DOI: 10. 1093/nar/gks1004. PubMed PMID: 23109552) with the identifier MTBLS792. The mass spectrometry proteomics data have been deposited to the ProteomeXchange Consortium via the PRIDE  [1]  partner repository with the dataset identifier PXD011721 and 10. 6019/PXD011721, and can be accessed via: ftp://PASS01292:YF2765va@ftp. peptideatlas. org/. The microarray data from SR9009 treated Huh-7 cells have been deposited at NCBI GEO with the identifier GSE123748 and can be accessed via http://www. ncbi. nlm. nih. gov/geo/query/acc. cgi?acc=GSE123748. The authors declare that all other data supporting the findings of this study are available within the article and its Supplementary Information files, or are available from the authors upon request.
pylori may result in the conversion of bacillary form to a coccoid form of H. pylori which is a morphological manifestation of bacterial cell death without an infective capacity  [24] , thus HpSA might detect antigens from the degradation of the two morphological forms of H. pylori  [52]. To overcome such limitations, all watery collected stool samples and volunteer participants under recent antimicrobial medications, bismuth, and potent proton pump inhibitors were excluded from the study. The study has provided a comprehensive overview of the prevalence of H. pylori in Sharjah, Ajman, Abu Dhabi, and Dubai taking into consideration the multinational UAE residents and the different factors associated with this infection. These data can be used to support national initiatives to prevent and eradicate H.
Industrial workers and Ethiopian nannies were assisted by research assistants speaking the same language. For stool sample collection from nurseries and schools, helpers were asked to cooperate with the assigned research assistant. Participants with equivocal questionnaire were taken out of the study. Inclusion criteria were UAE residents aged 1 year and above. Participants subjected to antimicrobials, proton pump inhibitors, and bismuth preparations within the last two weeks from the study period were excluded. The questionnaire consisted of three main sections. The first section consisted of demographic and socioeconomic data which included gender, age, nationality, profession, marital status, education level, family income, number of siblings, number of family members per room, and number of rooms per house.
Acknowledgments: The current study was supported by a research grant from the  University of Sharjah  ( 1601110211-P ) and  Boehringer Ingelheim. We express our deep gratitude to the  University of Sharjah  for the financial and technical support for this research and for all volunteer participants in this study. Special thanks are credited to the pharmacy student,  Mr. Bassel al Harbi , who volunteered to promote this research study in Ajman and helped enormously the research assistant in collecting the samples.
Acknowledgements BR is supported by  Fondation pour la Recherche Médicale , AC and RM are supported by  Ecole Normale Supérieure de Lyon. HD is supported by  INSERM. RM is part of the  French Laboratory of Excellence  project  ECOFECT  ( ANR-11-LABX-0048 ). The authors acknowledge the support from  Fondation pour la recherche médicale (équipe Labellisée ).
As mentioned above, annelid AMPs with BRICHOS are characterized by a short amino-acid sequence, a cationic net charge, a hydrophobic region, a β-sheet fold, and the formation of disulfide bonds between cysteine residues, increasing the rigidity of their open-ended cyclic structures (Table  4 )  [87] [88] [89]. Different specific software can easily determine all these structural characteristics. The Innovagen Pepcalc. com server (Innovagen AB, SE-22370 Lund, SWEDEN; https://pepcalc. com/) was used to calculate the net charge at neutral pH, and Peptide2. 0 server (Peptide 2. 0 Inc. , Chantilly, VA; https://peptide2. com/) to evaluate the peptide hydrophobicity. The positive charge (due to arginine residues) and the hydrophobicity (from valine, leucine, alanine, tryptophan, isoleucine, phenylalanine, and tyrosine) contribute to the amphipathic nature of the peptide.
These AMPs are also present in a major part of the nervous system, which suggests a possible involvement in the defense and the regeneration of the nerve cord as demonstrated for the cysteine rich AMPs of the leeches (see below)  [43, 89, 109]. Data given also evidences that alvinellacin shapes and controls the specific epibiotic microflora that allows it to thrive in the hydrothermal habitat  [48]. Recently, nicomicin-1 and -2 were identified in the artic polychaeta Nicomache minor  [110]. This worm lives in the cold water, inhabiting hard tubes attached to stones  [111]. Nicomicins consist of 33 residues (Table  1 ), containing BRICHOS domain in the sequences of their prepropeptide. They are characterized by many hydrophobic amino acids (51%) and a disulfide bond (Cys24 -Cys29)  [110]. While Nicomicin-2 has no effect on bacteria, Nicomicin-1 exerts strong antimicrobial activity towards Gram-positive bacteria by damaging their membranes; the presence of salt impedes its activity  [110].
Acknowledgments: We thank the captain of the crew of the  R/V Atalante , the  DSV Nautile and ROV group (IFREMER) , along with the chief scientists of the MESCAL 2010, 2012 (LE BRIS Nadine, LALLIER François MESCAL, https://doi. org/10. 18142/261 )and CHUBACARC 2019 cruises.
3nR group The 3nR group was produced by crossing 2nR females and 4nR males, both selected and provided by Ifremer. Usually, a cross involves several dozen or hundreds of 2nR females and one to six 4nR males. The 2nR and 4nR oysters were the progenies of families selected for their higher resistance to summer mortality during the MOREST program (MORtalités ESTivales)  (Dégremont et al. , 2010; Samain and McCombie, 2007). The founder populations of the 2nR and 4nR oysters were based on two males and four females  (Dégremont et al. , 2010). For PS1 and PS2, the 2nR oysters were the fifth generation of seven families (R1 to R7 -year of production 2007), and the sixth generation of two of them (R1 and R5 -year of production 2009), which were subsequently identified as resistant to infection by OsHV-1  (Dégremont, 2011).