dataesr/scientific-paragraphs-categorization huggingface dataset:
ATP and lactate concentrations Intracellular levels of ATP were determined with CellTiter-Glo ® 9 Luminescent Cell Viability Assay (Promega), following the manufacturer's instructions. Briefly, 1 × 10 5 cells were incubated for 10 min at room temperature in CellTiter-Glo ® Reagent, which contained lysis buffer and thermostable luciferase and the luminescent signal was analyzed in an Orion Microplate Luminometer with Simplicity software (Berthold Detection Systems, Oak Ridge, TN, USA). Intracellular and extracellular levels of l-(+)-Lactate were measured in cell lysates or supernatants using Lactate Assay Kit II (Sigma-Aldrich) accordingly to manufacturer's instructions. Briefly, 1 × 10 6 cells were lysed with 4 volumes of lysis buffer or pelleted to collect the subsequent supernatant and 50 μl of each sample was incubated with the commercial enzyme during 30 min at room temperature.
Intracellular ROS and glutathione levels Living Jurkat-Tat cells were adhered onto fibronectincoated plates and stained with DCF-DA 2′,7′-(5 μM) (Sigma-Aldrich), which after oxidation is converted into highly fluorescent DCF (2′7′-dichlorofluorescein)  [26]. Images were obtained with a Leica DMI 4000B Inverted Microscope (Leica Microsistemas, Barcelona, Spain). Cells from a total of 15 fields from three independent experiments were analyzed. Fluorescence from cells stained with DCF-DA-FITC was also measured by FACScalibur Flow Cytometer (BD Biosciences Clontech) using FL-1 channel and data were analysed by CellQuest software. Intracellular levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) were measured using the luminescence-based GSH/GSSG-Glo Assay (Promega). The luminescent signal (relative light units, RLUs) was quantified in an Orion Microplate Luminometer with Simplicity software and RLUs were converted into concentration (pM) using the glutathione standard curve included in the assay.
Apoptosis assays Living cells were adhered on PolyPrep slides, fixed with 2 %-PFA and treated with Dapi (4′,6-diamidino-2-phenylindole) (Sigma-Aldrich) for staining the nuclei. Images were obtained with a Leica DMI 4000B Inverted Microscope (Leica Microsistemas, Barcelona, Spain). The percentage of apoptotic events was calculated by acquiring 60 fields from three independent experiments-containing an average number of cells close to 40-and considering the total number of cells. Activation of casapse-3 was measured in non-treated cells with CaspaseGlo ® 3/7 systems (Promega). The luminescent signal (relative light units, RLUs), which was directly proportional to caspase activation, was quantified in an Orion Microplate Luminometer with Simplicity software (Berthold Detection Systems). Cells were stained with Annexin-V-PE (Immunostep, Salamanca, Spain) to measure apoptosis commitment.
Acknowledgements We greatly appreciate the secretarial assistance of  Mrs Olga Palao. This work was supported by  FIPSE  ( 360924/10 ),  Spanish Ministry of Economy and Competitiveness  ( SAF2010-18388 ),  Spanish Ministry of Health  ( EC11-285 ),  AIDS Network ISCIII-RETIC  ( RD12/0017/0015 ),  Instituto de Salud Carlos III ,  Spanish Ministry of Economy and Competitiveness  ( FIS PI12/00506 ). The work of  Sara Rodríguez-Mora  is supported by a fellowship of  Sara Borrell  from  Spanish Ministry of Economy and Competitiveness  (2013). The work of  María Rosa López-Huertas  is supported by a fellowship of the European Union Programme Health 2009 (CHAARM).
Therefore the primary aim of this study was to investigate CTh patterns in subjects with pro-DLB and we report MRI patterns of CTh in subjects with DLB at the stage of MCI (pro-DLB) and established dementia (DLB-d), AD at the stage of MCI (pro-AD) and dementia (AD-d),as well as data from healthy elderly controls (HC). We included comparator disease groups to explore how cortical thinning may evolve from an early stage of disease (pro-DLB and pro-AD) to later established disease (DLB-d and AD-d); similarly inclusion of pro-AD group was also considered relevant as this would be the group from which pro-DLB would most likely need to be most distinguished from in clinical practise. We hypothesised that in pro-AD, the pattern of cortical thinning would involve predominantly the temporal lobe, and parietal association cortices.
MRI data acquisition Subjects from NCL and SXB underwent T1 weighted MR scanning on a 3T MRI systemwithin 2 months of the study assessment. NCLused an 8 channel head coil (InteraAchieva scanner, Philips Medical Systems, Eindhoven, Netherlands) and SXB a 32 channel head coil (Veriosyngo MR B17, Siemens magnetom). The sequence was a standard T1 weighted volumetric sequence covering the whole brain (3D MPRAGE, sagittal acquisition, 1 mm isotropic resolution). 3D T1 of NCL had a matrix size of 240 (anterior-posterior) x 240 (superior-inferior) x 180 (right-left), a repetition time (TR) = 9. 6ms, an echo time (TE) = 4. 6ms, and a flip angle = 8°. 3DT1 of SXB had matrix size of 192 (anterior-posterior) x 192 (superior-inferior) x 176 (right-left), a repetition time (TR) = 1900ms, an echo time (TE) = 2.
Manual correctionswere then performed on these scans such as removal of dura mater and/orthe applicationof a set of WM control points as required, before regeneratingthe pialor WM surfaces or both. Modification to the processing stream resulted in successful cortical surface regeneration of31 scans. However, the remaining 16scans (1 healthy subject, 5AD-d, 1 pro-AD, 2 DLB-d and 7 pro-DLB), still exhibited significant pial or WM surface errors and were therefore excluded. The dataset for subsequent CTh analysis therefore comprised of 33 controls, 54 AD-d, 31 DLB-d, 27 pro-AD and 28 pro-DLB.
Statistical analysis The Statistical Package for Social Sciences software (SPSS ver. 21. 0. 0. 0, http://www-01. ibm. com/software/analytics/spss/) was used for further statistical evaluation as required. Where appropriate, differences in demographic and clinical data were assessed using parametric (ANOVA, t-tests) and non-parametric tests (Kruskall-Wallis H, Mann-Whitney U). Posthocanalyses employedTukey and Mann-Whitney U for ANOVA and Kruskall-Wallis tests respectively. For categorical measures, χ 2 tests were applied. For each test statistic, a probability value of <0. 05 was regarded as significant. Cortical thickness. Regional CTh between groups were examined on a vertex-wise basis using the general linear model (GLM), performed with the QDEC software (http://surfer. nmr. mgh. harvard.
Subject characteristics The demographic data for patients and healthy subjects are summarised in Table  1. Subject groups were well matched for education, gender and handedness. Patients with prodromal disease were younger than patients with dementia. Of the patients with pro-AD 9 presented with amnestic MCI single domain and 18 with amnestic MCI multiple domain. Of the patients with pro-DLB 2 presented with amnestic MCI multiple domain, 13 with non-amnestic MCI single domain and 13 with non-amnestic MCI multiple domain. For pro-AD and pro-DLB, MMSE scores were similar, and higher than in AD-d and DLB-d groups. For TMTA, patients with DLB (pro-DLB or DLB-d) were more impaired than the healthy control group. DLB-d patients were also more impaired than pro-AD. For TMTB, patients with dementia (DLB-d and AD-d), and pro-DLB were more impaired than healthy controls.
These findings were consistent with previous reports using cortical thickness and Voxel-Based Morphometry(VBM)  [14, 27]. In pro-DLB compared to healthy controls, there was evidence of cortical thinning in right frontal and insula regions, although this was only evident in uncorrected comparisons suggesting that cortical thinning, certainly in the prodromal stage of DLB is relatively mild. AD-d was characterised by cortical thinning in confluent areas of parietal and temporal lobes, and a significant part of frontal and occipital lobes. The CTh comparison of the DLB-d and AD-d showed more cortical thinning in AD-d patients in left entorhinal cortex and this observation is in line with cortical thinning patterns reported in other independent DLB-d and AD-d datasets from the NCL group  [14].
Acknowledgments The authors do thank MélanieStackfleth,  Heather Hunt  and  Laetitia Berly  for help for organization;  Mathias Bilger ,  Laure Di Bitonto ,  Emmanuelle Ehrhard ,  Jennifer Kemp ,  Alison Killen ,  Nicola Barnett ,  Catherine Kleitz ,  Nadine Longato ,  Laetitia Monjoin  and  Natacha Vogt  for neuropsychological assessment;  Paulo Loureiro de Sousa ,  Corinne Marrer ,  Camille Heitz ,  Stéphane Kremer  and  Daniel Gounot  for MRI and  Michael Firbank  for expert advice.
This study was funded by  Appel à Projet Interne (API)  of the  University Hospital of Strasbourg ,  Alsace Alzheimer 67 ,  Fondation Université de Strasbourg  and famille  Jean Amrhein , and  Projet Hospitalier de Recherche Clinique (PHRC) interrégional  ( IDRCB 2012-A00992-41 ). The work was also supported by the following: the  Newcastle Healthcare Charity  ( BH0070250 );  Academy of Medical Sciences, Wellcome Trust   Starter Grants scheme for Clinical Lecturers  ( BH090112  to J-P. T. ); demonstrated more CTh in AD-d in the left entorhinal cortex (p<0. 05,FDR corrected). in early stages of DLB distinct from AD. Right anterior insula involvement may be a key region at the prodromal stage of DLB and needs further investigation. Wellcome Intermediate Clinical Fellowship  ( BH083281  to J-P.
Study design and selection of participants The multicentre IBGP study performed a prospective recruitment of patients during two consecutive influenza seasons (from week 40 to 15): 2010-2011 (season 1) and 2011-2012 (season 2). Persons of any age with a lab confirmed diagnosis of influenza B made in the frame of established sentinel surveillance networks in France and Turkey were eligible for inclusion into the study. The trigger for the study recruitment was the positive notification of an influenza B case by the collaborating virological laboratory. This notification was sent from the laboratory to the GP coordinators who sought to recruit the identified patient if notification occurred early enough, i. e. before eleven days after the swab specimen had been taken for investigation. If for author  [GM]  who also contributed to the study design, but did not have any additional role in data collection and analysis, decision to publish, or preparation of the manuscript.
W. J. P. has served on an influenza advisory board for GSK. G. M. declares being employed by GlaxoSmithKline Vaccines which has financed the IBGP study. D. F. declares having received consultancy payments from Open Rome relating to the design analysis and reporting of this material and having provided advisory board consultancy services to several pharmaceutical companies on matters relating to the burden of illness due to influenza and its prevention. This does not alter the authors' adherence to all PLOS ONE policies on sharing data and materials. more than eleven days were elapsed from the date of swabbing, the influenza B patient was not included in the study. For each influenza B patient included in the study, the network coordinators searched for a correspondent influenza A patient, who has been swabbed within eleven days before and belonged to the same age group.
Data collection For each patient included in the study, the data collection was performed in three moments of the time horizon of the study: (1) at the swab test day (D0), (  2 ) on recruitment to the study at 9 ± 2 days (D9), (3) in case the subject had not recovered by day 9, at 28 ± 5 days (D28). At day 0, we used the virology investigation request form routinely used to collect data on: personal details (name, month and year of birth, gender and city code), date of onset of symptoms, presenting symptoms and syndromes, influenza vaccination status for the current season, and prescriptions of antibiotics or antivirals. Concerning vaccination status, patients were considered as vaccinated against the current seasonal flu if they had received at least one dose of seasonal vaccine in the current season and if the date of vaccination preceded by at least 14 days the onset of symptoms.
Patients for which the vaccination date was unknown, were considered as not vaccinated. Information about underlying conditions was based on each country own surveillance form, which means that heterogeneous and non comparable data were collected on this topic. Data were anonymised by the lab before entry into the computer database. Further information was obtained at the time of recruitment (day 9), using a patient specific questionnaire (illustrated by an English translation in Fig 1 ) completed by the sentinel physician (in France) or by the study coordinator (in Turkey) on the basis of a telephone interview. Some potentially eligible influenza B patients were not recruited in France because: the lab results were not transmitted to the physician in time to contact the patient within eleven days after the swab; or the patient/GP was not reachable or did not agree to participate.
Analysis Using data collected at day 0, 9 and 28, influenza A and B recruited patients were compared in terms of presenting symptoms and syndromes, vaccination status, drugs taken, duration of illness (days between symptom onset and return to normal activities), number of follow-up consultations, hospital admissions, days of absence from work or school. All comparisons were made separately for France and Turkey, and further stratified by season and age group (0-14, 15-64, 65+ years). The Fisher's exact test was used to compare the distribution of variables of interest. A p-value was considered statistically significant when less than 0. 05. We developed a multiple regression model to investigate the effect of patients and disease characteristics on the median duration of illness including influenza type and the other variables that were significant (p<0.
Discussion We successfully recruited 419 influenza B and 355 influenza A laboratory confirmed cases providing a database in which we would expect to detect important differences (if any) between influenza A and B presentation. We compared the main characteristics of influenza in two countries (France and Turkey) during two consecutive influenza seasons (2010-11 and 2011-12). To the best of our knowledge, this is the largest European community-based study that compares influenza A and B in recent years. This was made possible by the fact that influenza B circulated intensely in Europe during the 2010-2011 season  [20]. We found no significant differences between influenza A and B recruited patients for most of the aspects we considered, including presenting symptoms and syndromes, number of consultations and duration of illness.
Acknowledgments We acknowledge  Peter Spreeuwenberg  for his help in multilevel regression analysis. The IBGP study team is composed of all authors and the following persons:  Vanessa Escuret ,  Microbiology Laboratory, University of Lyon 1, Lyon, France ;  Sylvie Behilil ,  Virology Department ,  Unit of Molecular Genetics of RNA viruses, National Influenza Center, Pasteur Institute ,  CNRS UMR3569 ,  Université Paris Diderot Sorbonne Paris Cité, Paris, France ;  Tan Tai Bui  and  Elodie Nauleau ,  Open Rome  ( Organize and Promote Epidemiological Network ), Paris, France; the.
Finite element model The personalized FEM (5188 elements, 1997 nodes), implemented in ANSYS V11 (Ansys Inc. , Canonsburg, PA, USA), has been previously described  [23] [24] [25] [26] [27]. The main components of the model were the pelvis, sacrum, thoracic and lumbar vertebrae, intervertebral discs, ligaments and ribcage; material properties are summarized in Table  2. A custom made algorithm allowed transformation of vertebral volume models to beam models. The ribcage was composed of ribs, costal cartilage, intercostal membrane, intercostal ligaments, sternum and costovertebral and costo-transverse joints. Ribs and costal cartilage were modeled by elastic beams, and in the present study they were improved from previous works by adapting their Young's modulus according to the patient's Risser grade  [28] , while their second moments of area were adapted according to vertebral level from an existing database of scoliotic adolescent rib morphology  [29].
Acknowledgments GK is supported by the  Ligue contre le Cancer  (équipe labelisée);  Agence National de la Recherche (ANR) ;  Association pour la recherche sur le cancer (ARC) ;  Cancéropôle Ile-de-France ;  Institut National du Cancer (INCa) ;  Fondation Bettencourt-Schueller ;  Fondation de France ;  Fondation pour la Recherche Médicale (FRM) ; the  European Commission (ArtForce) ; the  European Research Council (ERC) ; the  LabEx Immuno-Oncology ; the  SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE) ; the  SIRIC Cancer Research and Personalized Medicine (CARPEM) ; and the  Paris Alliance of Cancer Research Institutes (PACRI).
These results are of importance and need to be confirmed by the ongoing randomized control trial (NCT01399593) comparing eculizumab to standard of care (including plasmaphereses and intravenous immunoglobulins) in the prevention of ABMR in living donor kidney transplant recipients requiring desensitization. The authors also point out the possible role of superimposed complement-independent mechanisms and proximal complement pathways to drive antibody-mediated injury in eculizumab-treated patients. This report from the Mayo group is valuable for the transplant community because it provides a better understanding that beyond acute, clinical overt, typical early onset ABMR cases, other forms or clinical courses of the disease can be observed. Especially under new potent drugs such as eculizumab clinical presentation of ABMR seems to be modified.
We next investigated the role of BM-derived macrophages from the various mice strains regarding myogenic precursor cells (MPCs) using in vitro assays. No differences were observed in MPC proliferation or fusion (Supplementary Fig. 7 ). Neither CX3CR1 nor CCR2 were detected on satellite cells  13  , on myoblasts or on regenerating myofibers (data not shown). To address more globally the mononuclear phagocyte functions that may promote muscle regeneration, we performed a genome-wide microarray analysis of the four mononuclear phagocyte subsets from WT, Cx3cr1 À / À , Ccl2 À / À and Cx3cr1 À / À Ccl2 À / À muscles on day 4 post injury (GSE73473). One-way analysis of variance analysis identified 434 genes (Po0. 05) that distinguished the four subsets (Fig. 2e ). Using hierarchical clustering and pathway analysis, we identified 10 clusters that confirmed the original identity and functions of each subset.
We used image J software to count three fields always chosen in the same overall injured area (representing 660±150 myofibers) for at least six different mice analysed per time point. Regenerating myofiber density was assessed in the same fields and is expressed as the number of regenerating myofibers per field. Phagocytosis was assessed on day 4 post injury on muscle cross-sections stained with haematoxylin/eosin by counting the ratio of infiltrated to non-infiltrated necrotic myofibers. Vascularization was quantified on muscle cross-sections stained with wheat germ/Griffonia simplicifolia agglutinin. We counted 8 ± 1 fields (at Â 20 magnification) chosen randomly over the entire injured area and representing 485±160 myofibers, in three different mice. Areas of fat, calcification and fibrosis were evaluated over the entire injured area of three muscle cross-sections at levels spaced 900 mm apart, stained, respectively, with Oil Red O, Alizarin Red and Masson Trichrome and recorded with a Nikon AZ100 macroscope connected to a DS-Ri1 camera (Nikon).
Appropriate thresholds were set with image J software to evaluate these areas. Each parameter was studied on days 4 (except fibrosis), 10 and 21 post injury in at least six different mice. Isolation of leukocytes and macrophages from muscle. Mice were flushed with 10 ml of PBS to remove blood. Muscles and fascia were weighed together, minced Analysis on day 10 post injury of muscle regeneration in Ccl2 À / À mice, transfected (n ¼ 3) or not (n ¼ 3) with a pLIVE plasmid encoding for human ApoE3, by measurement of mean CSA of regenerating myofibers, myofiber density and areas of fat and calcification. In this experimental system, systemic expression of ApoE3 was detected for at least 8 days after transfection (data not shown). Data are mean þ s. e. m. of a single experiment. Scale bar, 100 mm.
5-CD11b (clone M1/70, ebiosciences, 1:500) and APC-F4/80 (clone BM8, ebiosciences, 1:150). A PE-streptavidin (1:1,500, BD Biosciences) was used to reveal Mgl1 expression. Cells were analysed on a FACS Canto II (BD Biosciences) with Diva and FlowJo softwares. Sorting of macrophage cell subsets was performed on a FACSAria II cell sorter (BD Biosciences). Microarray analysis, normalization, data set analysis. The four subsets of mononuclear phagocytes were sorted from the injured muscle by flow cytometry on day 4 post injury with the gating strategy showed in Fig. 2. RNA was with the Ovation Pico WTA system V2 (NuGEN) and the resulting complementary DNA (cDNA) was hybridized on Illumina whole mouse genome oligo microarrays (WG6 V2. 0). Array data were analysed with Genome studio (Illumina) and MeV software.
Filter on background signals and quantile normalization were applied, and only probe sets showing significance (P-valueo0. 05) in 8 of the 16 samples were selected. One-way analysis of variance (Po0. 01) with subsequent hierarchical clustering was performed on median centred log2 intensity of the resulting 2,472 probes and identified 434 genes that discriminated between the four cell subsets and spread into 10 clusters. Genes showing differential expression in Ccl2 À / À mice compared with WT, Cx3cr1 À / À and Cx3cr1 À / À Cc2 À / À were selected according to Eisen et al. 56  and comparisons are presented with Venn diagrams (http://bioinfogp. cnb. csic. es/tools/venny/index. html). Ingenuity Pathway Analysis (IPA; Ingenuity Systems Inc. ) software was used to identify metabolic and signalling pathways.
Phagocytosis was expressed as the number of macrophages containing at least one microsphere per 1,000 cells, counted using and Image J software, in three distinct experiments. For some experiments, macrophage-enriched muscular cell suspensions were cultured for 16 h with or without addition of Apolipoprotein E3 (Leinco Technologies) at 10 mg ml À 1 , recombinant human cytokines CX3CL1 (R&D Systems) or CCL2 (PeproTech) at 100 nM. In vivo phagocytosis was assessed on day 4 post injury as the percentage of phagocytosed myofibers (infiltrated by mononuclear cells) among the total number of necrotic (not infiltrated) þ phagocytosed myofibers. In some case, Apolipoprotein E3 was injected in the muscle, twice per day (2 Â 10 mg), for 3 days. Statistical analyses. Data are presented as the mean plus the standard error of the mean (s.
Acknowledgements This work was supported by the  European Community's Seventh Framework  Project  FP7-Health-2009 ENDOSTEM 241440 ,  Association Franc¸aise contre les Myopathies (AFM)   15775 , the  Institut National de la Santeet de la Recherche Medicale (INSERM)  and the  UniversitePierre et Marie Curie (UPMC). We are deeply grateful to  Olivier Levy  and  Florian Sennlaub  from the  'Institut national de la vision ' for the generous gift of ApoE3-pLIVE and pLIVE plasmid controls.