dataesr/scientific-paragraphs-categorization huggingface dataset:
Because some datasets were not normally distributed, we used nonparametric statistical testing throughout (SigmaPlot 12; Systat Software). The Mann-Whitney U test was used for comparisons of unpaired data, whereas the Wilcoxon Signed Rank Test was used to compare paired datasets. For multiple group comparisons, we performed a Kruskal-Wallis ANOVA on Ranks, with Dunn's Test for further post hoc definition of comparisons. Significance for all statistical tests was set at p Ͻ 0. 05 unless noted otherwise. Data are represented as group mean Ϯ SEM unless stated otherwise.
Kingdom Awards  UU138197109  and  MC_UU_12020/5 ,  Parkinson's UK  Grant  G-0806  and  Monument Trust Discovery Award J-0901 ,  Wellcome Trust   Investigator Award   101821  to  P. J. M. ,  Association France Parkinson Ph. D. fellowship  to  A. A. ,  Fondation de France , and  Agence Nationale de la Recherche  Grant  08-JCJC-0087  and Grant  LABEX BRAIN ANR-10-LABX-43. A. S. was supported in part by the  European Union Marie Curie European Re-integration  Grant  SNAP-PD. K. C. N. was supported in part by the  Human Frontier Science Program  ( LT000396/2009-L ). S. V. A. was supported in part by a  Wellcome Trust   Doctoral Studentship in Neuroscience 099711. F. N. G. was supported in part by a  University of Oxford Clarendon Fund Scholarship.
Behavioral experiment Subjects. Eight volunteers (three females, aged 21-39, including two authors) participated in the first behavioral part of the study. All subjects had normal or corrected-to-normal visual function and no neurological disorders. Apparatus and stimuli. Intermittent photic stimulation was delivered through a ganzfeld (i. e. , a homogeneous visual field) flickering sinusoidally from black to white at various frequencies, with a small black fixation dot at the center (17 different frequencies  : 3, 5, 7, 8, 9, 10, 11, 12, 13,  14, 16, 18, 20, 24, 28, 33,  and 40 Hz). The stimulation was provided through a cathode ray monitor (resolution: 800 ϫ 600; refresh rate: 160 Hz) via the Psychophysics Toolbox  (Brainard, 1997)  running in MATLAB (The MathWorks). Procedure. Participants were seated at an ϳ60 cm distance from the flickering screen, with their head placed on a chin support, and instructed to fixate the black fixation dot at the center of the screen, keeping their eyes open.
This discussion procedure was also repeated at the end of each of the four experimental sessions. During the four experimental sessions, at the end of each 100 s trial, subjects were required to describe the experienced hallucinatory percept(s) in an open written report. Moreover, they were asked to indicate the experienced vividness (in a scale ranging from 0 to 10) of each reported percept; they were also encouraged to make sketches of the perceived shapes, either immediately after each trial, or at the very end of the experiment. Data acquisition and analysis. Behavioral reports were classified by the experimenters in main pattern clusters, considering complex percept classes resulting from sketches and descriptions of the hallucinatory phenomena. The shape clusters were initially defined based on those proposed by previous studies on flicker-induced illusions  (Becker and Elliott, 2006; Allefeld et al.
Electrophysiological experiment Participants. Twenty volunteers participated in the second electrophysiological experiment (11 female, aged 21-36, including one author). All subjects had normal or corrected-to-normal visual function and no neurological disorders. Apparatus and stimuli. EEG and EOG were recorded at 1024 Hz using an ActiveTwo BioSemi system (64 cranial and three ocular active electrodes), while stimulus presentation was delivered through a cathode ray monitor (resolution: 1024 ϫ 768; refresh rate: 100 Hz) via the Psychophysics Toolbox  (Brainard, 1997)  running in MATLAB (The MathWorks). Procedure. Participants were sitting at an ϳ60 cm distance from the screen, with their head placed on a chin support, and instructed to fixate the black fixation dot in the center of the screen.
They attended one experimental session during which the two static pictures were pseudorandomly presented, 120 times each in 12 s trials. EEG and EOG recordings were acquired concurrently. The pictures subtended 36. 5 ϫ 27 degrees of visual angle. Data acquisition and analysis. EEG recordings were downsampled offline to 256 Hz for data analysis via the EEGLAB  (Delorme and Makeig, 2004 ) toolbox for MATLAB. Data were re-referenced to average reference, notch-filtered (band-stop 45-55 Hz) and high-pass filtered (cutoff 0. 5 Hz), and then epoched from 1000 ms before to 12,000 ms after stimulus onset. Baseline EEG activity from the prestimulus interval (Ϫ1000 ms) was subtracted from each trial. Finally, all trials were visually inspected for artifacts and eye movements, and potentially rejected; channels containing abundant artifacts were discarded and replaced by an interpolation of adjacent electrodes.
Value of the data There is a limited number of publicly available datasets for comprehensive morphometric analysis of white matter microstructure. Our dataset illustrates the complex relationship between axon caliber and the myelin g-ratio in eight distinct regions of the corpus callosum of a cynomolgus macaque. The data is systematized in a way that makes it easy to explore the relationship between aggregate metrics (AVF, MVF, aggregate g-ratio) and the underlying distributions producing these metrics. 1. Data, experimental design, materials and methods.
Acknowledgments The authors would like to thank  Dr. Michael Petrides  for providing the animal scanning resources. This work was funded by the  Natural Sciences and Engineering Research Council of Canada  ( NSERC 17426-2012 ) and the  Canadian Institutes of Health Research  ( CIHR MOP-43871 ). The granting agencies had no involvement in study design, data collection, analysis and interpretation of data, writing of the report, or the decision to submit the article for publication.
Data analysis The inter-infusion intervals (III) for the 19 rats, during the last three sessions of the experiment were analyzed. Every point on Fig. 7i  is the average III over 19 rats and over the last three trials (averaged over 3*19=57 IIIs), for the n-th III after reducing the unit-dose of cocaine. To test the statistical significance of the IIIs being lower in the initial post dosereduction self-administrations, we assume that III becomes stable after 15 post-reduction responses. Thus, for each animal and for each of the three sessions, we can use the IIIs between the 15 th and the 25 th post-reduction responses as the baseline III for that animal and that session (25 is the minimum number of post-reduction responses among all animals; i. e. , the number of responses that all animals achieved).
ACKNOWLEDGEMENTS We thank  Peter Dayan  for critical discussions. M. K. and B. G. are supported by grants from  Frontiers du Vivant , the  French MESR ,  CNRS ,  INSERM ,  ANR ,  ENP  and  NERF. S. H. A. is supported by the  French Research Council (CNRS) , the  Université de Bordeaux , the  French National Agency (ANR ,  ANR2010-BLAN-1404-01 ), the  Conseil Régional d'Aquitaine  ( CRA20101301022 ;  CRA11004375/11004699 ) and the  LabEX BRAIN  ( ANR-10-LABX-43 ).
Protein analysis Protein extraction and Western blot (WB) were performed according to classical procedures. To detect OCAM in the medium, 10 ml of neurosphere-conditioned supernatant was syringefiltered (10 μm), precipitated with 4 vol. of cold acetone (-20°C) and resuspended in 200 μl Laemmli loading buffer. Antibody references and dilutions are: rabbit OCAM (  [13] ; 1:500), goat OCAM (R&D, #AF778, 1:2000), ErbB2 (Cell Signaling, #2165, 1:1000), phospho-ErbB2 (Cell Signaling, #2241, 1:1000). To detect phosphorylated receptors in neurospheres, we used a mouse phospho-Receptor Tyrosine Kinase array (phospho-RTK array R&D, #ARY014) which was probed with OCAM KO and OCAM WT neurosphere extracts according to manufacturer's recommendations. WB and arrays were quantified using ImageJ software.
cRNA preparation, microarray hybridization and analysis Hybridization targets were obtained following a double amplification procedure according to the protocol developed by Affymetrix (GeneChip Two-Cycle Eukaryotic Target Labeling Assay; Affymetrix, Santa Clara, CA, USA). A hybridization mixture containing 12 μg of biotinylated cRNA was generated and hybridized to Affymetrix HG-U133 Plus PM Array Strip (4 injured and 4 control animals). Chips were scanned using an Affymetrix GeneAtlas scanner and data files were generated with Affymetrix Expression Console v1. 2. 1. The Transcriptome Analysis Console (TAC) 2. 0 software was used for analysis. The full results obtained from this transcriptomics analysis of the adult spinal cord niche will be reported elsewhere.
Using immunoprecipitation, we have not been able to demonstrate a direct interaction between OCAM and ErbB2 and no clear co-localization of the two proteins was observed using confocal microscopy in neurosphere cells (data not shown). Thus it appears improbable that OCAM regulates ErbB2 by direct physical interactions as observed for instance between L1CAM and EGFR  [37]. It has been shown that NCAM1 can indirectly regulate the ubiquitin-mediated degradation of EGFR through phosphorylation of the ubiquitin ligase c-Cbl  [36]. Likewise, OCAM might influence the degradation of ErbB2 by its cognate ubiquitin ligases, notably CHIP  [38]  and c-Cbl ligase  [39]. Using electron microscopy and an internalization assay, we observed that OCAM localization is dynamic and that in addition to the membrane, OCAM was also associated with a pool of internal vesicles.
Background: Paracetamol's (APAP) mechanism of action suggests the implication of supraspinal structures but no neuroimaging study has been performed in humans. Methods and results: This randomized, double-blind, crossover, placebo-controlled trial in 17 healthy volunteers (NCT01562704) aimed to evaluate how APAP modulates pain-evoked functional magnetic resonance imaging signals. We used behavioral measures and functional magnetic resonance imaging to investigate the response to experimental thermal stimuli with APAP or placebo administration. Region-of-interest analysis revealed that activity in response to noxious stimulation diminished with APAP compared to placebo in prefrontal cortices, insula, thalami, anterior cingulate cortex, and periaqueductal gray matter. Conclusion: These findings suggest an inhibitory effect of APAP on spinothalamic tracts leading to a decreased activation of higher structures, and a top-down influence on descending inhibition.
Volunteers Participants were recruited through the database of the Clinical Pharmacology Centre of the University Hospital of Clermont-Ferrand, France. Male volunteers (to avoid pain thresholds variability due to menstrual cycle in females) were eligible if they were $18 years old, did not take analgesic or anti-inflammatory treatment in the last 7 days and were nonsmokers. Exclusion criteria included the following: a known hypersensitivity to APAP, concomitant pathologies, contraindications in the realization of the MRI without injection (claustrophobia, pacemaker, hearing aid, cerebral clip etc), consumption of alcohol and addiction to street drugs. Eligible volunteers were informed about the protocol and provided a signed informed consent.
Baseline fMRI was recorded using the thermal stimulation paradigm (described later). Each MRI session lasted 40 minutes. Subjects were then randomized at T0 in APAP or placebo groups. Double-blinding was fully respected with the volunteers and the members of staff. A research nurse who was only involved in drug allocation was in charge of drug administration. fMRI data acquisition was then repeated at T0+100 minutes (T0+100) during the application of the same thermal stimulation paradigm. Perceived pain was evaluated at the end of each fMRI session, at baseline and T+100 with a numeric pain rating scale ranging from 0 -no pain to 10 -maximal pain. Volunteers were then discharged after a clinical examination and came back a week later for the second period of the fMRI trial and were administered APAP or placebo in a crossover design.
The double-blind, randomized, and crossover design of this study was chosen in order to be able to discard all variable environmental factors, placebo analgesia, and have the subjects as their own controls. Such a clinical trial will isolate pure drug effects if expectations and beliefs of the subject are identical at each session to avoid any bias. The second test after administration of APAP was set at T0+100 based on published data on oral APAP with a maximal analgesic effect at 90-100 minutes  3  and also to allow the patient some time out of the MRI scanner to limit fatigue and poor compliance. The main outcome of the study was the impact of APAP compared to placebo on BOLD fMRI activity by the analysis of the regions-ofinterest (ROI). randomization Patients were randomized in the APAP group (2 g of oral APAP in four capsules of 500 mg APAP each) or in the placebo group (four capsules of 500 mg lactose each).
fMri data analysis The neuroimaging data were preprocessed and analyzed using SPM8 (Statistical Parametric Mapping, Version 8; Wellcome Department of Imaging Neuroscience, London, UK), in Matlab 7. 12 (MathWorks). Co-registration of T1 anatomical images was performed prior to spatial normalization into the MNI space. Functional images were first preprocessed with slice-time correction, and motion correction by realigning all images to the first image. The motion correction parameters were examined for each individual and instantaneous movement was always less than a third of the voxel size. The BOLD images were then spatially normalized into the MNI space using trilinear interpolation, with the normalization parameters determined during the normalization of the structural images. Subsequent spatial smoothing using isotropic 8 mm full width at half maximum Gaussian kernel was applied to the functional images to increase signal-to-noise ratio.
statistical analysis Previous pilot fMRI studies with analgesics, opioids, and non-opioids include a variable number of subjects. 32, 33, 37  double-blind, crossover, controlled fMRI study with nonopioids included 14 subjects  27  and an APAP pharmacological study with cerebral-evoked potentials included 12 subjects. 35  Considering these data, the estimated number of subjects was 16, and taking into account potential dropouts, 20 patients had to be included. Statistical analysis was performed using Stata software, version 13 (StataCorp LP, College Station, TX, USA). The tests were two-sided, with a type I error set at α=0. 05. The characteristics of patients between groups were compared using Student's t-test or Mann-Whitney test according to t-test hypotheses (assumption of normality studied by Shapiro-Wilk test and homoscedasticity by Fisher-Snedecor test) for quantitative parameters and using Fisher's exact test for categorical factors.
Acknowledgments To  Clermont-Ferrand University Hospital  for providing full financial support of the trial. SL and RV received funding from the  French program  " Investissement d'Avenir " run by the  "Agence Nationale pour la Recherche" ; grants " IHU-A-ICM, Paris Institute of Translational neuroscience " and " Infrastructure d'avenir en Biologie Santé - ANR-11-INBS-0006 ".
Image processing For image processing, we used SPM8 software (Statistical Parametric Mapping; Wellcome Department of Imaging Neuroscience, University College London  [24] ) running on MATLAB R2010a (MathWorks, Natick, MA, USA). SPECT images of each patient were spatially normalized to the Montreal Neurological Institute space. Intensities were linearly scaled using the average perfusion of the central regions of cerebellum because these areas are almost preserved in patients with DLB. Finally, images were smoothed with a Gaussian kernel of 12 mm.
Dysfunction of BA 18 causes errors in visual processing, with occurrence of object distortions that explain visual illusions particularly well. Patients with DLB report visual illusions more frequently than true hallucinations  [26]. The localized relative dysfunction of this visual area, which we found in the present study, is consistent with previous data  reported in the literature  [9, 10, 12, 15, 27]. It confirms the original hypothesis that the occipital dysfunction specific to DLB  [28, 29]  might be involved in the occurrence of VHs. The implication of visual areas was previously confirmed by other studies  [10, 12, 16] , in association with the parietal cortex  [10]  or the right temporo-occipital junction  [12]. In previous work by our group involving patients with AD chosen from the Alzheimer's Disease Neuroimaging Initiative database, we showed atrophy of the occipital cortex in patients with VHs.
40 oil) objective. data Presentation and Analysis Signals emitted at 620 and 520 nm were collected at the indicated times using time-resolved settings for the donor (1500 μs delay, 1500 μs reading time) and acceptor (150 μs delay, 400 μs reading time). Ratio 620/520 (R) was obtained by dividing the donor signal (620 nm) by the acceptor signal (520 nm) at a chosen time and multiplying this value by 10,000. Data are expressed as percent of maximal internalization ["% of max. internalization (620/520 nm)"] and were calculated using the following formula: [(Rt -Rmin)/(Rmax -Rmin)] × 100 where Rt corresponds to the ratio observed at a chosen time. Dose-response curves were fitted using non-linear regression dose-response "log [ligand] versus responses (with three parameters except for CXCR7)" routine of Prism 5 (GraphPad Software, La Jolla, CA, USA) to provide the maximal (Emax) and half maximal effective concentration EC50 values.
ACKNoWLedGMeNts This work was supported by SIDACTION (AI21-1/01708), AP-HP, Agence Nationale de la Recherche (ANR-07-MRAR-029). We thank the ARPEGE (Pharmacology Screening-Interactome) platform facility at the Institut de Génomique Fonctionnelle (Montpellier, France). MC was supported by the "Fondation pour la Recherche Médicale" and LK by the Laboratory of Excellence in Research on Medication and Innovative Therapeutics (LERMIT, Investissements d' Avenir-ANR-10-LABX-0033-LERMIT). We are grateful to Dr. Françoise Baleux (Unité de Chimie Organique, Institut Pasteur, Paris, France) and Dr. D. Bonnet (UMR7200, University of Strasbourg, Illkirch, France) for the generous donation of CXCL12 and Chalcone 4 respectively, and thank Dr. F. Arenzana-Seisdedos (Laboratoire de Pathogénie Virale, Institut Pasteur, Paris, France) for his support of the project.
Alternatively, immunolabeled astrocytes were examined at 633 and 203 with a confocal laser-scanning microscope (Leica TBCS SP2). Stacks of consecutive confocal images taken at 1 mm intervals were acquired sequentially with two lasers (argon 488 nm for GFAP-eGFP and 561 nm for Etd). Fluorescence was quantified in arbitrary units (AU) with image processing software Adobe Photoshop (Adobe Systems Software Ireland Ltd. ). Dye uptake intensity was evaluated as the difference (F 2 F 0 ) between the fluorescence (F) from astrocytes (20-30 cells per slice) and the background fluorescence (F 0 ) measured in the same field where no labeled cells were detected. At least three fields were selected in every slice for background evaluation.
3 EGTA (pH 7. 3; 280 mOsm). Patch-clamp recordings (10 kHz sampling and 2 kHz filtering) were performed with Pclamp9 software (Molecular Devices, Foster City, CA), membrane voltages and currents were amplified by a MultiClamp 700B amplifier and sampled by a Digidata 1322A Interface. Input resistance (R in ) was measured in voltage-clamp mode by applying hyperpolarizing voltage pulses (10 mV, 150 ms) from a holding potential of 280 mV. To evaluate the level of coupling, sulforhodamine B (559 Da; 1 mg/mL; Invitrogen, Eugene, OR) was added in the intracellular solution and loaded in the recorded cells during 15 min in current-clamp mode. Intercellular diffusion of sulforhodamine B was captured thereafter with the CCD camera (Pixelfly QE, The Cook Corporation, Romulus, MI) and the number of surforhodamine B positive cells (i.
Electrophysiology Slices (400 mm thick) were treated during 3 h with LPS (50 ng/ mL); in some experiments mimetic blocking peptides, Gap26 (0. 16 mM) and 10 Panx1 (0. 4 mM) were applied 15 min before and during LPS exposure. For synaptic recordings, a cut was made between the CA3 and CA1 region to prevent bursting, and slices were bathed in a modified ACSF containing 100 lM picrotoxin to block GABA A receptor-mediated inhibitory postsynaptic currents. Field excitatory postsynaptic potentials (fEPSPs) were recorded in CA1 area with glass pipettes (2-5 MX) filled with ACSF, and evoked by stimulating Schaffer collaterals in stratum radiatum (0. 1 Hz) with a monopolar stimulating electrode. Recordings were acquired with Axopatch-1D amplifier (Axon Instruments, Molecular Devices, Sunnyvale, CA), filtered at 2 kHz, digitized at 10 kHz, and analyzed online using Clampfit software (Molecular Devices).
Following several washes in PBS, slices were mounted in mounting medium (Fluoromount-G) and examined with a confocal laser-scanning microscope (Leica TBCS SP2). Stacks of consecutive confocal images taken at 300 nm intervals were acquired sequentially with two lasers (argon 488 nm for GFAP and 561 nm for CD11b) Z projections were reconstructed using the LAS AF Software.
Fluo-4 and SR 101 were excited at respectively 488 nm and 587 nm through a light emitting diode, controlled by the Axon Imaging Workbench software. Fluorescent emission of labeled cells at 515 nm (Fluo-4/AM) and 602 nm FIGURE 1: LPS treatment increases ethidium bromide uptake through astrocyte hemichannels in acute hippocampal slices. (A) Fluorescence representative contrasted images of acute hippocampal slices derived from GFAP-eGFP transgenic mice show GFAP-eGFP (green) astrocytes and Etd uptake (red) under control conditions (control), under exposure to LPS (50 ng/mL) alone (LPS) and in presence of the CxHC and Panx channel blocker carbenoxolone (200 lM) applied 15 min before and during dye uptake measurement (LPS 1 CBX). Images of hippocampal astrocytes were taken from the CA1 interpyramidal zone (CA1 stratum radiatum) as depicted by the square in the upper scheme of a hippocampal slice.
Analyses of the samples were performed with a commercial laser-induced fluorescence capillary electrophoresis (CE-LIF; CE: Beckman Coulter, P/ACE MDQ; LIF: Picometrics, LIF-UV-02, 410 nm 20 mW) as following. The samples were processed for micellar CE-LIF and were fluorescently derivatized at RT for 60 min with napthalene-2,3-dicarboxaldehyde (NDA) before being analyzed by CE using a hydroxypropyl-bcyclodextrin (HP-b-CD) based chiral separation buffer. All electropherograms data were collected and analyzed using Karat 32 software v8. 0 (Beckman Coulter, Fullerton, CA). Further analysis was made using GraphPad Prism 4. 03 software. The extracellular and intracellular amounts of L-glutamate were normalized to the protein content determined from pooled hippocampal slices by the Lowry method using the BCA protein Pierce (ThermoScientific, CA) assay with bovine serum albumin (BSA) as standards.
16 mM), the Px1 channel blocker 10 Px1 (0. 4 mM), the P2X 7 blocker BBG (1 lM) or a mixture of blockers, applied 15 min before and during Etd measurements. Data are obtained from 5 to 20 independent experiments. *P < 0. 05; ***P < 0. 001: effects of blockers compared with the effect induced by LPS alone on Etd uptake; &P < 0. 05; &&P < 0. 01: effects of blockers (BBG and 10 Px1) compared with LPS/CBX treatment effect (Kruskal-Wallis test followed by Dunn's Multiple Comparison post hoc test). The effect of LPS/CBX treatment is not significantly different from LPS/La 13 , LPS/Gap26, or LPS/Gap26/ 10 Px1 treatments while LPS/BBG and LPS/ 10 Px1 are statistically different from LPS/CBX treatment effect. Note that when compared with control condition (without LPS), Etd uptake is increased by LPS treatment (P < 0.