dataesr/scientific-paragraphs-categorization huggingface dataset:
Acknowledgments We thank our colleagues at  CAST  for many years of collaborative work and  R. de Oliveira  and his team at  CERN  for the manufacturing of the microbulk readouts. We also thank  D. Calvet  from  CEA/Saclay  for his help with the AFTER electronics. We acknowledge the support from the  European Commission  under the  European Research Council T-REX  Starting Grant ref. ERC-2009-StG-240054 of the  IDEAS program  of the  7th EU Framework Program. We also acknowledge support from the  Spanish Ministry MINECO  under contracts ref. FPA2008-03456  and  FPA2011-24058 , as well as under the  CPAN  project ref. CSD2007-00042  from the  Consolider-Ingenio 2010 program. These grants are partially funded by the  European Regional Development funded (ERDF/FEDER). Part of this work was performed under the auspices of the  U.
Acknowledgements We thank the  RHIC Operations Group  and  RCF at BNL , the  NERSC Center at LBNL , the  KISTI Center in Korea , and the  Open Science Grid consortium  for providing resources and support. This work was supported in part by the  Offices of NP  and  HEP  within the  U. S. DOE Office of Science , the  U. S. NSF ,  CNRS/IN2P3 ,  FAPESP CNPq of Brazil , the  Ministry of Education and Science of the Russian Federation ,  NNSFC ,  CAS, MoST and MoE of China , the  Korean Research Foundation ,  GA  and  MSMT of the Czech Republic, FIAS of Germany, DAE ,  DST , and  CSIR of India , the  National Science Centre of Poland, National Research Foundation  ( NRF-2012004024 ), the  Ministry of Science, Education and Sports of the Republic of Croatia, and RosAtom of Russia.
Although W bosons decaying to a lepton and a neutrino are more difficult to detect, their rate is about ten times larger than that of Z bosons decaying to leptonic final states. The production of W bosons in PbPb collisions was reported by CMS  [12]  and ATLAS  [13] , using data corresponding to an integrated luminosity of 7. 3 µb -1 and 150 µb -1 , collected in 2010 and 2011, respectively. The W boson yield per NN collision was shown to be compatible with the one measured in pp collisions, when taking into account isospin effects arising from the mixture of protons and neutrons in the colliding nuclei. However, the presence of 10-20% nPDF effects on Z and W boson production could not be excluded due to the relatively large experimental and theoretical uncertainties of these results. The 2013 pPb LHC run provides the best currently available data sample to look for initial-state effects (such as PDF modifications) using electroweak bosons.
[29, 30]. Table  1  gives the measured cross sections for each channel separately and combined, as a function of the lepton pseudorapidity, for positive and negative leptons. The theoretical predictions and their uncertainties (coming from the PDF set and from the renormalisation and factorisation scales) are also given. The agreement between the data and both theoretical predictions is within the uncertainties, although a small excess of W -candidates appears at negative η lab , i. e. in the Pb ion beam direction. The comparison between the CT10 and CT10+EPS09 calculations shows that the predicted modifications of the PDFs are of the same order as the theoretical uncertainties. This indicates that cross sections alone lack discriminating power, and motivates the study of various asymmetries of the + and -cross sections.
The frequency of adverse events (AEs) was low across all groups; 5 (12. 2%), 3 (7. 1%), and 2 (5. 0%) patients in the 14 mg, 7 mg, and placebo groups, respectively, discontinued treatment due to AEs. Teriflunomide reduced the number of T1-Gd lesions vs placebo (14 mg: 46. 6% relative reduction, p ¼ 0. 1931; 7 mg: 64. 0%: relative reduction, p ¼ 0. 0306). Conclusions: Teriflunomide added to stable-dose GA had acceptable safety and tolerability, and reduced some MRI markers of disease activity compared with GA alone. NCT00475865 (core study); NCT00811395 (extension).
Introduction Teriflunomide (AUBAGIO, Genzyme, Cambridge, MA) is a once-daily, oral immunomodulator approved for the treatment of relapsingÀremitting MS or relapsing forms of MS (RMS). 1, 2 In two pivotal phase 3 studies, TEMSO (NCT00134563) and TOWER (NCT00751881), teriflunomide 14 mg significantly reduced the annualized relapse rate (ARR) and the risk of disability progression compared with placebo; teriflunomide 7 mg also significantly reduced ARR compared with placebo. 3, 4 eriflunomide monotherapy demonstrated consistent efficacy on MRI parameters in addition to a similar and consistent safety profile with both doses. 3, 5  a 48-week phase 2 study, teriflunomide given as add-on therapy to interferon-b (IFN-b) (NCT00489489 [24-week study] and NCT00811395 [24-week extension]) was associated with an acceptable safety and tolerability profile and reductions in MRI disease activity compared with IFN-b alone.
6  a phase 3 study (TERACLES, NCT01252355), teriflunomide 14 mg added to a stable dose of IFN-b demonstrated an incremental benefit on ARR and a significant reduction (70. 8%; p ¼ 0. 0061) in the number of gadolinium (Gd)-enhancing T1 lesions/scan compared with IFN-b alone, although early study termination (sponsor decision) limited interpretation. Teriflunomide was well tolerated with no new safety concerns identified compared with other phase 3 monotherapy studies. 7  this study, we evaluated the safety and tolerability of teriflunomide added to ongoing glatiramer acetate (GA) for up to 48 weeks in patients with RMS.
Standard protocol approvals, registrations, and patient consents This study (NCT00475865 [24-week study] and NCT00811395 [24-week extension]) was conducted in accordance with the International Conference on Harmonisation Guidelines for Good Clinical Practice and the Declaration of Helsinki. The protocol complied with the laws and regulations of the countries where the study was conducted. All patients provided written informed consent prior to study initiation. An independent data monitoring committee evaluated the design, ethical conduct, and safety of the study.
6 Our data support the safety of teriflunomide when added to ongoing GA therapy and, by extension, as a sequential treatment for patients previously treated with GA. This study was not sufficiently powered to assess the efficacy of teriflunomide as an add-on therapy to GA; the lack of a teriflunomide-only arm, and the greater baseline MRI disease activity in the 7 mg group, further limit interpretation of efficacy outcomes. Nevertheless, we observed a general pattern of lower MRI activity in the teriflunomide groups compared with placebo, indicative of a lack of a negative drugdrug interaction between teriflunomide and GA. We also noted a significant reduction  The volume of Gd-enhancing T1-lesions for each patient divided by the number of scans for that patient. c Total lesion volume defined as the total volumes of hyperintense on T2 plus hypointense on T1 as measured by MRI scan.
Acknowledgements This study was funded by  Genzyme , a  Sanofi company. This manuscript was reviewed by  Stephanie Jurgensen ,  Deborah Dukovic  and  Karthinathan Thangavelu , of  Genzyme. Editorial support was provided by  Scott Chambers ,  Fishawack Communications Inc. , also funded by  Genzyme. Essential contributing members of the  MRI Analysis Center (Houston, TX, USA)  included  Professor Ponnada A. Narayana ,  Dr Flavia Nelson ,  Dr Sushmita Datta ,  Dr Irina Vainrub ,  Brandi Carrico ,  Kelly Ton ,  Rimma Brokhin , and  Lucille Lambert. Huiling Li , an employee of Sanofi, was responsible for statistical analyses. aventis, Santhera,  Siemens ,  Teva ,  UCB , and XenoPort; speaker fees from  Bayer HealthCare, Biogen Idec ,  Merck ,  Novartis , sanofi-aventis, and  Teva ; support for educational activities from  Bayer HealthCare, Biogen ,  CSL Behring ,  Genzyme ,  Merck ,  Novartis ,  Sanofi , and  Teva , royalties from  Neurostatus Systems GmbH ; and grants from  Bayer HealthCare, Biogen Idec ,  European Union ,  Merck ,  Novartis ,  Roche Research Foundation, Swiss MS Society , and the  Swiss National Research Foundation.
In contrast, HD flies overexpressing PINK1 did not show decreased ATP levels at the same age (Figure  3d ). PINK1 neuroprotection against mHtt toxicity is dependent on Parkin. To determine if PINK1-mediated neuroprotective effect involves Parkin, we examined whether Drosophila parkin overexpression (parkin OE ) alleviates HD phenotype in Drosophila. Unexpectedly, overexpressing Parkin failed to modify the life expectancy or the photoreceptor loss of flies expressing Httex1p Q93 under the control of the neuronal driver elav-GAL4 (Supplementary Figure  S1 ). Coexpression of Parkin with PINK1 was deleterious as no adult flies emerged from pupae. This observation is in agreement with previous data showing that ). Quantifications were performed as followed: n4150 neurons in six flies per condition coexpression of PINK1 and Parkin under the heat-shock-GAL4 driver leads to pupal lethality.
After staining with 2% uranyl acetate and dehydratation, samples were included in Epon resin. Ultrathin sections were examined with a Philips CM10 (Eindhoven, The Netherlands) or a Leo 912 Zeiss (Zeiss Microscopy, Jena, Germany) microscope at 100 kV. Pseudopupil analysis. Pseudopupil analysis was performed as described previously. 12 The number of photoreceptors was determined from 20 ommatidia per fly. Data from at least seven flies per condition were averaged and were presented PINK1 rescues mitochondrial mutant Htt toxicity B Khalil et al.
Acknowledgements. We thank  LThompson, JL Marsh ,  J Chung ,  P Verstreken ,  M Guo ,  LM Martins  and the  Bloomington Drosophila Stock Center  for constructs and mutant or transgenic flies. We also thank  R Youle ,  W Springer  and  R Vago  for Parkin and PINK1 plasmids;  Jean-Paul Chauvin  for providing his expertise on tissue preparation and electron microscopy analysis, as well as  Marie-Pierre Blanchard  for image analysis. The authors are grateful to  Julien Royet  for support. We wish to thank  Catherine Faivre-Sarrailh  and  Marie-Thérèse Besson  for helpful discussion. This work was supported by a grant from the  CHDI Foundation Inc.
Western blot analysis CD43 -B splenocytes (15 × 10 6 ) were stimulated with 15 μg of goat anti-mouse κ (Southern Biotech) for 10 min at 37°C. Cell lysates (30 μg) were analysed by SDS-PAGE and transferred onto polyvinylidene difluoride membranes (Millipore) as previously reported  [22, 23]. After blocking, membranes were incubated with antiphosphor-Tyr (Cell signalling), anti-phosphor-Erk (Cell signalling), anti-Erk (Cell signalling), anti-phosphor-Akt (Cell signalling), anti-Akt (Cell signalling) and anti-actin antibodies (Sigma), and revealed with HRP-labelled goat anti-rabbit Ig (Biorad) by chemoluminescence (ECL plus, Amersham). Results were analysed with the Java-based image processing program ImageJ that can calculate area and pixel value statistics of user-defined selections and intensity thresholded objects.
ACkNOWLEDgMENTS This work was supported by grants from  Conseil Régional du Limousin ,  Association pour la Recherche sur le Cancer  ( ARC SL 220100601332 ),  Ligue Contre le Cancer de la Corrèze ,  ANR  (Projets Blanc 2011) and " Lions Club de la Corrèze, Zone 33 district 103 Sud ". P. Rouaud  has a fellowship from  ARC  ( DOC20130606964 ). We thank  S. Desforges  and  B. Remerand  for help with animal care.
I. INTRODUCTION Measurement of the electric dipole moment (EDM) of the neutron (or of other fundamental particles) provides an extremely sensitive approach to investigating potential new sources of CP violation and physics beyond the Standard Model. The experimental technique underlying the most sensitive measurement to date  [1, 2]  of the neutron EDM has been discussed extensively in an earlier publication  [3]. The data were collected at ILL, Grenoble, between 1998 and 2002. In this article, we focus solely on the analysis, which we have carried out anew. We begin, in Section II, with a description of the determination of the neutron resonant frequency via the Ramsey method of separated oscillatory fields in conjunction with the cycle-by-cycle corrections from the mercury co-magnetometer.
Acknowledgments This work was funded in part by the  UK Science and Technology Facilities Council (STFC)  under grants  ST/K001329/1 ,  ST/M003426/1  and  ST/L006472/1 ; the  Fund for Scientific Research, Flanders ; grant  GO A/2010/10  of  KU Leuven ; and the  Swiss National Science Foundation  Projects  200020-144473  (PSI),  200021-126562  (PSI),  200020-149211  (ETH) and  200020-140421  (Fribourg). The  LPC Caen  and the LPSC acknowledge the support of the  French Agence Nationale de la Recherche (ANR)  under reference  ANR-09-BLAN-0046. Polish partners wish to acknowledge support from the  PL-Grid Infrastructure, Poland , and from the  National Science Centre, Poland , under grant no. UMO-2012/04/M/ST2/00556. The original apparatus was funded by grants from the  UK's PPARC  (now  STFC ), and we would like to thank the generations of engineers and Research Fellows who contributed to its development, including  I.
dAtA cOllectIOn And AnAlysIs Data regarding demographics, activity level, patient's history, previous treatment received were collected upon first clinical encounter. VAS was collected at the first patient visit, at 3 weeks and at 6 weeks. The need to switch to another treatment modality was assessed at the final follow-up visit. Data analysis was completed using SYSTAT ® 9 for Windows ®. Results will be expressed as a mean for continuous variables (VAS pain score at each time point, age, BMI, height, weight) and as a percentage for categorical variables (gender, laterality). To assess a difference in our primary outcome measure, we used a paired T-test comparing the mean of the differences between the initial VAS and VAS at 3 and 6weeks. A value of p<0. 05 was considered statistically significant.
Study design This was a non-randomized, single-arm, multicentre, open-label, 6month, prospective interventional study in patients with acute schizophrenia previously unsuccessfully treated with oral antipsychotics (Clinical trials. gov number: NCT01281527). A total of 160 sites in 21 countries took part in the study (see Appendix). Prior to trial initiation, the protocol was reviewed and approved by an independent ethics committee in all participating countries. The trial was performed in accordance with the Declaration of Helsinki. Patients were informed of the risks and benefits of the trial and written informed consent was obtained before commencement of any trial-related activities. The study consisted of a screening period, a 6-month study period, and an optional extension phase. This manuscript reports results from the 6-month study period.
Safety and tolerability Evaluation of safety and tolerability included the measurement of extrapyramidal motor symptoms (EPMS) according to Extrapyramidal Symptom Rating Scale (ESRS) total score  (Chouinard and Margolese, 2005)  and adverse events (AEs), reported either directly by the patient or indirectly obtained by means of interviewing patients at study visits. All reported AEs were coded using the Medical Dictionary for Regulatory Activities (MedDRA version 13. 0). Treatment-emergent adverse events (TEAEs) were defined as AEs that were new in onset or were aggravated in severity following initiation of PP. Recording of body weight and calculation of BMI were also performed. As this was a pragmatic study reflecting routine clinical practice, and data on prolactin plasma levels with PP have been extensively collected (in N3000 patients) during the clinical development program  (Gopal et al.
Data analysis The sample size estimation for patients with acute symptoms of schizophrenia switched from oral antipsychotics was based on the primary endpoint for this group. The proportion of patients with at least 30% improvement in PANSS total score was expected to be 40%. Using the large sample normal approximation, it was estimated at least 93 patients were required to reach a 95% confidence interval (CI) for a single proportion that maximally extends 10% from the observed proportion. Efficacy analyses were undertaken in the intent-to-treat (ITT) population, which comprised all patients who received PP at least once, and had at least one post-BL efficacy assessment. Actual values and changes from BL were summarized descriptively at each assessment time point and at the patient's last evaluation (LOCF EP).
Twenty days of field work in 1998 and 1999 that sampled also spring snails  (Haase et al. 2007 ) generated no less than 8,547 specimens of Diplommatinidae, representing 35 species. Segregating the Fiji diplommatinid fauna into species is relatively straightforward, but placing them in genera is problematic. After being relegated for decades in the backwater of land snails systematics, the Diplommatinidae have recently hit the front line of molecular data, integrative taxonomy, and even cybertaxonomy. At the generic level,  Webster et al. (2012)  reconstructed a 5-genes molecular phylogeny of 71 specimens of Diplommatinidae from SE Asia and the West Pacific, representing 54 recognized species and 7 putative genera. Their results indicate that (1) monophyletic clades correspond with both coiling direction and biogeographic patterns; and (2) the ancestral state in the family is sinistrality, with several shifts (three in their dataset) to dextrality.
Acknowledgements We are grateful to the collection managers and curators, who generously gave access to the collections under their care:  Jon Ablett  ( Natural History Museum, London );  Virginie Héros  ( Muséum National d'Histoire Naturelle, Paris );  Ronald Janssen  ( Research Institute Senckenberg, Frankfurt am Main );  Wolf Blankenhorn ,  Barbara Oberholzer  and  Trudi Meier  ( Zoological Museum of the University, Zurich );  Taehwan Lee  ( Museum of Zoology, University of Michigan ). We are much indebted to  Klaus Kittel  ( Wiesthal, Germany ), who undertook the sorting of microsnails from the leaf litter collected in 1998-99, and made the initial family sort. Estée Bochud  ( Naturhistorisches Museum der Burgergemeinde, Bern ) is acknowledged for preparing most of the photos, and  Gilberto Marani  ( Muséum National d'Histoire Naturelle, Paris ) for the maps and graphs.
Milori et al. 18  used excitation at blue wavelength (465 nm) to obtain an emission spectrum characteristic of more humified structures. In this case, the humification degree was calculated using the total area of emission (A 465 ). The fluorescence EEMs were acquired in the scan range 240-700 nm for emission and 220-510 nm for excitation. The spectra were obtained with a 290 nm cut off filter for the emission beam and an excitation increment of 10 nm, totaling 30 scans, slit width 10 nm for the excitation and emission and scan speed 500 nm min -1 for both monochromators. EEMs were extracted from the 30 scan using the three-dimensional-export from Perkin Elmer giving matrices with equal step for emission and excitation wavelength, 10 nm. CP/PARAFAC was used to extract information from the data obtained by classical fluorescence spectroscopy EEMs, allowing us to identify the contribution of the most representative intensities of the fluorophores.
Other biomarkers were measured using commercial ELISA kits according to manufacturer's instructions to assess the astrocyte marker glial fibrillary acidic protein (GFAP; BioVendor, Brno, Czech Republic) and S100b for astroglial cells (BioVendor), neuron-specific enolase (NSE; USCN, Hubei, China), and total tau protein for axonal/neuronal damage (Invitrogen, Carlsbad, CA). 12 CSF samples were used undiluted (S100b, GFAP) or diluted (tau 1:2; NSE 1:10). Optical density values at 450 nm were determined by spectrophotometer (Multiskan Go; Thermo scientific, Waltham, MA), and the albumin/biomarker concentration was calculated from standard curves. Data were summarized using medians (interquartile range, [IQR]) or frequencies (%). Pairwise associations between AI and biomarker levels with demographics, clinical signs and symptoms, severity and outcome measures, and laboratory    The demographics, clinical, and laboratory findings are summarized in Table  1.
Acknowledgments: We thank all the staff and patients at  Mahosot Hospital, Vientiane ,  Lao PDR , for their help in participating in this study and ensuing clinical care and sample collection from the patients involved. Further, we are very grateful to the  Minister of Health  and the Director of the  Curative Department, Ministry of Health , for their support for this study. We acknowledge the support of the  Centre d'Infectiologie Christophe Merieux du Laos  in molecular TBM confirmation. Financial support: This work was funded by the  Wellcome Trust of Great Britain  through the  LOMWRU and MORU grant   089275/Z/09/Z. Authors' addresses:  Sayaphet Rattanavong ,  Rattanaphone Phetsouvanh , and  Phonepasith Panyanivong ,  Wellcome Trust-Mahosot Hospital-Oxford TropicalMedicine Research Collaboration, Mahosot Hospital, Vientiane , Lao PDR, E-mails: sabine@tropmedres.
Procedure Subjects attended a single one hour test session in a temperature-controlled laboratory maintained at 24°C. Following clinical examination for intact sensory and pain pathways (warm/ cool, light touch and pin-prick), all subjects were asked to provide basic demographic data (age, gender, height, weight for BMI) and asked about presence and intensity (numerical rating scale 0-10) of low back pain. All subjects were also asked to detail their average weekly exercise in hours (examples provided such as lawn bowls, walking, cycling, dancing) and then completed the Spielberger State-Trait Anxiety Index (STAI) questionnaire. The OA group also completing the Western Ontario and McMaster (WOMAC) Knee-specific questionnaire. Pain thresholds for pressure (PPT), cold (CPT) and heat (HPT) were tested at three test sites (index knee, ipsilateral heel and elbow) using standardised procedures and scripted instructions.
Data Analysis SPSS (v19) statistical package was used, with the α-level set at 0. 05. Sample size was calculated using PPT and CPT data from previous studies. Using data from Suokas et al. , 2012  [16]  a mean difference in PPT between OA and controls across a range of joints of 155. 93kPa (standard deviation (SD) 150. 29kPa), required a sample size of 15 per group (α-level = 0. 05 and β = 0. 80). Knee joint PPT data from our own study (awaiting publication) showed that 22 subjects would be needed per group (mean difference 371. 18, SD 150. 28). Given the lack of available CPT data, our own data was used: a mean CPT difference between OA and controls of 4. 68°C (SD 6. 99°C) resulted in a sample of 15 per group. It was therefore decided that 20-25 subjects per group would provide adequate power.
M ucin-type (GalNAc-type) O-glycosylation is by far the most differentially and complex regulated type of protein glycosylation, and likely the most abundant with over 80% of all proteins passing through the secretory pathway that is predicted to be O-glycosylated  1. In metazoans, this post-translational modification is initiated by a large family (20 in humans) of polypeptide N-acetylgalactosaminyltransferases (GalNAc-Ts), which transfer a GalNAc residue from uridine diphosphate N-acetylgalactosamine (UDP-GalNAc) to Ser/Thr side chains in the presence of manganese  2. These isoenzymes are grouped in CAZy database as family 27 (ref. 3)  and further classified into several subfamilies based on the enzyme protein sequences and the genomic structures of the encoding genes  2. They are also classified into two major classes based on their primary acceptor substrate preferences for peptides and partially glycosylated GalNAc-glycopeptides.