dataesr/scientific-paragraphs-categorization huggingface dataset:
Evaluation of the number of atherosclerotic plaques Intima-media thickness (IMT) in the common carotid arteries was assessed with an ie33 ultrasound system (Philips, NL) using an 11 to 3 MHz linear array transducer. Measurements were performed by an experienced technologist and evaluated in the QLab software (Philips, NL). The presence of an atherosclerotic plaque was determined by an increment of 1. 5 mm or more in IMT when compared to a region without plaque 1 cm before the carotid bulb, averaging from left and right carotids. Plaques were counted in the common, external, and internal carotid arteries on both left and right sides  [9]. The phenotype considered was the count of plaques summed over both carotid arteries.
Microarray data processing RNA samples were hybridized to the Illumina HT-12 BeadChip v3 (Illumina, San Diego CA) containing 48,803 50-mer DNA probes. Probe-mapping to the genome was obtained from ReMOAT annotations  [50]  in the illuminaHumanv3. db package from Bioconductor v2. 8 (http://www. bioconductor. org). There were 13,445 probes with ''Bad'' scores for genome alignment, which were discarded. Probes were annotated with RefSeq and EntrezGene ids using the org. Hs. eg. db package from Bioconductor. Of the remaining 35,358 probes, 28,515 were annotated to Ensembl transcripts and 28,137 to EntrezGene ids. For the purpose of counting number of genes throughout, unannotated (but of good quality) probes were considered as targeting distinct genes. Note that probe annotations from Illumina were not used to discard probes, which is different from our previous analyses on this dataset  [9, 21].
However, 98% of probes that were removed in our previous analyses were also removed by at least one of the filtering steps applied here. Bead-level data were processed with BeadStudio (Illumina, San Diego CA) to perform quality control and summarization of intensity values at probe level. Data were further processed by quantile normalization. An arcsinh transformation was applied to stabilize the variance  [51]. A transcript was considered detected when the normalized intensity reported by its targeting probe was significantly above that of negative control probes on the same array (detection p-value,0. 04). Probes with ''detected'' calls in $5% of samples within any smoking/sex group were considered for analysis, representing 23,214 probes. All analyses were performed with R v2. 13  [52].
Correction for technical sources of variability in gene expression Major components of variance in the gene expression dataset were identified by singular value decomposition (SVD) using the La. svd function in R. The six largest components were not associated to any individual characteristic, and therefore were thought to reflect systematic effects from sample-processing protocols. The first 6 SVD components were then used as surrogate variables of technical effects and were adjusted for in expression analyses  [53]. In addition, potential sample contamination with B and T cells, and megakaryocytes was corrected as previously described  [21]  (Text S1).
GO enrichment analysis Gene set enrichment analysis of gene ontology (GO) terms was performed with the topGO (v 2. 4. 0) package in R. GO data were obtained from the GO. db Bioconductor metadata package v 2. 5. 0 (March 2011). Enrichment was tested by a Fisher's exact test using the set of 18,364 unique known detected genes as a reference. In order to account for the redundancy and hierarchy of GO terms, the weight01 algorithm was used, which is a hybrid between the elim and weight algorithms described in  [58]. Control for multiple testing was done by a Bonferroni correction on the number of GO terms represented in the reference set.
SVD was initially performed to determine the a priori number of components for the ICA algorithm as explained in  [21]. This number was found to be 59. The fastICA algorithm identifies major variance components by iteratively estimating the ''mixing'' matrix A that satisfies the equation X = SA, where X is an m6n data matrix, S is a m6p matrix of signatures across genes, A is p6n matrix of patterns across samples, n is the number of samples (n = 936), m is the number of genes (m = 3,368), and p is the number of ICA components set a priori (p = 59). The iterative algorithm minimizes dependency among signatures (columns of S), while maximizing non-Gaussianity, i. e. negentropy, of signature distributions  [20]. The fastICA function in the R-package of same name was used  [59]. The algorithm was run multiple times to avoid trapping in a local maximum.
The term Pr(X i DPa M (X i )) denotes the conditional probability of observation X i given its set of parents Pa M (X i ) in graph M. The graph with the lowest BIC is selected as the most likely model, which produces identical values for equivalent networks  [61]. Here, however, because different density functions were used for different variables, equivalent networks may results in slightly different scores. Therefore, we computed BIC scores for all models in a class, which was selected if any network in the class had the minimum score. The probability of selecting a model class, estimated by 1000 bootstraps of the data was used as a measure of confidence in the Bayesian network inference  [62].
Inference of network skeleton The skeleton of the network connecting genes, smoking, risk factors and plaques was learned by conditional associations using the PC algorithm 1 implemented in the pcalg R package v 1. 1-4  [22]. Briefly, the algorithm starts with a matrix of marginally associated variables (nodes connected by edges) and for each pair of connected, i. e. adjacent, nodes it successively tests whether the pair becomes independent after conditioning on any group of adjacent nodes. If for any set of conditioning nodes the pair is independent, the edge is removed. The Pearson correlation with significance level of 0. 05 was used to test independence. The process was repeated for 1000 data bootstraps and the proportion of samples where the edge is recovered was recorded. Shortest paths between smoking and plaques were inferred with the Dijkstra's algorithm on a reduced graph after removing nodes corresponding to covariates.
Whenever more than one shortest path existed, the algorithm chooses one according to a greedy search. The Dijkstra's algorithm implemented in the sp. between function of the RBGL package for R was used  [63]. Note that although in its full version the PC algorithm (Algorithm 2 in  [22] ) can asymptotically infer causal associations in a network by directing some of the edges of the skeleton, when applied to samples of finite size the algorithm may lead to inconsistencies that make such inference impossible  [64]. This was the case with the present data. Therefore, we decided to limit to inferring the skeleton of significant partial correlations among variables using a first part of the PC algorithm.
Acknowledgments We appreciate the contribution of participants of the  Gutenberg Health Study. We gratefully acknowledge the excellent medical and technical assistance of all technicians, study nurses and coworkers involved in the Gutenberg Health Study. We thank  Raphae ¨le Castagne  ´for her invaluable assistance in the organization of the many files associated with this project. EN is a Director of  Research in Centre National de la Recherche Scientifique.
To get further insight into the mechanism of fragmentcapture, the measured yields of the evaporation residues obtained from the particle-gamma coincidence data were compared with the predictions from platypus + pace2 for different excitation energies (E * ) of the primary composite system as discussed below. The spectrum of the surviving α-particles, after capture of the complementary fragment (t), represents the cross-section for breakup-fusion as a function of the kinetic energy of the α-particles (E α ). This can be expressed as a function of E * of the composite system 201 Au, by obtaining the E * for each value of E α , using the dynamical variables at the instant of breakup of 7 Li into α+t on an event by event basis. The calculated E * and the corresponding breakup fusion cross-section as a function of spin (σ J vs J) were given as input to the statistical model code pace2  [15]  for calculating the evaporation residue cross-sections from decay of 201 Au formed after triton-fusion.
Nucleotides are numbered according to GenBank accession numbers [NM_001081. 3] (CUBN) and [NM_030943. 3] (AMN) with +1 corresponding to the A of the ATG translation initiation codon and the initiation codon corresponding to codon 1. CUBN and AMN exons, with flanking intronic regions, were amplified using standard PCR procedures with sequence specific primers (primer sequences are available upon request) and a polymerase (HOT FIREPol ® DNA polymerase; Solis Biodyne, Estonia). AMN exons were amplified in 7 fragments with addition of the PCR additive S-Solution for amplification of GCrich templates. Amplified products were enzymatically purified (ExoSAP-IT; USB Corporation, Cleveland, Ohio, USA) and used as template in sequencing reactions (Big Dye ® Terminator v1. 1 Cycle Sequencing Kit; Applied Biosystems, Naerum, Denmark).
Sequencing products were purified using pre-soaked Sephadex G-50 (GE Healthcare Orsay, France) 96-well multiscreen filter plates (Millipore, Molsheim, France). Purified products were analysed on an automated 48-capillary sequencer (ABI 3730 Genetic analyser; Applied Biosystems, Courtaboeuf, France) and the results interpreted using the SeqScape ® software (Applied Biosystems). Novel sequence variants were compared to commercially available control alleles (Human random control panels; Health Protection Agency Culture Collections, Salisbury, United Kingdom) to exclude commonly occurring polymorphisms. In silico splicing prediction analyses was performed using the NNSPLICE server (0. 9 version) (http://fruitfly. org/seq_tools/splice. html). No additional patient material was available for analyses of AMN splicing.
*Based on analyses of urinary excretion of selective cubilin and megalin ligands in patient urines using immunoblotting or high-resolution gel electrophoresis, see Table  3. † Based on in vitro functional analyses. ♦ Based on in silico protein predictions. A Previously described as c. 208-2A>G, skipping of exon 4, fs  [5]. B Previously described by  [4]. C Functional analyses previously described by  [39]. acceptor splice sites could be detected in AMN intron 9 or exon 10 using the NNSPLICE server (0. 9 version). RT-PCR and cDNA sequencing of total RNA isolated from CHO-K1 cells expressing either genomic wt AMN exon 8-12 or AMN exon 8-12 (c. 1006 + 11_1008del) showed abrogated splicing with retention of the remaining 10 bp of intron 9 in the mutant mRNA transcript (Figure  2 ). The deletion consequently causes a translational frameshift and a premature stop codon most likely resulting in nonsense mediated decay of the aberrant mRNA and thus functional AMN null alleles (Table  2 ).
Consistent with this, both parents were heterozygous at this position and the 70 bp deletion was not detected in 158 control alleles. Direct sequencing, of the AMN gene in family 4, revealed compound heterozygous mutations in the two affected children (Table  1 ). In both patients the c. 208-2A>G mutation, described above, was observed on the maternal allele whereas a novel deletion-insertion of exon 10 (c. 1041_1042delinsCTC) was identified on the paternal allele (Figure  1A ). The insertion-deletion Figure  3  G1112 is located in the tight interface between CUB 5, 6 and 7. A: Overview of the structure of cubilin CUB domains 5-8i n complex with IF (PDB accession 3KQ4)  [16]. The CUB domains are illustrated in green cartoons and IF domains in blue cartoons. The G1112 residue is located in the interface between CUB domains 5, 6 and 7 and shown as red spheres.
B: Zoom-view of the interface between CUB domains 5, 6 and 7. Residues lining the interface are here indicated in green sticks. The space occupied by the interface residues is indicated by a transparent surface. This clearly shows that G1112 is centrally located within the tight interface and accordingly, that a substitution to a larger and polar residue could potentially cause severe sterical clash with surrounding residues as well as disturb inter-domain interactions. The figure was generated using Visual Molecular Dynamics  [43]. resulted in a translational frameshift and no alternative stop codon could be detected upstream of the AMN 3′ UTR region (Table  2 ). Due to the aberrant and elongated AMN transcript product, the c. 1041_1042delinsCTC may result in an unstable amnionless protein and thus in functional null alleles.
Acknowledgements The authors would like to thank the families and clinicians ( Dr. Ogier de Baulny  and  Dr. Deschênes ,  Robert Debré Hospital , Paris;  Dr. Petit ,  Trousseau Hospital, Paris  and  Dr. Douillet ,  Fontainebleau Hospital, France ) who participated in this study. This work was supported in part by the  University of Aarhus , the  Danish Medical Research Council , the  NOVO-Nordisk Foundation ,  The Lundbeck Foundation , The  Danish Kidney Association ,  Region Viborg ,  Fondation Voir et Entendre , and the program of the  European Community , EUNEFRON ( FP7, GA# 201590 ). We sincerely thank  Dr. S. K. Moestrup  ( Department of Biomedicine, University of Aarhus ) for kindly providing the rabbit anti human cubilin antibody and furthermore,  Hanne Sidelmann ,  Pia K. Nielsen ,  Marie-Elise Lancelot  and  Damien Latour  for skilful technical assistance.
6A ). The diet of the Cape Gannet was quantified during the 1950s in the SB by Davies (cited by  Crawford and Shelton 1978 ) and in the central NB by  Matthews (1961)  and  Matthews and Berruti (1983). More recent data on gannet diet were collected in the SB between 1978 and 1990 (R Crawford unpubl data) and in the NB between 1980 and 2006 (Ministry of Fisheries and Marine Resources, Namibia, unpubl data and R Crawford unpubl data). In the 1950s the energy density of the Cape Gannet diet was >6 kJ g -1 in both ecosystems (Fig. 6B ) and was estimated at 5. 86 kJ g -1 in the SB in the more recent period, whereas it was slightly less than 5 kJ g -1 in the NB (between 21% and 24% less than in the other studies). The Cape Gannet is probably the most specialized predator considered here, consistently deriving the largest portion of its diet from pelagic fishes  (Berruti et al.
Total mortality rates for the juvenile stanzas of the three species were estimated to retain biomass levels per model group as close as possible to those in the previous model version. The model was then refitted to time-series data by the procedure previously adopted and reported in  Shannon et al. (2008). First, a search was run for vulnerability values describing the 25 most sensitive predator/prey interactions in the model. Second, a hypothetical forcing function that improved model fits to available time-series data was fitted to interactions between anchovy and its predators. Third, a hypothetical forcing function was fitted to sardine-predator interactions. Finally, a small hypothetical forcing function was applied to primary productivity to optimize the fit of the model. Dynamic trajectories of model groups were consistent with published trajectories  (Shannon et al.
Acknowledgments We would like to thank the organizers of the 8th William R. and  Lenote Mote International Symposium in Fisheries Ecology. R Cooper ,  RJM Crawford ,  J Kemper ,  C Kirchner , and  K Ludynia  are acknowledged for making unpublished data available;  C Grobler ,  J Kemper ,  C Bulman ,  P Johnson , and  A Thistle  commented on earlier drafts; and  S Kohler  and  P Lopez  assisted with the figures. Two anonymous reviewers are thanked for their constructive comments. This paper is a contribution to the  SEACODE research group in Namibia.
Population Study The Epipage study covered all births between 22 and 32 completed WG in 1997 and all births between 22 and 26 completed WG in 1998 in 9 regions of France and, after parental consent, included all children discharged alive from the hospital. At recruitment in the maternity or neonatal unit, investigators told parents about the study, gave them written information, and obtained verbal consent. Because only 3 infants born at 23 WG survived, the study was limited to children born between 24 and 32 WG. This study is limited to survivors at 8 years of age. In accordance with French regulations, the study and the verbal consent were approved by the Comiteconsultatif sur le traitement de l'information en matiere de recherche dans le domaine de la santeand the Commission Nationale de l'Informatique et des Libertes (the French data protection agency).
Data Collection At recruitment, medical and social information was collected in maternity and neonatal units. The follow-up included the following stages: 1) At 2 years, a standard questionnaire was completed by the child's physician  [10] ; 2) At 5 years, a standardized medical examination, including a short version of the Touwen neurologic examination and a developmental evaluation with the Kaufman Assessment Battery for Children (K-ABC), was conducted by trained examiners in special centers set up for the study  [6, 11] ; 3) At 8 years of age, parents received a mail questionnaire asking about the child's health and school situation  [12]. In 5 regions, the local office for people with disabilities (Maison Departementale des Personnes Handicapees, MDPH), re-sponsible for meeting specific needs of disabled people at all ages, completed an additional questionnaire, after searching both for children already known to have a neuromotor or sensory deficiency or learning disability or to be in a specialized center or school and for those whose parents did not return the questionnaire at 8 years.
Outcome Indicators (Table 1) Six deficiencies or disorders were considered: motor deficiencies, cognitive deficiencies/learning disabilities, psychiatric disorders, epilepsy, visual deficiency, and hearing deficiency. To reduce bias due to loss to follow-up and to be able to classify as many children as possible, we used all available data from all stages of follow-up (2, 5, and 8 years) for each deficiency to determine if it affected the child and how severely. Severity was assessed according to the most recent information available. Moreover, when information in one domain of development was missing at one stage of follow up, the child was considered free from this deficiency at that stage. Two combined indicators were considered. The first describes any combination of motor and cognitive deficiencies, regardless of other deficiencies or disorders.
Statistical Analysis Results are presented as proportions of the number of survivors included in the follow-up after discharge from neonatal care. Deficiencies and their grouping were reported according to gestational age and categories of neonatal brain injuries diagnosed by ultrasonographic studies. We used the chi 2 test to compare outcomes between the different gestational age groups of VPT children. Finally the neonatal characteristics of children complete-ly lost to follow-up were compared with those for whom we had at least one stage of follow-up. Statistical analyses were performed with SAS software (version 9. 2).
(2) Moderate Neuromotor Dysfunction (MND-2) at the short version of the Touwen neurological examination at the age of 5 years 11. (3) Including children free of CP or other neuromotor disorders but who were not assessed with the Touwen examination. (4) Except for visual or hearing deficiency only; for 25 children in special school/class at 8 years of age with MPC at 5 years $70 or missing, other data in their record allowed us to classify 14 with a severe cognitive deficiency, 10 with moderate, and 1 with none identified record allowed to classify 14 as severe crecords. (5) MPC = Mental Processing Composite of the K-ABC test 14. (6) MDPH = Maisons departementales des Personnes handicapees. (7) Regardless of all other deficiencies. doi:10. 1371/journal. pone. 0062683. t001 examination, and 1594 (64%) were assessed with the K-ABC  [14].
Acknowledgments We thank all the parents and children who have participated in this study over the years. We acknowledge  Jo Ann Cahn  for help in editing the manuscript and all the members of EPIPAGE group. INSERM U149:  B Larroque  (national coordinator),  PY Ancel ,  B Blondel ,  G Bre  ´art,  M Dehan ,  M Garel ,  M Kaminski ,  F Maillard ,  C du Mazaubrun ,  P Missy ,  F Sehili ,  K Supernant ,  L. Marchand. Alsace:  M Durand ,  J Matis ,  J Messer ,  A Treisser  ( Hopital de Hautepierre, Strasbourg ). Franche-Comte:  A Burguet ,  L Abraham-Lerat ,  A Menget ,  P Roth ,  J-P Schaal ,  G Thiriez  ( CHU St Jacques, Besancon ),  Haute-Normandie :  C Le  ´veque,  S Marret ,  L Marpeau  ( Hopital Charles Nicolle, Rouen ). Languedoc-Roussillon:  P Boulot ,  G Cambonie J-C Picaud  ( Hopital Arnaud de Villeneuve, Montpellier ),  A-M Donadio ,  B Lede  ´sert (ORS Montpellier).
An Italian expert panel published guidelines for the management of nodal indolent lymphomas  [10]. They recommended involved field (IF) radiotherapy in low tumor burden localized disease, with adjuvant chemotherapy being reserved for cases of high tumor burden or high-risk disease (FLIPI score >2). The experts did not retain the eventuality of a "watchful waiting" option in a low burden case, which was associated with a good outcome in the Stanford experience  [8]. More recently, a report mentioned that upfront RT was associated with improved OS compared with alternate management approaches (surveillance, epidemiology and end results database analysis)  [11]. At present, new low-toxicity therapies that prolong progression-free survival periods and the interval period to new anti-lymphoma therapies are available and include rituximab monotherapy or the combination of rituximab plus chemotherapy  [12].
Statistical analysis Statistical analyses were performed using SPSS software version 12. 0. Demographic characteristics were compared across the groups using chi-squared tests for qualitative characteristics, while the t-test, Mann-Whitney test, and ANOVA test were used for quantitative characteristics. The event-free survival (EFS) and the OS were calculated according to the Kaplan-Meier product limit estimator method. Survival was calculated from the time of diagnosis to death for any given case. PFS was calculated from the time of diagnosis to the moment of progression or relapse. Univariate comparisons of survival curves were made using the log-rank test. Two side P-values of <0. 05 were considered statistically significant.
ACKNOWLEDGMENTS This work was funded by  MICINN  ( MAT2010-21156-C03-02 ,  MAT2011-22491 , and  FIS2011-23230 ),  SurMott ANR , and  CNRS PICS. We are grateful to  L. Patthey  of the SIS beamline at the  Swiss Light Source  for his help during the photoemission experiments.
Acknowledgments Financial support from the  NSERC   Discovery Grant  and  Canada Foundation for Innovation (CFI-Leaders Opportunity Funds and CFI-New Opportunity Funds)  is greatly acknowledged. We are also thankful for the technical support from  Alison Ser ,  Yang Qiu ,  Pat Kenyon ,  Lovemore Malunga  and  Victoria Ndolo  of the  Department of Food Science, University of Manitoba. Special thanks to  S. Arntfield  for her guidance during the initiation of this project.
Protein concentration estimation Total membrane protein concentration was determined using a Bio-Rad DC Protein assay, using bovine serum albumin as standard. Purified protein concentration was determined using a NanoDrop Spectrophotometer, measuring the absorbance at 280 nm and using an extinction coefficient at 280 nm of 99945 M -1 cm -1 for hSERCA2a; or by SDS-PAGE quantification, using known amounts of native rabbit SERCA1a as standard. The software used to quantify the SERCA2a yield was ImageJ  [36].