dataesr/scientific-paragraphs-categorization huggingface dataset:
(c) Roche 454 and Illumina Solexa sequencing Transcriptome data were obtained from RNA of wing discs that were dissected from seven individuals of each sex in the last larval instar or in a pre-pupal stage. Reverse transcription was performed using the PrimeScript reverse transcription enzyme (Takara, Otsu, Japan). Double-stranded cDNA was normalized using the Kamchatka crab duplex-specific nuclease method (Trimmer cDNA normalization kit, Evrogen, Moskow, Russia) and shotgun sequenced with a 454 GS-FLX Titanium pyrosequencer (Roche Applied Science). Long-range PCR was conducted using Takara LA Taq on a single f. lamborni specimen, and amplicons were shotgun sequenced with 454 pyrosequencing. Raw data were preprocessed using Prinseq-lite  [27]. Retained reads were mapped onto the BAC tile path (RepeatMasker masked  [28] ) using Burrows-Wheeler aligner (BWA)  [29].
(d) Molecular evolution The McDonald -Kreitman  [33]  and HKA tests  [34]  were applied to test for non-neutral evolution and balancing selection. These tests compare the within-species variation to the between-species divergence using a close relative. Sequence data from Short Read Archives SRR850327 and SRR850325 for P. polytes and Papilio glaucus  [35]  were used as outgroups. Because these species were only distantly related to P. dardanus, tests of molecular rates may be affected by multiple hits at variable sites, which was corrected by applying a Jukes -Cantor model of sequence variation  [36]. For P. dardanus, haplotypes were inferred using Phase  [37]  as implemented in DnaSP  [38]. Diversity and divergence values were obtained using DnaSP, and McDonald -Kreitman tests were performed using Fisher's exact tests.
Acknowledgements. The  Wellcome Trust Sanger Institute  is acknowl- edged for BAC sequence data generation with  Carol Churcher ,  Claire Davidson ,  Richard Clark ,  Rebecca Glithero ,  Christine Lloyd ,  Lucy Matthews ,  Karen Oliver  and  Sarah Sims  as major participants. We thank  Austin Burt  for invaluable discussions. Data accessibility. DNA sequences: GenBank accessions:  FP243376 ,.
Methods Search Strategy. This study was conducted in adherence to the PRISMA Statement guidelines  49. A systematic literature search was performed using Pubmed, MEDLINE, EMBASE and CNKI (China Knowledge Resource Integrated Database) databases. No restriction was set for languages or date of publication. The following search key words were used: surgical resection, hepatic resection or hepatectomy; radiofrequency or radio-frequency; and liver cancer or hepatocellular carcinoma. Data Extraction and Quality Assessment. Data were extracted independently by two authors (Q. X and K. S) and cross-checked to reach a consensus. The following variables were extracted from each study: (1) first author and year of the publication; (2) study design and patients characteristics; (3) clinical outcomes. The primary endpoint was efficacy, including overall and disease-free survival rates at 3, and 5 years.
The following studies were also excluded: 1) those dealing with liver metastases or recurrence after hepatectomy; 2) those with no clearly reported outcomes of interest; 3) those sample size for either the RFA group or HR group smaller than 30. Statistical Analysis. The meta-analysis was performed using the RevMan 5. 2 software and R software with ''meta'' package from the Bioconductor project  51, 52. For dichotomous variables, OR was estimated with a 95% CI. For continuous variables, WMD was calculated. The significance of the pooled effects was determined by Z-test. Statistical heterogeneity among studies was evaluated with Q-test and I 2 statistics  53. Study-specific results were combined using a random-effects model, which considers both within-study and between-study variation  54. Sensitivity analysis was performed to evaluate the stability of the results.
Each study involved in the meta-analysis was removed each time to reflect the influence of the individual data set on the pooled effects. An estimation of potential publication bias was executed by the funnel plot, in which the SE of log (OR) of each study was plotted against its log (OR). Funnel plot asymmetry was assessed by the method of Egger's linear regression test, a linear regression approach to measure funnel plot asymmetry on the natural logarithm scale of the OR  54. The significance of the intercept was determined by the t-test suggested by Egger (p-value , 0. 05 was considered representative of statistically significant publication bias).
Chemical maps were created and analyzed with the Omnic software (Thermo Fisher) by measuring and plotting the intensity of the specific bands of the second derivative of the spectra: PLGA, 1,770-1,740 cm -1 ; 35 amide I, 1,670-1,625 cm -1 ; lipids, 2,970-2,950 cm -1. PyMCA (European Synchrotron Radiation Facility) and Origin 8. 0 (OriginLab, Northampton, MA, USA) were used for data analysis.
For hypoxic treatment, cell monolayers were cultured in chondrogenic medium in an atmosphere containing 2% O 2 using a Scientific Innova CO-48 incubator with O 2 control option (New Brunswick, NJ). Microarray Analysis-Hybridization of Affymetrix HG-U133 (version plus 2. 0) arrays has been described in a previous study  (15). Raw gene expression data were processed for normalization and signal calculation with the Expression Variation software described previously  (16). To determine differentially expressed genes, comparative occurrence analysis was performed using a recently described approach  (17). RNA Extraction, Reverse Transcription, and Quantitative PCR-Total RNA was isolated using RNeasy mini kit (Qiagen) and reverse-transcribed using GeneAmp Gold RNA PCR Core kit (Applied Biosystems).
Quantitative PCR (qPCR) was performed using LightCycler 480 SYBR Green I Master mix and real-time PCR instrument (Roche Diagnostics). Reaction conditions were 95 °C for 5 min followed by 40 cycles of 15 s at 95 °C, 10 s at 64 °C and 20 s at 72 °C. For each reaction, a single amplicon with the expected melting temperature was obtained. Primer pairs are listed in Table  1. These were designed using the web-based applications, Primer3  (18)  and BLAST at the National Center for Biotechnology Information. Of note, for ␣-1 type II collagen, primers amplify specifically transcript variant 2, which is the splice form expressed by mature chondrocytes. Expression of the housekeeping gene encoding ribosomal protein S9 (RPS9) was measured for normalization. The threshold cycle (Ct) of each amplification curve was calculated by Roche Diagnostics LightCycler 480 software using the second derivative maximum method.
Total soluble collagens were then quantified using a Sirius Red-binding assay according to the manufacturer's instructions (Biocolor). Colorimetry was performed at 550 nm. Quantitation of DNA-Pellets were homogenized and ultrasonicated in PBS. Samples and the PicoGreen reagent were diluted in 10 mM Tris, 1 mM EDTA, pH 7. 5, following the manufacturer's recommendations (Molecular Probes). Fifty l of sample or DNA standard were incubated for 5 min with an equal volume of PicoGreen reagent in a microtiter plate. Fluorescence was then excited at 480 nm and recorded at 520 nm. Statistical Analysis-Data are expressed as the mean Ϯ S. E. of at least three independent experiments. Student's t test was used to compare two treatment groups. Statistical significance was set up at p Ͻ 0. 05.
ANGPTL4 Expression Is Strongly Up-regulated Specifically During Chondrogenic Differentiation of MSCs-Transcriptomic analysis was performed using Affymetrix gene chips. MSCs obtained from three donors were differentiated into chondrocytes using either TGF-␤-3 or BMP-2 as inducers and their mRNA analyzed at different time points. In silico analysis was performed by varying the stringency for selection of regulated genes. Parameters that were adjustable included normalized fold change over control value at day 0, occurrence in the samples depending on the chondrogenic inducer, the donor, or the time point. Interestingly, ANGPTL4 was singled out as the sole gene encoding a secreted factor to be up-regulated with a fold change Ͼ 6 by both inducers in at least two donors and one time point. Data obtained on the three donors indicated that ANGPTL4 expression was greatly increased at the early time points (days 1 and 3) and to a lesser extent at the later time points (days 7 and 21) (Fig.
1A ). Of note, the two ANGPTL4 probe sets spotted on Affymetrix arrays correspond to transcript variant 1 encoding ANGPTL4 isoform a. The other transcript of ANGPTL4, known as variant 3, lacks an alternate inframe exon and encodes a shorter protein named ANGPTL4 isoform b. We therefore performed qPCR analyses with primers that amplify each splicing variant individually. Data showed that both variants shared a similar regulation profile during TGF-␤-3-induced chondrogenesis with a sharp rise at day 2 and progressive decrease until day 21 (Fig. 1B ). Thus, all subsequent qPCR experiments were performed with primers that amplify a region common to both variants to measure overall expression of ANGPTL4. Early up-regulation of ANGPTL4 mRNA level during chondrogenic differentiation was confirmed (Fig.
1C ). Differentiation into the three lineages was checked by measuring the expression of various markers (data not shown). Induction of ANGPTL4 Expression in MSCs Requires Hypoxia or Micromass Culture-Hypoxia has been shown to occur inside three-dimensional culture systems  (21)  and is a well known inducer of ANGPTL4 expression in various cell types  (22, 23). Therefore, we examined the contribution of hypoxia, threedimensional culture, and TGF-␤-3 in the induction of ANGPTL4 expression in MSCs. Cells were cultured in monolayers in either 21 or 2% O 2 for up to 7 days. In comparison with normoxic conditions, the hypoxic environment strongly induced expression of ANGPTL4 at the RNA and protein level (Figs. 2, A  and B ). TGF-␤-3 treatment produced some stimulating effect on ANGPTL4 release at day 2 of culture in both conditions (Fig.
Using recombinant ANGPTL4 and a RNA interference approach targeting this factor, we show that extracellular matrix deposition of type II collagen and aggrecan, two major components of the cartilage, is markedly decreased by ANGPTL4 during chondrogenic differentiation. We provide evidence that this regulation occurs not only through repression of type II collagen and aggrecan expression but also through induction of MMP13, MMP1, and MMP3 synthesis. Indeed, both MMP13 and MMP1 are known to digest type II collagen and aggrecan  (8 -10, 12) , whereas MMP3 activates the precursor form of these MMPs  (11). The possible involvement of ADAMTS aggrecanases in the degradation of aggrecan during chondrogenesis was unlikely because no aggrecanase activity was detected in any medium samples using a sensitive activity assay (data not shown).
We used live trapping experiments to produce a large and robust spatio-temporal dataset of tropical rat home range and measures of home range overlap. Within individual home ranges, we also aimed to determine whether rats range uniformly within the total space they use or if they differentially use parts of their home range. For this purpose we compared results from daily movement and simulated home range sizes. Finally, for each island we looked at what could be the recommended treatment period and conservative bait gap threshold, i. e. the maximum tolerable distance between bait broadcast or stations of baits to ensure all rats rapidly encounter baits. For each combination of island and habitat we used the smallest home range scenario depending on age and sex of the rats but also according to season.
For the spatially explicit capture probability model we assumed a hazard-rate function defined by three parameters, g0 (probability of capture at the home range centre), σ (scale parameter) and the shape parameter z, with sex and age as individual covariates and season, habitat and island as session covariates. Individual capture histories were implemented with R package 'secr'  (Borchers & Efford 2008; Efford, Borchers, & Byrom 2009). The three model parameters were estimated using conditional maximum-likelihood on covariates. Different sub-models were tested to determine whether covariates had an effect on the scale parameter sigma. Each model was considered a competing best model when dAIC c < 2. Using a circular hazard distribution we calculated the 95% and the 50% probability density area of detection as surrogates for black rat home range (HR 95 ) and home range core area (HR 50 ): HR 95 = π × (3.
Discussion Our mark-recapture study conducted twice a year over five years provided a substantial dataset to test for complex environmental effects which may alter rat space use on tropical islands. In particular, we were able to test for higher order interactions among variables, such as the consistency of sex, habitat and season effects across both islands. We were also able to compare various statistical measures of range use, including multiple measures derived from our capture-recapture data (the 95% and 50% areas of the SECR detection function and the MMDM) and independent estimates derived from tracking a subset of rats using spool-and-line.
Acknowledgements D. Ringler  benefited from a Ph. D. grant given by the  Région Réunion  and the  European Social Fund. This research is part of the ' ALIENS' programme funded by ANR, 'Ecosystèmes Tropicaux' programme funded by MEDD  and ' MIRE ' programme funded by  INEE. Thanks to TAAF for authorisation to work on  Juan de Nova  and Europa. We thank  Araceli Samaniego  and two anonymous referees for comments on a draft version of the manuscript.
Materials and Methods We used a case-control design to investigate EOBC risk among Caucasian women in relation to 1,265,546 single-nucleotide polymorphisms (SNPs) included in the HapMap3 project (http://hapmap. ncbi. nlm. nih. gov/downloads/phasing/2009-02phaseIII/ HapMap3_r2/). Specifically, we used Illumina SNP arrays to genotype 3523 EOBC cases and 2702 control women and to impute their genotypes for the HaMap3 SNPs (hereafter called the discovery set). We then conducted two SNP-based analyses and a gene-based analysis. The results of these analyses were examined in two sets of independent data (called replication sets). We begin with a description of subject recruitment, genotyping and quality control for the discovery set. We then describe the SNP-based analysis and replication, followed by the gene-based analysis and replication.
), using the protocol described in the Supplement. Two hundred and twenty seven population control subjects from the Colon Cancer Family Registry (CCFR) were genotyped at TGEN (http://www. tgen. org) using the Illumina Human1M and HumanOmni1-Quad BeadChips. In addition, 27 blinded and 22 un-blinded quality control replicates from the study sample were genotyped on the Human1M. Replicates showed concordance of called genotypes >99. 94% (for samples with call rates >90%). Standard laboratory quality control procedures were applied and have been described previously  (15). Quality control was implemented using a combination of PLINK  (16)  and custom programs written in C, R, Perl, and the Unix bash shell. Data quality control procedures are described in more detail in the Supplement and summarized in Table  S3.
For step 1, we used eQTL mapping of SNPs to genes, as implemented in the online database SCAN  (20, 21)  and used the eQTL significance levels to quantify the likelihood that a SNP (or one in strong LD with it) regulates gene transcript levels  (22). That is, we assigned a SNP to a gene if the SNP encoded a missense, nonsense or frameshift (MNF) variant in the gene, or if it met our criteria for an expression-quantitative trait locus (e-QTL) SNP for the gene. While not all the SNPs annotated to a gene are likely to be functional, they are clearly enriched for those with functional consequence. We were able to annotate 19,684 genes with one or more putative functional SNPs, 11,040 of which were annotated with at least one e-QTL SNP. In step 2 we calculated a gene-based P-value for each of the 19,684 genes by combining the EOBCassociation P-values for all its putative functional SNPs using methods described elsewhere  (23).
Replication of gene-based results -To replicate the gene-based association analyses, we used available GWAS data from the CGEMS breast cancer study of 1,145 Caucasian case women and 1,142 Caucasian control women aged 55-74 years. Details of subject selection, genotyping methods and QC analyses for CGEMS breast cancer project have been published  (31, 32). The identical gene-based analytic method, described above and in the Supplement, was applied to the CGEMS data obtained from dbGaP. The gene-based Pvalues from both discovery and replication datasets were combined for the gene with smallest gene-based P-value in discovery data using Fisher's method for meta-analysis  (33). Further details of both the SNP-based and gene-based replication sets can be found in the Supplement.
Financial Support National Institute of Health Grants  U01CA122171 ,  RC1CA145506 ,  R01CA094069 , and  U19CA148065. The  Breast Cancer Family Registry (BCFR)  is supported by the  National Cancer Institute, National Institutes of Health  under  RFA-CA-06-503  and through cooperative agreements with members of the BCFR and Principal Investigators, including  Cancer Care Ontario  ( U01 CA69467 ),  Cancer Prevention Institute of California (CPIC)  ( U01 CA69417 ), and  University of Melbourne  ( U01 CA69638 ). Samples from the CPIC were processed and.
40E-01 8. 59E-01 3. 66E-01 rs16955826 5. 51E-01 6. 99E-01 3. 22E-01 rs8095381 5. 57E-01 4. 51E-01 2. 37E-01 rs11114379 5. 70E-01 4. 99E-01 2. 59E-01 rs6999405 5. 81E-01 N/A * N/A * rs1245012 5. 86E-01 5. 04E-01 2. 66E-01 rs7199193 6. 01E-01 1. 85E-01 1. 27E-01 rs11777718 6. 76E-01 6. 30E-01 3. 45E-01 rs12470945 7. 00E-01 8. 83E-01 4. 43E-01 rs1376386 7. 45E-01 6. 22E-01 3. 66E-01 rs12476834 7. 50E-01 9. 22E-01 4. 76E-01 rs9952079 8. 14E-01 3. 86E-01 2. 78E-01 rs17775523 8. 14E-01 6. 57E-01 4. 03E-01 rs17505688 8. 38E-01 1. 12E-01 1. 12E-01 rs1920398 8. 50E-01 5. 16E-01 3. 52E-01 rs8057807 9. 08E-01 4. 32E-01 3. 26E-01 rs7031588 9. 36E-01 1. 48E-01 1. 51E-01 rs12306431 9. 43E-01 4. 54E-01 3. 46E-01 rs17505369 9. 61E-01 1. 53E-01 1. 58E-01 rs6984368 9. 98E-01 8. 69E-01 5. 48E-01 * missing in replication datasetCancer Epidemiol Biomarkers Prev.
Background: N-methyl-D-aspartate receptor antagonists are potential therapies for neuropathic pain, and memantine has a good tolerance profile. A preclinical study recently reported that presurgery memantine may prevent neuropathic pain development and cognition dysfunction. Considering the high prevalence of breast cancer and of post-mastectomy neuropathic pain, a clinical trial is carried out to evaluate if memantine may prevent neuropathic pain development and maintain cognitive function and quality of life in cancer patients. Methods/Design: A randomized clinical trial (NCT01536314) includes 40 women with breast cancer undergoing mastectomy at the Oncology Hospital, Clermont-Ferrand, France. Memantine (5 to 20 mg/day; n = 20) or placebo (n = 20) is administered for 4 weeks starting 2 weeks before surgery.
Methods/Design We are conducting a randomized, placebo-controlled clinical trial in the Oncology Hospital, Clermont-Ferrand, France, in 40 women undergoing total mastectomy for breast cancer. The study has been approved in December 2011 by the regional Ethics committee (CPP Sud-Est, France, number AU917) and registered on 16 February 2012 at "http://www. clinicaltrials. gov" (NCT01536314). Women provide written informed consent prior to their participation in the study during their anesthesiology visit. After baseline assessments (day (D) -15 ) of pain intensity, cognition, quality of life and quality of sleep questionnaires, participants are randomized into two parallel groups: memantine (n = 20) or placebo (n = 20). Memantine or placebo (lactose) is given orally for 4 weeks starting 2 weeks before surgery.
Statistical analysis Statistical analyses will be performed with Stata software (version 13, StataCorp, College Station, USA). Concerning the primary objective, comparison between the randomized groups will be performed using an analysis of covariance with baseline score as a covariate  [33]. The correlation between baseline and follow-up scores was also proposed. For other secondary parameters, the comparisons between the randomized groups will be performed using the Student test or the Mann-Whitney test (if the conditions for validity of the Student test are not met, normality will be verified by the Shapiro-Wilk and homoscedasticity by the Fisher-Snedecor test). To study the evolution of the main endpoint (numerical scale pain), data analyses will be performed using mixed models which allow us to consider, on the one hand, time, group and interaction time versus group as fixed effects, and, on the other hand, the within-and betweensubject variability in order to visualise the assumption of a difference at 2 months between the two randomized groups that increases up to 3 months and stabilizes at 6 months.
Residual normality will be checked for all considered models. When appropriate, anticancer chemotherapy (yes/no) will be studied as a fixed effect in these models before considering subgroup analyses. The comparison between the treatment groups will be performed systematically: (1) without adjustment; and (2) by adjusting other factors whose repartition could be, despite the randomization, unbalanced between the treatment groups. The tests will be two-sided, with a type I error set at α = 0. 05. A sensitivity analysis of missing data will be performed to ensure the pertinence of the longitudinal data (MAR (Missing at random) or MCAR (Missing completely at random)). In order to assess the problem caused by missing longitudinal data at 6 months, estimation methods developed by Verbeke and colleagues  [34]  will be proposed.
Electronic nose An array of 14 gas sensors was constructed using inorganic metal oxide (MOX) sensing units that were selected according to a previously published method  (Villanueva et al. , 2008). Sensors were polarised using a constant voltage of 5 V. The resistance was measured every 0. 5 s. Data were monitored in real time and the graphs could be followed using a program written in Visual Basic software from Microsoft. The SPME (Solid Phase Microextraction) sampling method was used as the injection method equipped with a bipolar fibre of polydimethylsiloxane coated with carbowax and divinylbenzene (PDMS/CW/DVB, Supelco). Data matrix used for the different chemometric treatments had a dimension of 96 Â 14, where the rows represent the wine samples analysed (six replicates per type of wine) and the columns correspond to the value of the maximum variation of the resistance registered upon exposure of each sensor to the headspace of the wine samples.
Similarly, HDL subfractions can be categorized into large, intermediate, and small subfractions  [38]. The system includes tube gels and proprietary data analysis software to determine the subfraction concentrations based on area under the curve  [38]. Coefficient of variation (CV) varies according to the level of lipoproteins. Intra-and interassay  Fasting blood samples were drawn between 7. 00 and 7. 30 a. m. , aliquoted and stored at -80°C until analyses. Basic biological assays were performed in the biochemistry laboratory of the University Hospital (Clermont-Ferrand, France), including ApoA1 and ApoB. Individual risk factor scores were summed to determine the 10-year absolute risk of cardiovascular disease using Framingham score  [15]. The common carotid artery structure was evaluated using a high-resolution B-mode ultrasound (MyLab30, Esaote SpA, Firenze, Italy) The CIMT was defined as the distance from the leading edge of the lumen-intima interface to the leading edge of the media-adventitia interface of the far wall.