dataesr/scientific-paragraphs-categorization huggingface dataset:
Acknowledgements Funding: This work has been supported by the  European Communities 7th Framework Program Funding  under Grant agreement no. 603629-ENV-2013-6. 2. 1-Globaqua. We thank  Verena Huber-García  from the  Ludwig-Maximilians-Universität (Munich)  and  Laura Vergonyos  from the  Catalan Institute for Water Research (ICRA, Girona)  for their valuable help in collecting and preparing the data. We also thank the two anonymous reviewers who contributed to improving this paper. This article was edited for proper English language, grammar, punctuation, spelling, and overall style by two highly qualified native English-speaking editors at American Journal Experts (certification verification key:  3C40-1321-C1E8-190F-6B34 ).
monocytogenes infection from blood (gene-Ifna4) and upregulated in the spleen (gene-Ifnb1). Using the Interferome v2 database  [30]  we identified from the significantly expressed transcript lists in both blood and spleen a set of genes classified as being type I, type I & II or type II IFN responsive (Fig  2B ). However in both blood and spleen there were more genes associated with type I IRGs than type II IRGs. The transcriptional fold change varies differentially at different time points after L. monocytogenes infection in WT and Ifnar1 -/-mice Since type I IFN contributes to pathogenesis of intracellular bacterial infection  [14] [15] [16]  and type I IFN-inducible genes were highly represented in both the blood and tissue transcriptional signature during L. monocytogenes infection we sought to determine how a lack of type I IFN receptor signaling in Ifnar1 -/-mice affected the global transcriptional response to infection as compared to that observed in the WT controls (C57BL/6 background).
monocytogenes infection we set out to identify those transcripts, which temporally differed between WT and Ifnar1 -/-at days 1, 2 and 3 post infection, using a two-step filtering process. From the two-way ANOVA lists generated in Fig 3B  , S2  Table, blood transcripts which were inducible in the WT or the Ifnar1 -/-mice by at least 1. 5FC upon infection were identified (Figs 4A and 5B) for each time point post infection. Since significant numbers of transcripts were perturbed at each time point post infection the datasets were analyzed using Ingenuity Pathway Analysis (IPA) and the top 15 p-value ranked pathways were first identified in infected versus uninfected WT mice at each time point, yielding a total top 30 canonical pathways unique or shared within each of the three time points (Fig  4A ).
Absence of type I IFN signaling leads to enhanced or reduced type I and type II IFN responsive gene expression at day 1 or day 3 post L. monocytogenes infection respectively Using the Interferome v2 database  [30]  we identified from our significant transcript lists  (Fig 3B and S1 Table)  genes that were classified as either type I IFN responsive, type II IFN responsive or both type I and type II IFN responsive  (Fig 8A and S2 Table). Statistical filtering (2-way ANOVA with Benjamini Hochberg multiple testing correction, P <0. 05) revealed 588, 618 and 605 significantly differentially expressed IFN responsive transcripts in blood, spleen and liver during the course of infection (i. e. days 1, 2 and 3) which were differentially expressed in infected and uninfected Ifnar1 -/-or WT mice (Fig 8A  and 8B ).
Our findings that increased Ifng expression was accompanied by increased levels of Il10 could suggest that Th1 cells which have been shown to produce both cytokines  [40]  are reduced in the WT possibly by type I IFN inhibition of IL-12 production by myeloid cells as we have previously demonstrated during Mycobacterium tuberculosis infection  [41]. Changes in gene expression were also seen in the blood of the Ifnar1 -/-as compared to WT mice in the absence of infection (approximately 25%), suggesting that type I IFN signaling is already evident in uninfected mice. The small number of transcripts shown to be perturbed in the blood and tissue of Ifnar1 -/-as compared to WT mice in the absence of infection were shown a cohort of genes dependent on IFNαβR signaling. A proportion of these type I IRGs match known type I IFN responsive genes as identified in the Interferome v2 database.
-/-compared to the uninfected WT mice (Fig 3C and data not shown from independent experiment using the same methods as Fig 3C, which validated the findings) we set out to identify transcripts whose expression was at least 1. 5FC lower in the uninfected Ifnar1 -/-compared to the uninfected WT group using the same analysis method as in Fig 3C (Fig 7A-7C and data not shown from an independent experiment which validated our findings). These 134, 475 and 260 transcripts in the blood, spleen and liver respectively were enriched for IFN related pathways when analysed by IPA canonical pathway analysis (Fig 7A-7C). Identifying the common transcripts across the three tissues revealed 50 transcripts, which comprised 35 unique genes (using IPA annotation) of which 25 were identified as being type I IRGs from the Interferome v2 database (Fig 7D).
Acknowledgments We thank  Harsha Jani  and  Abdul Sesay  from  The Francis Crick Institute, Mill Hill Laboratory, Advanced Sequencing Facility , for their assistance and for the running of the Illumina microarray platform. We thank  The Francis Crick Institute, Mill Hill Laboratory Biological Services and Procedural Services , and Safety Operations Group at The  Francis Crick Institute, Mill Hill Laboratory  for technical help and assistance.
This work was supported by the  Medical Research Council ,  United Kingdom  ( U117565642 ), The  Francis Crick Institute, Mill Hill Laboratory (Crick 10126 ) and the  European Research Council  ( 294682-TB-PATH ). SB was in part jointly funded by the  UK Medical Research Council (MRC)  and the  UK Department for International Development (DFID)  under the  MRC/DFID  Concordat agreement ( MR/ J010723/1 ). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Linkage Mapping The mapping population was genotyped with two previously developed SSRs flanking the ABSr locus  (Cuenca et al. , 2013)  and nine new SNP markers developed from the sequences shown in Table  1. Besides, it was phenotyped as described above. The fine linkage map was constructed using the JoinMap 4. 1 software package  (Stam, 1993) , where markers were coded as lm × ll (i. e. , pseudo-test cross), using Kosambi's mapping function. The recombination threshold was of 0. 35, and default values were set for all other parameters. Markers were subjected to segregation distortion analysis.
SNP Mining from Sequencing With the objective to perform fine mapping, useful SNPs were searched in the previously defined 3. 3 Mb region spanning the ABSr locus. In a first step, 20 DNA fragments within the ABSr region were Sanger-sequenced in the parents of the analyzed population and two additional genotypes (one resistant and one homozygous susceptible) to find informative polymorphisms potentially correlated with the response to the disease. A total of 9. 7 kb corresponding to these sequences were finally obtained. Consensus sequences have been submitted to Genbank (accession numbers from KX368965 to KX368984). Twenty-two SNP were found to have useful polymorphisms (data not shown). An example for SNP08 development from sequencing (fragment #16) is shown in Figure  2. At this position, "Fortune" (heterozygous susceptible parent; Figure  2A ) is heterozygous G/T and "C × SO-1" (resistant parent; Figure  2B ) is homozygous T/T; additional genotypes are "Clemenules" (resistant, T/T; Figure  2C ) and "Minneola" (homozygous susceptible G/G; Figure  2D ).
In addition to these genes, there are other four genes with no functional annotation in www. phytozome. org website. These genes were then blasted against the NCBI database (https://blast. ncbi. nlm. nih. gov), where no similarity with any previously characterized protein was found for Ciclev10019166, Ciclev10022922, and Ciclev10023674 genes. Blast results for the Ciclev10024474 gene showed high similarity with a predicted putative RPP13-like protein annotated in Citrus sinensis. Therefore, this gene was also considered as annotated for disease resistance.
The identified region contains eight genes harboring NBS-LRR repeats, which should be considered as candidate genes for ABS resistance. Nevertheless, the RLM3, a Toll/interleukin 1 receptor domain R-protein in Arabidopsis is the only NBS-LRR gene found to be responsible for resistance to necrotrophs  (Mengiste, 2012). A BLAST with this protein results in 200 hits in the citrus genome. Surprisingly, 170 of them are located within chromosome 3, showing the highest score (E = 8. 1e-58), and 37% of them are physically mapped around the region of interest (i. e. , from 21 to 28 Mb in chromosome 3); however, none of them is within the region identified by fine mapping. Among the identified resistance genes, Ciclev10018637 and Ciclev10023511 encode for a Leucine-Rich Repeat (LRR) receptor-like protein with serine/threonine kinase domain.
Despite endophthalmitis being the most feared complication, antibioprophylaxis remains controversial in intravitreal injections. Therefore, we conducted a systematic review and meta-analysis on the effects of antibioprophylaxis in intravitreal injections in the prevention of endophthalmitis. The PubMed, Cochrane Library, Embase and Science Direct databases were searched for studies comparing groups with and without antibiotics in intravitreal injection, with the use of the following keywords: "antibiotic*", "endophthalmitis" and "intravitreal injection*". To be included, studies needed to specify number of participants and number of endophthalmitis within each group (with and without antibiotics). We conducted meta-analysis on the prevalence of clinical endophthalmitis including both culture-proven and culture negative samples.
Literature Search We reviewed all cohort studies found on Medline via Pubmed that compared two groups after intravitreal injections: one with antibiotics and one without. Keywords for the search strategy were "antibiotic Ã ", "endophthalmitis" and "intravitreal injection Ã ". The following databases were searched on December 23 rd , 2015: PubMed, Cochrane Library, Science Direct and Embase. The search was not limited to specific years and no language restrictions applied. To be included, studies needed to specify the number of participants and quantify the incidence of endophthalmitis within each group (with and without antibiotics). All kinds of intravitreal injections were included i. e. corticoids (triamcinolone, dexamethasone) or anti-VEGF such as monoclonal antibodies (mab-bevacizumab, ranibizumab), recombinant proteins (aflibercept) and pegatnamib.
Statistical considerations Statistical analysis was conducted using Comprehensive Meta-analysis software (version 2, Biostat Corporation) and Stata software (version 13, StataCorp, College Station, US). Extracted data were summarized for each study and reported as mean (standard-deviation) and number (%) for continuous and categorical variables respectively. Prevalence of endophthalmitis and 95% confidence intervals were estimated using random-effects models assuming between and within study variability (DerSimonian and Laird approach). Statistical heterogeneity between results was assessed using forest plots, confidence intervals and I². The I 2 statistic is the most common metric for measuring the magnitude of between-study heterogeneity and is easily interpretable. I² values range between 0 and 100% and are typically considered low for values <25%, modest for 25-50%, and high for >50%.
Other meta-analyses and meta-regressions An insufficient number of studies reported the specific types of antibiotics used and types of products injected (bevacizumab, ranibizumab, triamcinolone). Therefore, low numbers of studies precluded meta-analyses on the influence of types of products injected to reduce the risk of endophthalmitis. Insufficient sample sizes also precluded meta-analyses on bacteries retrieved in culture proven endophthalmitis. Similarly, only two studies reported the number of patients, only two studies reported age, and no studies reported gender (S1 Database). Consequently, no meta-regressions were conducted.
Pepper (Capsicum spp. ) is an important vegetable crop in the world. Now the pepper in China contributes one-third of the world's peppers production. Genetic diversity of the pepper germplasm of China is expected interesting to know. To explore the structure of genetic diversity in Chinese pepper germplasm resources and possible relationship with cultivar types or geographic origin, we sampled and compared 372 GenBank pepper accessions (local cultivars and landraces) from 31 provinces, autonomous regions and municipalities of China and 31 additional accessions from other countries. These accessions were genotyped using 28 simple sequence repeat (SSR) markers spanning the entire pepper genome. We then investigated the genetic structure of the sampled collection using model-based analysis in STRUCTURE v2.
Data analysis Genetic diversity analysis GeneMapper 4. 0 software was used to evaluate the sizes of amplified fragments (SSR alleles) from different samples. The number of alleles, allele frequencies, number of genotypes, Nei's unbiased gene diversity index (He), observed heterozygosity (Ho), and polymorphism information content (PIC) were calculated using Power Marker v3. 25 software (http://www. powermarker. net). Genetic distances (chord distances) were calculated by the.
Acknowledgements This work was supported by the  National Key Technology Research and Development Program of China  ( 2011BAZ01732 ), the  Project of the Ministry of Agriculture of China  ( CARS-25 ), the  Core Research Budget of the Non-profit Governmental Research Institute, China (ICS, CAAS ;  1610032011011 ), and the  Science and Technology Innovation Program of the Chinese Academy of Agricultural Sciences  ( CAAS-ASTIP-IVFCAAS ).
Study population The data used in this analysis are from the colon and rectal cancer case-control components of the Canadian National Enhanced Cancer Surveillance System (NECSS), a collaborative effort between Health Canada and the cancer registries in 8 Canadian provinces. The NECSS collected data from a population-based sample of 21022 cases of 19 different cancers and 5039 controls between 1994 and 1997. Data for rectal and colon cases were not collected in Ontario, therefore this analysis is based on male participants from 7 provinces. Cancer-free controls were recruited using a random sample of the provincial population obtained from health insurance plans in 5 provinces (Prince Edward Island, Nova Scotia, Manitoba, Saskatchewan and British Columbia) and random-digit dialing in Newfoundland and Alberta  [16].
Statistical analysis Odds ratios (OR) and 95 % confidence intervals (CI) were estimated using unconditional logistic regression for each of the exposure metrics. Trends were also examined using logistic regression. Ordinal metrics of diesel and gasoline exposure were treated as continuous in the regression model in order to obtain an estimate of the slope and associated p-values (p-trend). Descriptive analyses were conducted and the influence of possible risk factors suggested by the literature and by previous analyses of NECSS data was investigated. These included the characteristics presented in Table  1 , as well as additional nutritional factors, including consumption of red meat and intake of added fat. Exposure metrics for diesel and gasoline emissions were entered into the statistical models together in order to account for the simultaneous exposure to both of these constituents of motor vehicle exhaust.
Discussion Exposure to diesel and gasoline emissions is widespread, and accurately assessing its impact on multiple health outcomes continues to be a public health priority. In this study, our aim was to conduct a comprehensive investigation of occupational exposure to diesel and gasoline emissions on colon and rectal cancer risk, using data from a large population-based case-control study. Despite the robust associations previously observed for lung cancer in these data  [22]  and other studies, the increases in colon and rectal cancer risk appeared to be attenuated. Statistically significant excesses in rectal cancer risk were observed for exposure to diesel emissions at high Composite index of physical activity was derived y summing the hours/month of moderate and strenuous activity levels of concentration, as well as for long durations of exposure at high levels of concentration.
The hypothesis linking diesel emissions to increased risk of colon and rectal cancer postulates that clearance of inhaled the gases and particulate matter by mucocilliary transport and diffusion into the pulmonary capillaries is likely the pathway by which these particles translocate to other organs  [32]. Although the carcinogenic mechanism of PAHs has been attributed to genotoxic effects, such as the formation of bulky DNA adducts  [33] [34] [35] , the underlying process is less clear for other constituents of motor vehicle exhaust, such as elemental carbon  [35, 36]. Toxicology data suggest that generation Adjusted for age, province of residence, use of proxy respondents, BMI categories, percent change in weight from maximum lifetime weight, cigarette pack years, combined physical activity index (hours/month), alcohol consumption (servings/week), consumption of processed meat (servings/week), occupational exposure to asbestos (yes/no), occupational exposure to aromatic amines (yes/no) c Cumulative metric of exposure to diesel emissions was derived from estimates of concentration of exposure, frequency of exposure and duration of employment of reactive oxygen species (ROS) and the resulting mutations represent another potential carcinogenic mechanism.
In a large Canadian population-based case-control study in the 1980's, exposure to diesel engine exhaust was linked to increased risks of colon cancer (OR = 1. 7 for long-term, high-level exposure)  [12]. Contrary to our findings, gasoline engine exhaust was associated with elevated risks of rectal cancer (OR = 1. 6 for long-term, high-level exposure)  [12]. However, this analysis was based on small case series (364 colon and 190 rectal cancers), and lacked information on BMI, diet and physical activity. In another analysis of the same dataset, Goldberg et al. [13]  assessed the association of colon cancer with diesel engine emissions in 497 male cases compared with 1514 other cancer patients (excluding cancers of the lung, peritoneum, esophagus, stomach and rectum) and 533 population controls.
Acknowledgments The  Canadian Cancer Registries Epidemiology Research Group  comprised a principal investigator from some of the provincial cancer registries involved in the National Enhanced Cancer Surveillance System:  Farah McCrate ,  Eastern Health , Newfoundland;  Ron Dewar ,  Nova Scotia Cancer Registry ;  Nancy Kreiger ,  Cancer Care Ontario ;  Donna Turner ,  Cancer Care Manitoba. This project was funded by a research grant provided by the  Workplace Safety and Insurance Board  (Ontario) -WSIB#  10011. We thank the chemists/industrial hygienists at  INRS Institute Armand-Frappier ,  Louise Nadon ,  Benoit Latreille ,  Ramzan Lakhani , and  Mounia Rhazi  for their contribution to this work. We also acknowledge the support of the  Ontario Occupational Cancer Research Center (OCRC)  and  Health Canada.
A photograph of a fractured microdevice sitting on a dime is shown in Fig. 1D , revealing the microfluidic channels along the edge of the device. The cell culture chamber is covered with a thin glass cover slip (≈3 mm×3 mm×0. 17 mm). To optimize the design and operation of the microdevice, we employed modeling software (COMSOL) to elucidate diffusion profiles within the cell chamber (Fig. 2 ). The physical laws governing the operation of the microdevice are Fick's laws of diffusion and the Navier-Stokes equations  (Smith et al. , 2010). The judicious placement of sources and sinks allows a wide variety of diffusion profiles to be engineered in the microdevice. Initially, a simple two-port system was used that is suitable for generating a linear concentration gradient. This gradient within the chamber corresponds with SHH diffusion profiles found in the dorsoventral axis of the neural tube (Fig.
Acknowledgements This study has been funded by the  Swedish Research Council  ( 2011-3916 ,  2012-4944 ), The  Swedish Heart and Lung Foundation ,  Swedish Medical Society, The Medical Faculty of Lund University, Sweden , and  Region of Scania, Sweden. Funding for the CHILL-MI trial was received from  Philips Healthcare. Funding for the MITOCARE trial was received from the  European Commission  within the 7 th  Framework Programme for RTD -Project MITOCARE -Grant  Agreement  HEALTH-2010-261034.
Statistical analysis All patients were followed up until death or the end of data recording  (31 January 2015). The time under treatment was defined as the period between the first and last cure of FOLFIRINOX, without progression during this period. Progression free survival was calculated from the date when therapy started to the date of disease progression, and Overall Survival was calculated from the date when therapy started to the date of death. Median follow-up with its 95%CI was calculated using the reverse Kaplan-Meier method. Patient or disease characteristics were examined using the χ 2 test or Fisher's exact test for qualitative variables, and the Student t or Mann-Whitney tests for continuous variables, as appropriate. Survival probabilities were estimated using the Kaplan-Meier method and survival curves were compared using the log-rank test.
patients with metastatic pancreatic adenocarcinoma. Oncology 2011; 80: 301-306 [PMID: 21778770 DOI: 10. 1159/000329803] 32 Ychou M, Viret F, Kramar A, Desseigne F, Mitry E, Guimbaud R, Delpero JR, Rivoire M, Quénet F, Portier G, Nordlinger B. Tritherapy with fluorouracil/leucovorin, irinotecan and oxaliplatin (FOLFIRINOX): a phase II study in colorectal cancer patients with non-resectable liver metastases. Cancer Chemother Pharmacol 2008; 62: 195-201 [PMID: 17901955 DOI: 10. 1007/ s00280-007-0588-3] 33 Institut de Cancérologie de l'Ouest. Phase 2 trial: Efficacy and Tolerance Evaluation in FOLFIRINOX Dose Adjusted in Elderly Patients with a Metastatic Pancreatic Cancer (PAMELA70), 2014. Available from: URL: https://clinicaltrials. gov/ct2/show/ NCT02143219 P-Reviewer: Kleeff J, Lakatos PL, Yoshitomi H S-Editor: Qi Y L-Editor: A E-Editor: Zhang FF.
Qualitative simulation of the PL model The model in Table  1  has been implemented in and simulated with the publicly available software tool Genetic Network Analyzer (GNA 8. 4, Genostar, http://userclub. genostar. com/en/genostar-soft ware/gnasim. html). The corresponding model file is given in the supplementary data in GNAML and qualitative SBML formats  [20]. An example of qualitative simulation with the simple network model is given in Panel D of Fig. 1. Running the attractor search functionality of GNA shows that there are two stable steady states for the osmotic stress response model, one characteristic for normal growth in the absence of osmotic stress and one reached in case of osmotic stress. We can simulate how the system responds to salt addition and leaves the non-stressed state for the stressed one, by perturbing the state of normal growth with the signal of stress switched on u 4 t u ð Þ.