dataesr/scientific-paragraphs-categorization huggingface dataset:
Data availability The 30 s disdrometer data from a 2-month measurement campaign with collocated devices in the Paris area are presented in this paper. Raw data, along with Python-formatted data with corresponding scripts, are described. The Hydrology, Meteorology, and Complexity laboratory of École des Ponts ParisTech (HM&Co-ENPC) has made this data set available at http://doi. org/10. 5281/zenodo. 1240168. The following citations should be used for every use of the data. -For this paper: Gires, A. , Tchiguirinskaia, I. This data set is available for download free of charge. License terms apply. These disdrometers and others similar ones have been used in other campaigns by HM&Co and are still collecting data. Regular updates of their status along with updates of the database are to be provided through Earth Syst.
, and Schertzer, D. : Two months of disdrometer data in the Paris area, Earth Syst. Sci. Data, 10, 941-950, https://doi. org/10. 5194/essd-10-941-2018, 2018. For the database: Gires, Auguste, Tchiguirinskaia, Ioulia, and Schertzer, Daniel. (2017). Data for "Two months of disdrometer data in the Paris area" (Version v2 of the dataset) [Data set]. Zenodo. http://doi. org/10. 5281/zenodo. 1240168.
Acknowledgements. The authors greatly acknowledge partial financial support from the  Chair of Hydrology for Resilient Cities  (endowed by  Veolia) of the École des Ponts ParisTech ,  EU NEW INTERREG IV RainGain Project  (www. raingain. eu,last access: 18 May 2018),  EU Climate KIC Blue Green Dream  (www. bgd. org. uk, last access: 18 May 2018), and the  Île-de-France region RadX@IdF Project. The authors thank  Serge Botton  (from the  Departement Positionnement Terrestre et Spatial of the ENSG ) for facilitating access to the roof where the disdrometers are installed. Edited by: David Carlson Reviewed by: two anonymous referees.
- , and Schertzer, D. : Two months of disdrometer data in the Paris area, Earth Syst. Sci. Data, 10, 941-950, https://doi. org/10. 5194/essd-10-941-2018, 2018. For the database: Gires, Auguste, Tchiguirinskaia, Ioulia, and Schertzer, Daniel. (2017). Data for "Two months of disdrometer data in the Paris area" (Version v2 of the dataset) [Data set]. Zenodo. http://doi. org/10. 5281/zenodo. 1240168.
Together, these data indicate that cell death and loss of heterochromatin integrity induced by KAP1 depletion can be rescued by Suv39h1 overexpression. Noteworthy, in spite of their persistent association with H3K9me3, the expression of major satellite transcripts increased in Kap1 KO MEFs (Figure  6E ). It suggests that this chromatin mark does not primarily influence transcription from these loci. We then examined by ChIP-qPCR the enrichment in H3K64me3 and H4K20me3, two other marks of constitutive heterochromatin. While H4K20me3, as H3K9me3, was lost at KAP1 binding sites but preserved at major satellite repeats in Kap1 KO MEFs, H3K64me3 was reduced at both places (Figures  3C  and 6F ). Thus, the H3K64me3 histone mark appears to play an important role in repressing transcription at major satellite repeats.
ACKNOWLEDGEMENTS We thank  S. Ait-Si-Ali  for providing all KMT expression plasmids,  C. Green  for the His-PCNA,  C. Rachez  for the  FLAG-KAP1  and  F. Rauscher  for the GST-KAP1(RVEE) vectors,  T. Jenuwein  for WT and Suv39h1/h2 KO MEFs,  M. Friedli ,  E. Allemand ,  O. Mauger ,  A. De Iaco  for discussion,  C. Raclot  and  B. Quentin  for technical assistance, the  University of Lausanne Genomics Core Facility  for sequencing and  Yuri Kim  for drawing Figure 7. Authors Contributions: S. M. J. conceived the study, designed and performed experiments, analyzed and interpreted data, and wrote the manuscript. A. K. , J-P. Q. and B. R. designed, performed and analyzed experiments. J. P. and J. D. performed bioinformatics studies. A. C and P. T. made intellectual contributions. G. A. designed experiments, analyzed and interpreted data.
FUNDING Swiss  National Foundation  and the  European Research Council  [ ERC-2010-AdG-268721  " KRABnKAP " and Nucleic Acids Research, 2018, Vol. 46, No. 17 8801 ERC-2015-AdG-694658  " TRANSPOS-X " to D. T. ]; la  Ligue National contre le Cancer (Equipe labellisée Ligue)  [ ANR-11-LABX-0044   DEEP  and  ANR-10-IDEX-0001-02   PSL ,  ANR-12-BSV5-0022-02  ' CHAPINHIB ',  ANR-14-CE16-0009  ' Epicure ',  ANR-14-CE10-0013  ' CELLECTCHIP ',  EU  project  678563 'EPOCH28', ERC-2015-AdG-694694  ' ChromADICT ',  ANR-16-CE15-0018  ' CHRODYT ',  ANR-16-CE-12-0024  ' CHIFT ' and  ANR-16-CE11-0028  'REPLICAF' to G. A. ]. Funding for open access charge:  Swiss National Foundation  and the  European Research Council.
Primary outcomes include hospitalisation rates, length of stay, leaving against medical advice, readmission and in-hospital mortality. In total, five databases will be searched (MEDLINE, EMBASE, CINAHL, PsycINFO and Web of Science). Titles, abstracts and full texts will be independently reviewed by two investigators in three separate stages. The methodological quality of included quantitative research studies will be assessed using a validated tool. Data from included articles will be extracted using a standardised form and synthesised in a narrative account. Ethics and dissemination Results of this systematic review could provide a better understanding on how to optimise health systems and services to improve patient outcomes and care. The results of this study may provide future research with a foundation to guide decisionmaking and for designing and implementing systems-level interventions to improve treatment and care delivery for people living with HCV.
Information sources and search strategy We will conduct a comprehensive search strategy to identify articles that meet the eligibility criteria. Specifically, we will search the following databases: MEDLINE, EMBASE, CINAHL, PsycINFO and Web of Science. As indicated above, search terms will be based on the PEO framework, and these terms will be mapped to database-specific medical subject headings and controlled vocabulary terms when available (online supplementary additional file 2). Additionally, we will search reference lists of research articles and systematic reviews to identify relevant articles not otherwise captured in the search strategy. To ensure the robustness of the search strategy, we have consulted with a medical reference librarian with expertise in systematic reviews and population and public health at the University of British Columbia (U.
study records We will conduct database searches and import the full-text articles from the search strategy into Endnote X8. Then, we will remove any duplicates prior to reviewing the titles, abstracts and full-text articles. This will be conducted independently in three separate stages by two investigators. At each review stage, studies clearly not meeting the inclusion criteria will be excluded from further review and the reason for exclusion will be recorded. If the two investigators are not able to come to a consensus regarding the inclusion or exclusion of an article, this will be resolved by discussion with a third investigator.
Open access risk of bias in individual studies The methodological quality, including risk of bias, of included quantitative research studies will be assessed using the Downs and Black checklist for the reporting of healthcare studies. 22 23 This 27-item checklist has been shown to be a valid and reliable tool in assessing the quality of research studies. Higher scores represent higher overall methodological quality. Each article will be independently scored by two investigators. If the two investigators are not able to come to a consensus regarding the inclusion or exclusion of an article, this will be resolved by mutual consent and discussion with a third investigator. data synthesis A PRISMA flow chart will be created to outline the article selection process. 24 Data from included studies will be extracted using a standardised form developed to capture study characteristics and main findings and summarised in a table.
Specifically, information on study characteristics (eg, geographical setting, study design, study period (including therapeutic periods, ie, interferon-based therapy era, first-generation DAA-based therapy era, second-generation DAA-based therapy era), study population), participant characteristics (eg, age, sex/gender); study objectives; outcome variable(s) and main study findings will be extracted from individual studies. Should there be multiple articles pertaining to the same study population and setting, we plan to extract comprehensive data across the articles but they will be linked together as one unique study. Findings from the included studies will then be synthesised in a narrative account that addresses the objectives of this systematic review.
The second, the SST measurement method (SIM) is derived from WMO Publication 47-hereafter Pub47 (e. g. ,  Kent et al. , 2007) -and is available from ~1960 onward. Unfortunately, the available metadata is not always correct; both SI and SIM can lead to misidentified reports  (Kent & Taylor, 2006; K11b). For discussion on the reliability of the metadata see section S1 of the supporting information. Both HadSST3 and COBE-SST2 bias adjustments require estimation of the fraction of observations associated with each measurement method, inferred using either SI or SIM. In K11b, additional information was derived from the literature and from the typical method adopted by the country that recruited the ship. By contrast, in  Hirahara et al. (2014) -hereafter H14-time-varying ratios of bucket to ERI observations were calculated such that global mean SST anomalies, following method-dependent bias adjustment, agreed for the data sets with extant and missing metadata.
5  (Woodruff et al. , 2011). Subsets of data expected to use the same measurement method were identified and analyzed. Typically, each ship-operating country has a preference for a particular measurement method (K11b), and some ICOADS data sources (known as decks) derive from archives of particular countries. Country is expected to be more consistently associated with method than deck, but is not available for every observation, so subsets are also analyzed according to deck. The approach is described in more detail in section S2 in the supporting information. To account for variations over time and regionally, the analysis was performed for 10 year intervals and by 60°latitude band. Five different realizations were performed changing the start date by 2 years  (1850, 1852, 1854, 1856, and 1858).
In contrast, our results confirmed the presence of a small percentage (less than 4%) of U. S. bucket observations in the 1980s and 1990s, according to SI(M). K11b assumed that all U. S. observation post-WWII were made by ERI. In the period 1960-1975 observations from Dutch and Russian ships have sparse method information, which indicates bucket observations. However, we identified the much larger proportion with unknown method from these countries as ERI, explaining much of the Geophysical Research Letters 10. 1002/2017GL076475 reduction in bucket measurements in this period. Data from Russian deck 732 were analyzed separately (see section S3 in the supporting information) and were also classified as ERI. Different classifications will impact on long-term SST trends because different observational biases characterize each SST method  (Kent et al.
Acknowledgments The authors wish to acknowledge use of the R software for analysis and graphics in this paper ( R Development Core Team ,  2016 ). G. C. , E. K. , and D. B. were funded by the  Natural Environment Research Council (NERC)  through grant  NE/J020788/1. S. M. -B. and C. J. M. were funded by  NERC  through grant  NE/J02306X/1. J. K. was supported by the  Joint UK BEIS/Defra Met Office Hadley Centre Climate Programme  ( GA01101 ). S. H. was supported by the  Environment Research and Technology Development Fund of the Ministry of the Environment, Japan. The data used in this study can be obtained from https://rda. ucar. edu/datasets/ds540. 0/.
This loop may be relevant in human tumors, because MYC and FGFR3 expression levels were found to be positively correlated in tumors bearing FGFR3 mutations in two independent transcriptomic datasets (n = 63 and n = 271), and because FGFR3 inhibition in a patient-derived tumor xenograft (PDX) model harboring an FGFR3-S249C mutation decreased the levels of both MYC and FGFR3. We found that MYC mRNA levels and protein stability were dependent on p38 and AKT activation, respectively, downstream from FGFR3 activation. Finally, we showed, in xenograft models, that FGFR3 activation conferred sensitivity to FGFR3 and p38 inhibitors and to a BET bromodomain inhibitor (JQ1) preventing MYC transcription. These findings therefore suggest new treatment options for bladder cancers in which FGFR3 is aberrantly activated.
We identified 741 and 3,124 genes displaying significant differential expression after FGFR3 depletion in MGH-U3 and RT112 cells, respectively (adjusted P-values < 0. 05, |log2(FC)| > 0. 5; Dataset EV1). An analysis of these two lists of FGFR3-regulated genes using the upstream regulator function of Ingenuity Pathway Analysis (IPA) software identified upstream regulators activated and inhibited by FGFR3  (Fig 1A, left panel). The top 10 transcriptional regulators with activity modulated by FGFR3 were common to the two cell lines and are listed in the right panel in Fig 1A. The transcription factor predicted to be the most strongly inhibited here after FGFR3 depletion, in both cell lines, was the proto-oncogene MYC, for which mRNA levels were downregulated. This downregulation of MYC mRNA levels after FGFR3 knockdown with siRNA was further confirmed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) (30-70% decrease, depending on the cell line used; Fig  1B ).
Western blot analysis showed that the downregulation of MYC induced by the inhibition of FGFR3 was abolished by MG132, in both cell lines. Overall, our results indicate that the inhibition of aberrantly activated FGFR3 decreases MYC mRNA levels and favors proteolysis of the MYC protein by the proteasome, thereby decreasing its transcriptional activity. We then investigated the possible contribution of MYC to the oncogenic activity of aberrantly activated FGFR3. We compared the effects on viability of depleting FGFR3 and MYC alone or together, with siRNA, in RT112 and MGH-U3 cells (Fig  1I ). FGFR3 and MYC siRNAs efficiently knocked down the levels of the targeted proteins  (Appendix Fig S3B). The depletion of either MYC or FGFR3 resulted in significantly lower cell viability than for cells treated with the control siRNA (Fig 1I, right and left panels and Dataset EV2 for the P-values).
This result was confirmed in two other cell lines expressing constitutively activated FGFR3: UM-UC-14 (FGFR3-S249C) and RT4 (FGFR3-TACC3 breakpoint exon 18 FGFR3-exon 4 TACC3, whereas FGFR3-TACC3 breakpoint exon 18 FGFR3-exon 11 TACC3 is expressed in RT112;  Williams et al, 2013; Earl et al, 2015; Fig 2D). These four cell lines express low levels of FGFR1, FGFR2, and FGFR4, as assessed with an Affymetrix U133plus2 array, suggesting that the observed effect was mostly due to FGFR3 inhibition (data not shown). However, treatment had no effect on MYC and FGFR3 expression in UM-UC-5 cells, which express wild-type FGFR3 (Fig 2D.
C ChIP-qPCR for MYC at the FGFR3 locus in MGH-U3 and RT112 cells (lower panel). The qPCR target loci of FGFR3 are schematized (upper panel). Data presented are representative of two replicate experiments. Error bars show standard deviation of three replicate qPCR reactions. D RT112, MGH-U3, UM-UC-14, RT4, and UM-UC-5 cells were treated for 48 h with a pan-FGFR inhibitor (500 nM PD173074). Lysates were obtained, and levels of FGFR3 and MYC were analyzed by Western blotting with appropriate antibodies. An anti-tubulin antibody was used as a loading control. E MGH-U3 and RT112-derived xenograft tumors from mice treated for 9 days with vehicle or PD173074 (25 mg/kg/day) were lysed and immunoblotted with anti-FGFR3 and anti-MYC antibodies. Actin was used as a loading control. Black and white arrowheads indicate WT FGFR3 and FGFR3-TACC3 bands, respectively.
Data are presented as means AE SEM. Results were compared in Wilcoxon's test. E MGH-U3 and RT112 cells were treated for 72 h with (+)-JQ1 and PD133074 alone or in combination. Cell viability was measured with CellTiter-Glo. Data are presented as means AE SD of three experiments carried out in triplicate. Results for the drug combination were compared with those for each individual drug separately, in unpaired Student's t-tests, ***0. 0001 < P < 0. 001; ****P < 0. 0001. Source data are available online for this figure. particular using pan-FGFR inhibitors. A multi-drug phase II clinical trial including pan-FGFR inhibitor (BGJ398) together with a MEK inhibitor (MEK162) and a RAF inhibitor (LGX818) is currently ongoing in advanced BRAF melanoma (NCT02159066). A phase Ib trial of BGJ398 in combination with BYL719 (PI3K inhibitor) on solid tumors showed encouraging results as eight patients over 24 showed a partial response, among them, one patient with a urothelial carcinoma bearing FGFR3-TACC3 had a complete tumor shrinkage for 4 months (NCT01928459).
ncbi. nlm. nih. gov/geo/) under accession number GSE84733. The LIMMA algorithm was used to identify genes differentially expressed between FGFR3 siRNA-treated (two and three different siRNAs were used for RT112 and MGH-U3 cells, respectively) and Lipofectaminetreated cells (three replicates;  Ritchie et al, 2015). The P-values were adjusted for multiple testing by Benjamini-Hochberg FDR methods. Genes with a log 2 fold-change of at least 0. 58, in a positive or negative direction, with a FDR below 5%, were considered to be differentially expressed.
Reverse-phase protein array (RPPA) Reverse-phase protein array with specific anti-phospho-AKT (S473; Cell Signaling Technology # 4058, used at 1/1,000) and anti-phospho-p38 (T180/Y182; BD Biosciences #612288, used at 1/500) antibodies was performed and analyzed as previously described  (Calderaro et al, 2014). The specificity of the antibodies used for RPPA for the protein of interest was checked by Western blotting with 18 tumor lysates, before the study. We obtained a Pearson coefficient for the correlation between RPPA and Western blotting of 0. 84 for P-AKT (66) and 0. 88 for P-p38 (data not shown).
FGFR3 mutational status and data for eight normal samples were kindly provided by Dr. Ellen Zwarthoff (Erasmus MC Cancer Institute, the Netherlands) and Dr. Lars Dyrskjøt (Aarhus University Hospital, Denmark). The microarray for MGH-U3 and RT112 cells treated with FGFR3 siRNA are available from GEO (https://www. ncbi. nlm. nih. gov/geo/) under accession number GSE84733. The paper explained Problem Bladder cancer is the ninth most common cancer worldwide. FGFR3 alterations (mutations or translocations) are among the most frequent genetic events in bladder carcinoma. They lead to constitutive activation of the receptor and to oncogene addiction to FGFR3. Anti-FGFR therapies have recently yielded promising results, but the efficacy of such targeted therapies is currently limited by the emergence of resistance.
Tomlinson et al, 2012)are the means of three independent experiments carried out in triplicate, error bars represent standard deviations. Tukey's multiple comparisons tests were performed to evaluate the significance of differences. The results of the statistical analysis are summarized in Dataset EV2. Tomlinson et al, 2012), in some blood-derived cell lines and in one lung cancer-derived cell line. MYC activation did not seem to be sufficient to induce FGFR3 regulation. Indeed, MYC ChIP-Seq data acquired for two inducible models of MYC overex-.
Acknowledgements We thank  David Gentien  and  Leanne De Koning  from the genomics and RPPA platforms, respectively, of  Institut Curie. We thank  Ellen Zwarthoff  ( Erasmus MC Cancer Institute, the Netherlands ) and  Dr. Lars Dyrskjøt  ( Aarhus University Hospital, Denmark ) for providing FGFR3 mutations for their cohort of tumors for which transcriptomic data were publicly available and transcriptomic data for eight normal samples, respectively. This work was supported by a grant from  Ligue Nationale Contre le Cancer  ( IBP, FR, MM, HNK, RN, CK, MDG ) as an associated team (Equipe labellisée), the " Carte d'Identité des Tumeurs" program  initiated, developed, and funded by  Ligue Nationale Contre le Cancer , the " LIONS " project funded by  INSERM/ ITMO Cancer  and the " Tumult " project funded by  INCa.
Data availability Transcriptomic data obtained with Affymetrix U133plus2. 0 DNA arrays for our CIT-cohorts of bladder tumors, encompassing 82 NMIBCs and 85 MIBCs, were previously deposited on the publicly available ArrayExpress databases E-MTAB-1803 and E- MTAB-1940,  respectively (El Behi et al, 2013; Biton et al, 2014; Rebouissou et al, 2014). RNA-Seq data for an independent cohort of 416 tumors were available from ArrayExpress E-MTAB-4321  (Hedegaard et al, 2016).
Tomlinson et al, 2012)are the means of three independent experiments carried out in triplicate, error bars represent standard deviations. Tukey's multiple comparisons tests were performed to evaluate the significance of differences. The results of the statistical analysis are summarized in Dataset EV2. Tomlinson et al, 2012), in some blood-derived cell lines and in one lung cancer-derived cell line. MYC activation did not seem to be sufficient to induce FGFR3 regulation. Indeed, MYC ChIP-Seq data acquired for two inducible models of MYC overex- checked, by ChIP-qPCR, that the selected FGFR3 promoter and enhancers did harbor the expected histone activation marks (H3K27ac and H3K4me3) in RT112 cells (Appendix Fig S4B). Finally, we showed that the two FGFR3 enhancer regions tested were enriched in MYC, consistent with the direct regulation of FGFR3 expression by MYC, at the transcriptional level (Fig 2C).
This regulation of FGFR3 by MYC seemed to be quite specific to bladder The significance of differences was assessed in Mann-Whitney tests, and means and standard errors are represented. cancer, because MYC binding to the FGFR3 enhancers or promoter D MYC and FGFR3 mRNA levels in human bladder tumors harboring either mutated FGFR3 (upper panel) or wild-type FGFR3 (lower panel). Spearman's coefficient and was rarely observed in a publicly available dataset encompassing P-values are indicated for the correlations between MYC and FGFR3 mRNA levels in each group. 118 MYC chromatin immunoprecipitation and sequencing (ChIP- E MYC mRNA levels in a PDX model bearing a FGFR3-S249C mutation and treated daily, for 4 days, with 30 mg/kg BGJ398, a pan-FGFR inhibitor, or with vehicle (n = 4 Seq) in different tissues (Appendix Fig S5A).
| Literature survey, clustering and ancestral host reconstruction analysis The literature survey was conducted by typing the terms (using Boolean operators): "Bemisia tabaci" AND botanical family name (e. g. , "Acanthaceae") AND "Cytochrome oxidase I" OR "mtCOI" (both options) in Google Scholar, using the "Any time" option. Only reported insect collections in which the plant host was associated with a specific mtCOI barcode were maintained (papers are listed in Supporting Information Table  S1 ). Due to too sporadic sampling reports, data of species within the Mediterranean (MED), New-World (NW), Sub-Saharan Africa (SSA), Italy, Asia II and China genetic groups were collapsed. The combined data set (the absence/ presence matrix) was used as input for the HEATMAP. 2 function (Euclidean distance with a complete linkage method) of the R GPLOTS package (R Core Team, 2017).