dataesr/scientific-paragraphs-categorization huggingface dataset:
(G) WM115 cells were treated with various doses of doxycycline, and apoptosis induction was measured in real time using PI staining and live-cell imaging (data represent mean with SEM of a representative experiment). (H) Gating strategy used to sort and further characterize cells undergoing failed apoptosis (VC3AI + /Annexin V À ). (I) Representative images of sorted VC3AI + /Annexin V À WM852 cells immediately after and 12 h after sorting (scale bar, 75 mm). (J) Cell proliferation was determined using live-cell imaging based on the confluency parameter (data represent mean with SEM of a representative experiment). (K) Responsiveness to tBID expression challenge was measured using SYTOX Green staining (data represent mean with SEM of a representative experiment). Cell Reports 31, 107731, June 9, 2020 3 Article their role as anchors, focal adhesions are also involved in cell migration, especially during metastasis  (Roussos et al.
As the Venn diagram in Figure  7G  shows, the failed apoptosis signature in WM852 cells significantly overlaps with the ''invasion'' gene expression signature in melanoma published by  Verfaillie et al. (2015)  (p < 3. 563eÀ56, 13. 5 times more represented than expected by chance), whereas minimal overlap is observed with the ''proliferative'' group. WM115 cells follow a similar trend (Figure  S7I ). Interestingly, the failed apoptosis gene signature is different from that published for anastasis (Figure  S7J ), suggesting that failed apoptosis is a distinct process  (Sun et al. , 2017). To calculate a score of failed apoptosis, we further selected genes with a higher level of expression (logCPM [counts per million] > 1) to ensure overall higher detection across different datasets (Figure  7H ).
(G) WM115 cells were treated with various doses of doxycycline, and apoptosis induction was measured in real time using PI staining and live-cell imaging (data represent mean with SEM of a representative experiment). (H) Gating strategy used to sort and further characterize cells undergoing failed apoptosis (VC3AI + /Annexin V À ). (I) Representative images of sorted VC3AI + /Annexin V À WM852 cells immediately after and 12 h after sorting (scale bar, 75 mm). (J) Cell proliferation was determined using live-cell imaging based on the confluency parameter (data represent mean with SEM of a representative experiment). (K) Responsiveness to tBID expression challenge was measured using SYTOX Green staining (data represent mean with SEM of a representative experiment).
ACKNOWLEDGMENTS This work was supported by funding from  LabEx DEVweCAN  ( University of Lyon ),  Fondation ARC pour la Recherche sur le Cancer  (grant  20171206348 ),  Agence Nationale de la Recherche (ANR)   Young Researchers Project  ( ANR-18-CE13-0005-01 ), and the  ANR PLAsCAN Institute. We thank  Brigitte Manship  and  Stephany Fiore  for reviewing the manuscript;  Florine Mugnier ,  Sara Guedda ,  Thomas Barre  ( AniCan Image, Lyon, France ), and  Priscillia Battiston-Montagne  for technical assistance;  David Bernard ,  Germain Gillet , and  Ruth Rimokh  for discussing this project; and  Stephen Tait  for the pLZRS DD-FLAG-BCL-xL plasmid.
Acknowledgements We acknowledge support by grants from  European Research Council  (advanced grant  340485 ),  Human Frontier Science Program  ( RGP0029-2014 ),  Swedish Research Council  ( K2015-99X-22877-01-6 ),  Mizutani Foundation  for Glycosciences (reference n° 200014),  Agence Nationale pour la Recherche  ( ANR-16-CE23-0005-02 ,  ANR-19-CE13-0001-01 ),  Institut National du Cancer  ( n°2018-1-PLBIO-01-ICR-1, n°2019-1-PL BIO-05-CEA-1 ),  Plan Cancer program  LipoCanPredict. The Johannes team is member of  Labex CelTisPhyBio  ( ANR-11-LBX-0038 ) and  Idex Paris Sciences et Lettres  ( ANR-10-IDEX-0001-02 PSL ).
GENERAL FEATURES OF CTIP2/BCL11B An Overview of Its Role in the Immune and Nervous Systems Murine CTIP2, along with CTIP1, was first identified as a zinc finger protein implicated in transcriptional repression by interacting with the COUP-TF orphan nuclear receptors protein family  (Avram et al. , 2000). It was "rediscovered" independently as a tumor suppressor gene based on allelic loss mapping on chromosome 12 in γ-ray induced mouse thymic lymphomas  (Wakabayashi et al. , 2003a). Its human ortholog (Rit1/Bcl11b) was described in human gene databases and mapped to chromosome 14 (14q32. 1) (Satterwhite et al. , 2001). It was later reported that these chromosomal loci undergo recurrent cryptic chromosomal rearrangements t(5;14). These translocations induce ectopic expression of TLX3 or NKX2.
Hence in this work, only experimental data by AGE and PFGE are compared to the simulated number of DSBs as benchmark, because of the difficulty of evaluating absolute values of DSB yields by foci measurements. Whilst foci measurements cannot be used to determine the number of DSBs, they can be used to evaluate DNA repair processes with respect to time. The calculated time-curve of protein accumulation which is newly implemented into the simulation application is compared with experimental γ-H2AX yield irradiated with gamma rays from a 137 Cs source. The scavengeable damage fraction can be measured from the maximum degree of protection (DP) at infinite dimethylsulfoxide (DMSO) concentration. DMSO has been used as scavenger of radiolysis free radical species, in particular hydroxyl radical. DMSO is permeated among the Chinese hamster cell V79 before irradiation with different concentration up to 1.
Acknowledgements We would like to acknowledge the financial support from the  CNRS PICS  # 7340  and  PICS #8235 France -Greece , from the  CNRS PICS #8070 France -Serbia , the  IdEx Bordeaux University -France  - International Post-doctorates program  in the framework of the " France-Japan Particle Physics Laboratory" International Associated Laboratory , and the  IdEx Bordeaux University -France  - International Doctorates program  in the framework of the "France- Korea Particle Physics Laboratory" International Associated Laboratory  ( 2017-2020 )  S. Guatelli ,  D. Sakata ,  S. Incerti ,  I. Kyriakou  and  D. Emfietzoglou  acknowledge financial support from the  Australian Research Council ,  ARC DP170100967. I. Kyriakou  and  D. Emfietzoglou  acknowledge financial support from  ESA  (Contract No.
Protein Identification and Label Free Quantification MS/MS spectra were assigned to peptide sequences using the MASCOT Daemon 2. 6. 1 search algorithm (Matrix Science). A reference database from C. canephora  (Denoeud et al. , 2014)  of 25,574 polypeptide sequences totaling 10,251,572 residues was downloaded from Genoscope (http://coffee-genome. org/sites/ coffee-genome. org/files/download/coffea_cds. fna. gz) on July 1 st 2019 and used for peptide and protein inference. The following parameters were used in the search: trypsin as proteolytic enzyme, maximum of two missed cleavages, mass tolerances of 5 ppm on the precursor ion and 0. 02 Da on the MS/MS, fixed modification of cysteine into carboxyamidomethylated cysteine (+57. 0215), and oxidized methionine (+15. 9949) as variable modification.
Statistical Analysis Physiological and biochemical data were analysed using a twoway ANOVA to evaluate the differences between water treatments (WW or SWD), between temperature treatments, and their interaction, followed by a Tukey's test for mean comparisons. For the proteomic data, a two-way ANOVA was used to evaluate the differences between water treatments, between the several temperatures, and their interaction, followed by a Fisher's LSD test for mean comparisons between each condition and the double control (WW at 25/20°C). A 95% confidence level was adopted for all tests, which were performed always independently for each genotype.
DATA AVAILABILITY STATEMENT The mass spectrometry proteomics data have been deposited to the ProteomeXchange Consortium via the PRIDE partner repository with the dataset identifier PXD019474 and DOI: 10. 6019/PXD019474 for C. arabica proteome, and the dataset identifier PXD019541 and DOI: 10. 6019/PXD019541 for C. canephora proteome.
D300N, the Marian group showed using bulk RNA sequencing strategy that an increase of DNA damage response/TP53 pathway was contributing to the pathogenesis of cardiomyopathy associated with EDMD  [51]. All these datasets led to the hypothesis of a model of how abnormalities of A-type lamins and emerin may lead to EDMD  [52]. Using a transcriptomic approach from regenerating skeletal muscle from emerin-deficient mice,  Melcon et al. [34]  have shown delayed myogenic differentiation, which is regulated by Rb and MyoD genes. Since then, small molecules have been used by others to rescue the impaired myogenic differentiation in emerin deficiency, which could represent a potential strategy for improving the muscle wasting phenotype seen in EDMD  [53]. Hence, abnormalities in satellite cell behavior may be responsible in part for the skeletal muscle disease in EDMD.
In this process, bacteria perform a C4 demethylation reaction of lanosterol (a 4a,4bdimethylsterol) with an enzyme classified as a Rieske-type oxygenase belonging to a sterol-C4-demethylation complex Fig. 1. Orthologous groups of sterol-C-methyltransferases in eukaryotes. Orthologous groups were retrieved from the OrthoDB database (Group 661953at2759 at Eukaryota level). The common tree was based on the NCBI taxonomy database using species names. Sterol autotroph organisms with SMT genes (shown in green), versus organisms without SMT genes (shown in purple). Sterol auxotroph organisms with 4-SMT (shown in orange), versus organisms without 4-SMT genes (shown in brown). Organisms that do not produce sterols are shown in black. 4-SMT, sterol-C4a-methyltransferase; SMT1, cycloartenol-C24-methyltransferase; SMT2, 24-methylenesterol-C24-methyltransferase; ERG6, zymosterol-24-methyltransferase.
Stained cells were analyzed by flow cytometry (FACS-Canto II or LSR II-Fortessa, Becton Dickinson, San Jose, CA) and 1-2 × 10 e6 events/sample were routinely acquired. The gating strategies for human and murine thymocytes are shown in Supplementary Figure  1. When indicated, molecules of equivalent soluble fluorochrome (MESF) were evaluated by Quantum MESF beads (Bang Laboratories, Fisher Indiana). Delta geometric mean fluorescence intensity (dGeo MFI) was calculated as the Geometric MFI of specific staining minus the Geometric MFI of the FMO. Data analyses were performed using Diva (BD Biosciences), and FlowJo Mac v. 10. 6. 2 software (Tree Star).
ACKNOWLEDGMENTS We thank all members of our lab for their scientific critique and support and are indebted to  Marc Sitbon ,  Cédric Mongellaz ,  Valérie Dardalhon ,  Sandrina Kinet ,  Jawida Touhami , and  Alfred Singer  for their critical input. We are grateful to  Metafora biosystems  for their support and production of RBD ligands. We thank the  La Timone pediatric cardiothoracic team and Eric Freeman from Children's National Medical Center (CNMC)  for providing thymic tissue samples. The authors thank  Myriam Boyer of Montpellier Rio Imaging  for support in cytometry experiments. We thank  Hongxia Yan ,  Narla Mohandas ,  Keith Kauffman ,  Shunsuke Sakai ,  Daniel Barber , and  Gregoire Altan-Bonnet  for precious support in assisting with reagents during the COVID crisis. AM, MP, VF, UL-S, and MC were supported by fellowships from the  French Ministry of Health, EpiGenMed/ FRM ,  AFM , EpigenMed, and the  Portuguese Foundation for Science and Technology , respectively.
However the whole cohort was not concerned by this issue. Only MVCTs including all PTVs areas were analysed which represents a total of 120 MVCT scans and 30 MVCT images per immobilization device. In routine, the registration between the planning CT and MVCT is performed first using the automatic bone-matching algorithm followed by manual adjustement on the vertebra. For the present study, all the data were processed after the end of the patients treatments using different ROIs as described below.
Data processing The repositioning accuracy of the different IDs was first assessed by calculating the translation vectors for each ID and each registration ROI separately after patient setup on the reference skin markers, using the following formula: T = [Tx 2 +Ty 2 +Tz 2 ] 1/2 Tx, Ty and Tz representing the translation values obtained in the left-right (LR), superoinferior (SI) and antero-posterior (AP) directions, respectively. This enabled us to see if the different shifts were constant or if they were increasing with the treatment duration (thus demonstrating that the ID was not reliable for maintaining reference position during the whole treatment). Furthermore it allowed us to determine which ID minimized local deformation for each ROI. Rotations were thereafter calculated. Residual setup errors resulting from the subtraction of the shifts obtained using a specific ROI for registration and reference matching based on automatic bone registration+manual adjustment were calculated according to the methodology described by van Herk et al.
This work was performed within the framework of the SIRIC LYriCAN Grant INCa-INSERM-DGOS-12563, and the LABEX PRIMES(ANR-11-LABX-0063) of Université de Lyon, within the program Investissements d'Avenir (ANR-11-IDEX-0007) operated by the ANR. We are grateful to Sophie King for her involvement in this work.
Funding This work was supported by  Région Hauts-de France ,  University of Lille  and  Centre National de la Recherche Scientifique  (projet exploratoire premier soutien PEPS),  Inserm ,  CHU of Lille (the Bonus H, PHRC Convergence ),  Dementia in Neurological and Mental Diseases  ( DN2M ), the  Lille FHU- VasCog  project , Fondation Vaincre Alzheimer  and  ANR  MetDePaDi. EC received a research fellowship from  Agence Régionale de Santé Hauts-de-France. MAB received a doctoral scholarship from the  Doctoral School "Biology and Health" of Lille  ( 446 ).
1d  and Supplementary Fig. 1B ). MT samples as seen by  13  C and 31 P ssNMR spectroscopy. To evaluate the sample quality, we first recorded a 2D 13 C-  13  C dipolar-based correlation spectrum using radio frequency-driven recoupling (RFDR)  29  recoupling and compared our data to chemical-shift predictions for MTs (PDB ID: 5SYF) using FAN-DAS 2. 0  30. Overall, the spectrum agreed with in silico estimates (Fig. 2a , left). For example, in Cα-Cβ regions of serine, threonine and alanine residues, signals were observed in qualitative agreement with predictions for α-helical and β-strand conformations (Fig. 2a , right). Interestingly, alanine signals that were not observed (Fig. 2a , top right) resided in random-coil conformation and related to residues in tubulin loops. The latter observation would be consistent with the occurrence of loop motion as discussed elsewhere 7 at the experimental temperature (~298 K) in our dipolar-based experiments.
HiLyte488-and rhodamine-tubulin were purchased from Cytoskeleton Inc. All in vitro experiments were conducted at 30 °C. Data were collected using total internal reflection fluorescence (TIRF) microscopy on an inverted research microscope Nikon Eclipse Ti-E (Nikon) with the perfect focus system (Nikon), equipped with Nikon CFI Apo TIRF 100× 1. 49 N. A. oil objective (Nikon, Tokyo, Japan), Photometrics Evolve 512 EMCCD (Roper Scientific) and Photometrics CoolSNAP HQ2 CCD (Roper Scientific) and controlled with MetaMorph 7. 7 software (Molecular Devices, CA). The microscope was equipped with TIRF-E motorized TIRF illuminator modified by Roper Scientific France/PICT-IBiSA, Institut Curie. For excitation lasers we used 491 nm 100 mW Stradus (Vortran), 561 nm 100 mW Jive (Cobolt) and 642 nm 110 mW Stradus (Vortran).
4. https://github. com/ekatrukha/KymoResliceWide; copy archived at https://github. com/elifesciences-publications/KymoResliceWide). Transmission EM. Taxol-stabilized MTs were prepared with and without MAS spinning as described above. The protein samples were negatively stained with 2% uranyl acetate on glow-discharged carbon coated copper grids. Images were recorded on a Tecnai 20 electron microscope with a LaB6 filament, operating at 200 kV with a BM Eagle 4 K CCD camera (ThermoFisher, Eindhoven, The Netherlands). Images were acquired with a defocus of approximately 5 μm The magnification used at 19,000 × g resulting in an effective pixel size of 1. 14 nm on the specimen level. Preparation of CAMSAP1 CKK N1492A in complex with MTs. [ 13 C,  15  N] labeled MTs were prepared as described above.
Acknowledgements We thank  Gert Folkers  for helpful discussions and  Johan van der Zwan  for technical support. This work was supported by the  Dutch Science Foundation NWO: VENI  grant  722. 016. 002  to  S. X. ,  ALW Open program  grant  824. 15. 017  to A. A. ,  NWO-Groot  (no. 175. 010. 2009. 002 )and  TOP-PUNT  (no. 718. 015. 001 )grant to M. B. and by uNMR-NL, the  National Roadmap Large-Scale NMR Facility of the Netherlands  (grant  184. 032. 207 ). C. J. is supported by the grants  ANR-10-IDEX-0001-02   PSL ,  ANR-11-LBX-0038 ,  FRM DEQ20170336756. S. B. was supported by the  FRM  grant  FDT201805005465 , and  CEFIPRA 5703-1 , and J. A. S. by the  European Union 's  Horizon 2020 Marie Skłodowska-Curie  grant agreement No. 675737 , and the  FRM  grant  FDT201904008210.
4:c. 520-1G>T; NG_008130. 2:g. 8288G>T; Genomic location: 3:132719145 (GRCh38); ClinVar accession number VCV000812666). Allele frequency of this mutation was below the 0. 0001 thresholds for recessive gene according to the Genome Aggregation Database (gnomAD), the largest and most comprehensive public source of genetic information of individuals of different ethnic backgrounds to date. The c. 520-1G>T variant was further validated using PCR and Sanger sequencing of the amplicons, confirming the diagnosis in all affected family members (II:1 and II:3) and the paternal origin of the mutation (Fig. 1 ). We speculated that the c. 520-1G>T of the NPHP3 gene is responsible for either the use of cryptic splice sites or exon skipping. We tested this hypothesis by RT-PCR, using total RNAs from leukocytes obtained from affected and control family members.
2:g. 9528C>G; Genomic location: 3:132717905 (GRCh38); ClinVar accession number VCV000812665) located in the third intron of NPHP3, which was inherited from the mother and segregated with the disease in the expected autosomal recessive mode (Supplementary Table  1 ). These results were confirmed by Sanger sequencing. No variant at the c. 671-996C>G position in NPHP3 was identified in public databases (1000 Genomes, gnomAD, Bravo), providing further support for the hypothesis that it is likely disease-causing. To gain insight into the functional consequences induced by this deep intronic variant, we performed cDNA sequencing. This analysis revealed that the c. 671-996C>G mutation was associated with the insertion of a 163-nucleotide cryptic exon within intron 3 (Genomic location: 3:132717955-132718117 (GRCh38)), located 48 bp downstream of the splice donor site and generating a frameshift as well as a premature stop codon at codon 240 (Fig.
Bioinformatics analysis Data of each sample were mapped to the human reference genome (GRCh37/HG19) using Burrows-Wheeler Aligner software (v0. 7. 17). Variant calling was performed using Genome Analysis Toolkit. Variant quality score recalibration method, which uses machine learning to identify annotation profiles of variants that are likely to be real, was applied to get highconfident variant calls. In order to decrease the noise of sequencing data, data filtering was performed and included (1) removing reads containing sequencing adapter; (2) removing reads whose low-quality base ratio (base quality less than or equal to 5) is >50%; (3) removing reads whose unknown base ratio is >10%. Statistical analysis of the data and downstream bioinformatics analysis were performed on this filtered, high-quality data.
2% of diet). During days 15-28, dogs remained on their placebo or yeast treatments but were rapidly transitioned to a canned diet or high-fiber diet. Fresh fecal samples were collected on days 13, 16, 20, 24, and 27 for measurement of pH, dry matter, calprotectin, immunoglobulin A (IgA), Escherichia coli, and Clostridium perfringens. Blood samples were collected on days 14, 17, and 28 to measure serum lipopolysaccharide-binding protein concentrations. All data were analyzed using the Mixed Models procedure of SAS 9. 4. Fecal pH, dry matter, calprotectin, IgA, and E. coli were not affected (P > 0. 05) by treatment before diet transition. Dogs supplemented with yeast cell wall fraction tended to have higher (P = 0. 06) fecal C. perfringens counts than the controls. After diet transition, most parameters were not altered (P > 0.
Statistical Analysis For the baseline samples, data were analyzed using the Mixed Models procedure of SAS (version 9. 4; SAS Institute, Cary, NC, United States) to test the main effect of treatment, with treatment as a fixed effect and dog as a random effect. For post-diet transition samples, data were expressed as change from baseline and analyzed using the Mixed Models procedure of SAS (version 9. 4; SAS Institute, Cary, NC, United States) as repeated measures. The main effects of treatment, diet and time as well as interactions of diet and treatment, diet and time, and treatment and time were tested, with dog as a random effect. Data are reported as means ± standard error of the mean (SEM) with statistical significance set as P ≤ 0. 05 and trends set as 0. 05 < P ≤ 0. 10.
Colorectal cancer GWAS data We obtained SNP estimates from the most comprehensive GWAS of CRC to date  [26] , including 58,221 cases and 67,694 controls (sexes combined) from 45 studies within 3 consortia: Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), Colorectal Cancer Transdisciplinary Study (CORECT), and Colon Cancer Family Registry (CCFR). Across these studies, there were 28,207 CRC cases and 22,204 controls among men, and 24,568 CRC cases and 23,736 controls among women. Cases were diagnosed by a physician and recorded overall and by site (colon, proximal colon, distal colon, rectum). Approximately 92% of the participants were White-European (~8% were East Asian). Case distributions are outlined in Additional file 1: Table  S3 ; other study characteristics are detailed elsewhere  [26].
Statistical approach First, we examined the associations of BMI and WHR with overall and site-specific CRC using SNP estimates from sex-combined GWAS of exposures as well as outcomes. We then examined the associations of BMI and WHR with overall CRC based on SNP estimates from sex-specific GWAS of exposure as well as outcome (sexspecific GWAS were not available and thus not used for site-specific CRC). Summary statistics were harmonized using the harmonise_data function within the TwoSam-pleMR R package  [36]. All GWAS were assumed to be coded on the forward strand, and harmonization was confirmed as consistent using option 2 of the "action" argument. As sensitivity analyses, up to four MR methods were used to generate effect estimates using the TwoSampleMR R package  [36]  which make differing pleiotropy assumptions (detailed in Fig.
Adiposity was measured indirectly using BMI and WHR because these correlate highly with more objectively measured fat indexes  [50, 51]  and allow much larger GWAS sample sizes than otherwise possible (comparably strong GWAS were unavailable for waist circumference). UK Biobank data are included within GWAS for both the exposure and outcome used for MR estimates of adiposity for CRC risk. Sample overlap in a two-sample MR setting is reported to contribute to weak instrument bias and inflated type one error rates, resulting in MR estimates that are biased towards confounding-prone observational estimates  [71]. However, given that the proportion of sample overlap is presently low (< 5%) and estimated Fstatistics are relatively high (each > 70 for adiposity traits), we do not expect considerable bias here.