dataesr/scientific-paragraphs-categorization huggingface dataset:
5 µm were carried out. The local orientation data of the α-laths were used to calculate the average misorientation of neighboring α within an 11 × 11 kernel to produce LAM maps in Channel 5 software (version 5. 0). A calibration method was used to convert LAM maps into a strain that is explained in detail elsewhere  [39]. It is important to highlight that the maximum strain that can be determined by this method is 12% and the minimum is approximately 4%, due to the saturation and noise of the method, respectively. The strain field maps were captured in regions similar to the one represented in Figure  4b , and the captured areas varied depending on the geometry of the bead and MHP parameters. As the step size is smaller, the scanning time is significantly increased and consequently the map size is limited to more localized measurements.
Acknowledgments: The authors would like to thank several staff members of  ECOROLL AG  for providing the ECOpeen-C MHP tool and for the operational support, and to  Flemming Nielsen ,  Nisar Shah , and  Steve Pope  for the technical support throughout the experiments carried at the  WAMC and metallurgy laboratory of Cranfield University. Furthermore, the intellectual support by  Filomeno Martina ,  Jan Hönnige , and  Jialuo Ding  was greatly appreciated.
Each experiment was performed using a CytoFLEX LX cytometer (Beckman Coulter, Brea, CA, USA), and the obtained data were then analyzed with the CytExpert software (Beckman Coulter). For flow cytometry analysis of adult mice, dissected hearts were minced into small fragments, washed in PBS, and dissociated in a 0. 5 mg/mL Liberase TM solution in PBS (Sigma, 5401127001) at 37 • C for 7 min in agitation. The digestion was stopped with four volumes of cold 10% fetal bovine serum in PBS. The dissociated cells were centrifuged, resuspended in cytometry buffer (PBS plus 2% fetal bovine serum and 10 mM HEPES), and filtered through a 70 µm nylon mesh. Then, cells were incubated on ice in the dark with the fluorochrome-conjugated antibodies and DAPI (Sigma, D9542). Cardiomyocytes were identified using a mitochondrial staining reagent (MitoTracker Deep Red, Thermo Scientific, M22426)  [17].
We incubated the cell suspension, previously stained with anti-CD31, in the MitoTracker solution (100 nM in cytometry buffer) at 37 • C for 30 min. Another mitochondrial marker, TMRE, was also used to assess changes in the mitochondrial membrane potential  [18]. Cardiac cell suspensions previously stained with anti-CD31 were incubated with TMRE (100 nM in cytometry buffer) for 30 min at 37 • C in the dark before analysis. Analytical flow cytometry was performed in an FACS Verse flow cytometer. Data were analyzed with Kaluza Analysis software (version 2. 1) and are displayed in tables as mean ± standard error of mean. Negative controls (Cre-negative littermates) and isotypic antibodies allowed setting of the gates. Details of the antibodies used for flow cytometry are provided in Supplementary Table  S3.
Electrocardiography (ECG) The anesthesia used to perform the ECGs was ketamine (64 µg/g body weight)/xylazine (10 µg/g) in PBS (i. p. ). After 15 min, electrocardiograms were obtained from mice using BioAmp PowerLab 8/35 (AD Instruments, Dunedin, New Zealand) for the data acquisition. The negative electrode and positive electrode were placed in the upper right and lower left limbs, respectively. The neutral pole was placed in the lower right limb. We analyzed a section of the ECG for 1 min and we used the ECG module of the LabChart 8. 0 software and the preset mouse settings. The number of analyzed mice is detailed in Tables  1  and 3.
2 kV ion spray voltage; 320 • C ion capillary temperature; 350-1500 mass scan range for full MS and 350-1500 scan range for MS/MS; MS resolution 120,000 for full MS and 30,000 for data-dependent MS/MS; collision energy 32 with high-energy collisional dissociation mode; MS/MS isolation window 0. 7 m/z; and dynamic exclusion 20 s. The peptides and proteins were identified and quantified using Proteome Discoverer TM 2. 4 (Thermo Fisher Scientific) platform and SwissProt Mus musculus protein database ver-sion 2017. 10. 25 (25,097 sequences). The search parameters were set as follows: two missed tryptic cleavage sites were allowed; full MS and MS/MS tolerances were 10 ppm and 0. 02 Da, respectively; fixed modification of carbamidomethylation on Cys, variable modification of oxidation on Met, and N-terminal acetylation on protein were specified; proteins required a minimum of two peptides.
Proteomic Analysis Shows Alterations in Cardiomyocyte Metabolism after Conditional Deletion of Wt1 To further characterize the cellular phenotype of WT1-deficient cardiomyocytes, we performed proteomics assays one month after tamoxifen administration. The results were analyzed following two different approaches using the WebGestalt platform (http: //www. webgestalt. org/ accessed on 21 April 2023). On one hand, over-representation analysis (ORA) was performed on a list of 130 proteins (17 downregulated, 113 upregulated) with an abundance ratio <0. 9 or >1. 1 and a p-value < 0. 05. On the other hand, the whole list of 826 proteins with a high protein FDR confidence level and a minimum of two peptides identified was analyzed with a gene set enrichment analysis method (GSEA). According to ORA analysis (using the KEGG pathway database), biological processes significantly over-represented in the 130 proteins selected mainly included metabolic pathways, including amino acid degradation, glutathione metabolism, and oxidative phosphorylation.
and R. C. All authors have read and agreed to the published version of the manuscript. Funding: This work was funded by the Spanish Ministry of Economy, Industry and Competitivity (BFU2017-83907-P) to R. M. -C. and R. C. , Consejería de Salud, Junta de Andalucía (PC0066-2017/PC-0081-2017) to R. C. , Instituto de Salud Carlos III-TERCEL network (RD16/0011/0030) to R. M. -C. , R. C. , Consejería de Economía y Conocimiento, Junta de Andalucía (UMA18-FEDERJA-146) to R. M. -C. and R. C. European Commission H2020 program grant (SC1-BHC-07-2019. Ref. 874764 "REANIMA") to M. T. , Spanish Ministerio de Ciencia e Innovación grant (PGC2018-096486-B-I00) to M. T, the Fondation pour la Recherche Medicale, grant number FRM DPC20170139474 (K. -D. W. ); the Fondation ARC pour la recherche sur le cancer, grant number n • PJA 20161204650 (N.
-D. W. , R. M. -C. and R. C. All authors have read and agreed to the published version of the manuscript. Funding: This work was funded by the Spanish Ministry of Economy, Industry and Competitivity (BFU2017-83907-P) to R. M. -C. and R. C. , Consejería de Salud, Junta de Andalucía (PC0066-2017/PC-0081-2017) to R. C. , Instituto de Salud Carlos III-TERCEL network (RD16/0011/0030) to R. M. -C. , R. C. , Consejería de Economía y Conocimiento, Junta de Andalucía (UMA18-FEDERJA-146) to R. M. -C. and R. C. European Commission H2020 program grant (SC1-BHC-07-2019. Ref. 874764 "REANIMA") to M. T. , Spanish Ministerio de Ciencia e Innovación grant (PGC2018-096486-B-I00) to M. T, the Fondation pour la Recherche Medicale, grant number FRM DPC20170139474 (K. -D. W. ); the Fondation ARC pour la recherche sur le cancer, grant number n • PJA 20161204650 (N.
On the contrary, CD123-IgG1 + was completely inactive on OCI-AML2, OCI-AML3, THP-1 and SKM-1 CD64-positive cell lines, and showed limited activity on NB-4 and MV4-11 compared to the NKCE that was significantly highly superior to CD123-IgG1 + (Extended Data Fig. 1c , P < 0. 0001), confirming with AML cell lines the results observed on primary AML samples. An autologous NK cell activation assay performed with additional samples from patients with AML, two CD64-positive (AML nos. 8 and 9) and one CD64-negative (AML no. 10) (Extended Data Fig. 2a, b ), further confirmed that, unlike CD123-IgG1 + , which was active only against the CD64-negative sample (AML no. 10), CD123-NKCE mediated the autologous activation of NK cells from the three patients against their own blasts regardless of CD64 expression (Extended Data Fig.
Article https://doi. org/10. 1038/s41587-022-01626-2 We evaluated the pharmacokinetic/pharmacodynamics of CD123-NKCE administered by a single 1-hour i. v. infusion of a high (3 mg kg -1 ) or low (3 and 0. 5 µg kg -1 ) doses in male cynomolgus monkeys (two animals each for the 3 mg kg -1 and 3 µg kg -1 doses and one animal for the 0. 5 µg kg -1 dose). Treatment with CD123-NKCE promoted a sustained and complete depletion of CD123 + cells in the blood of all monkeys, for more than 10 days, at both the 3 mg kg -1 and 3 µg kg -1 doses (Fig. 6a, b ), with only very small amounts (<50 pg ml -1 ) of the proinflammatory cytokines IL-6 and IL-10 released (Fig. 6c  and Extended Data Fig. 3a ) without any associated clinical signs. A transient and partial depletion of CD123 + cells was observed in the monkey treated at the lowest dose (0.
The capture surface was regenerated with regeneration solution (3 mol l -1 MgCl 2 ) at a flow rate of 30 µl min -1 for 60 s. The data were evaluated with Biacore T200 Evaluation Software v. 3. 0 (Cytiva) using a 1:1 binding model with a mass transport limitation. For FcR binding studies, CD123-NKCE molecules and control human IgG1 antibodies were immobilized (at about 700 RU) onto the dextran layer of a CM5 Series S sensor chip on flow cells 2 and 3 by amine coupling chemistry. Flow cell 1 activated with NHS/EDC alone and deactivated with ethanolamine served as a reference flow cell for online blank subtraction. For all experiments other than the FcRn binding study, HBS-EP + 1× was used as the running buffer. For the FcRn binding study, acetate buffer pH 5. 6 replaced HBS-EP +. Serial dilutions of FcRn and FcγRs were sequentially injected over a period of 2 min, at a constant flow rate of 40 µl min -1 over the CM5 chip and allowed to dissociate for 10 min before regeneration (10 s of 10 mM NaOH 500 mM NaCl and 10 s of HBS-EP + at a constant flow rate of 40 µl min -1 for FcγRs and FcRn, respectively).
CalceinAM released by dead target cells was determined by measuring the number of relative fluorescence units (RFU) with a luminometer (EnSpire Multimode Plate Reader, Perkin Elmer; excitation at λ = 495 nm and emission at λ = 516 nm). The percentage specific lysis was calculated with the following formula: Specific lysis (%) = (ER (cpm or RFU) - SR (cpm or RFU))/(MR (cpm or RFU) - SR (cpm or RFU)) × 100 where ER = experimental release, SR = spontaneous release and MR = maximal release. EC 50 were determined by fitting the data with nonlinear regression curve model (log(agonist) versus response-variable slope (four parameters)) with GraphPad Prism Software v. 8. 0. 2.
NK cell degranulation assay with AML samples Tested items and PBMCs from patients with AML were added to each well of round-bottomed 96-well plates. After overnight coincubation with the NKCE molecules or antibodies, antihuman CD107a and CD107b antibodies (Miltenyi, 130-111-621 and 130-118-818) were added for 4 h. Cells were then washed and stained with the following mixture: viability markers, anti-CD45 (Miltenyi, 130-110-771), anti-CD33 (BD Biosciences, 564588), anti-CD56 (BD Biosciences, 557747) and anti-CD3 (BD Biosciences, 740187) antibodies. Cells were then washed, fixed and analyzed by flow cytometry. The data obtained were analyzed with Flowjo Software to assess NK cell degranulation by monitoring the expression of CD107a/b on NK cells identified as living CD45 + CD33 -CD56 + CD3 -cells.
An intracellular staining was performed for IFN-γ (Biolegend, 502536), TNF-α (BD Biosciences, 563996) and MIP-1β (BD Biosciences, 550078). Cells were analyzed by flow cytometry (Supplementary Fig. 3 ). Parameters were recorded with BD FACSDiva v. 8. 0 software and the analyses were done with FlowJo v10. 5. 2 software. Analysis of the percentage of NK cell activation was done with GraphPad prism v. 8. 0. 2.
A mixture of PBMC subset-specific antibodies and the viability reagent were added to the PBMC suspension according to the supplier's instructions. As a fluorescence minus one control, additional points were obtained by labeling PBMC with the same mixture, but with each labeling antibody replaced in turn by its corresponding isotype control. Cells and antibody mixtures were incubated for 1 h at 4 °C in the dark, and then washed twice with 200 µl of staining buffer by centrifugation at 300g for 5 min at 4 °C. Cells were analyzed with a MACSQuant Analyzer from Miltenyi Biotec. Raw data were analyzed with VenturiOne v. 6. 1 software (Applied Cytometry Inc. ). The gating strategy can be found in Supplementary Fig. 4. For MSD assay, cell supernatant was diluted in MSD buffer following the manufacturer's instructions.
Diluted samples or prediluted multi-analyte calibrator samples were added to the precoated plate supplied in the kit. A solution of detection antibodies conjugated to electrochemiluminescent labels (MSD SULFO-TAG) was added and the plates were incubated at room temperature for 2 h before measurements. Data were analyzed with Excel 2019 software. The concentrations of IL-6, IL-1β, IFN-γ and TNF-α were determined from electrochemiluminescent signals by back-fitting to a calibration curve established with a four-parameter logistic model with 1/Y2 weighting.
Quantification and statistical analysis Detailed information concerning the statistical methods used is provided in the figure legends. Statistical analyses were performed with GraphPad Prism software v. 8. 0. 2, and v. 8. 3. 0. Kaplan-Meier methods were used for survival analysis. When sample size was sufficiently large, the normality of populations was assessed with the d'Agostino-Pearson omnibus normality test. If the data were not normally distributed, the statistical significance of differences between paired sample populations was determined with the two-sided Wilcoxon matched-pair signed rank test.
Acknowledgements We thank  A. Tang ,  L. Bassinet  and  V. Boisrobert-Dheilly  for performing some cellular studies,  L. -M. Meyer  et  Ravi Rangara  for animal pharmacological studies,  F. Windenberger  for the statistical analyses, and all members of  Sanofi Immuno-Oncology Research, Pharmacology ,  Drug Metabolism  and  Pharmaco-Kinetics, Preclinical Safety, Biomarker and Clinical Bioanalysis, Large Molecule Research  and  Chemistry Manufacturing  and Control teams who contributed to this project. We thank  M. Seillier  and  L. Pouyet  ( MI-mabs, Marseille France ) for performing some cellular and animal studies. We thank  C. Naussac  for her help in the coordination of the collaborative work. The study was performed and supported by two private companies, namely  Sanofi and Innate Pharma , without the help of any funder or grant.
Data availability All data supporting the results are available in the main text or the supplementary materials. The detailed molecular organization and the sequences of the NKCE used in the present study can be found in Supplementary Figs. 1  and 2 , and in patents WO2016207273 and WO2022144836A1. Recombinant proteins were built from sequences found at https://www. ncbi. nlm. nih. gov.
Design, population and data linkage We conducted a European, population-based linked cohort study. The full cohort included all live births with a major CA collected and validated by population-based CA registries which are members of EUROCAT (https://eu-rd-platform. jrc. ec. europa. eu/eurocat_en). Each registry has ethics permissions and procedures for routine surveillance, data collection and transmission of anonymised individual-level data to a central database according to national guidelines. For the EUROlinkCAT study, local ethics approvals or other permissions to link registry data with local mortality data sources were obtained by 12 registries, one registry (Norway) obtained permission to use data that were already linked. Data on all children with a major CA born alive between 1 st January 1995 and 31 st December 2014 recorded in the 13 registries in nine Western European countries were linked to administrative mortality data sources up to the child's 10 th birthday or to 31 st December 2015, whichever was earlier, so that all children have at least one year of follow-up information.
Statistical analysis The study included the development of a common data model to standardise the local variables available in the national/vital statistics or mortality databases (https://www. eurolinkcat. eu/wp2-  18 This formed the basis for the development of centrally written syntax scripts used for checking the data linkage quality and for the local analyses to be run by the participating registries. 18, 19 ch registry calculated the survival probability of children with T13 and T18 at pre-specified ages by running Kaplan-Meier survival analysis on the individual case data to account for censoring, as not all children reached their 10 th birthday during the study period. The registry specific Kaplan-Meier survival estimates with 95% confidence intervals (CIs) (all 13 registries), the number at risk (alive at the beginning of each age point), and the number of deaths at each age (all registries, except Netherlands: Northern) were then uploaded to the Central Results Repository at Ulster University (UK) using a secure web platform.
The Netherlands: Northern registry rounded the number of deaths to the nearest 0 or 5 after age 4 weeks due to the national small number restrictions, therefore their data could not be included in the meta-analysis. https://mc. manuscriptcentral. com/adc Archives of Disease in Childhood C o n f i d e n t i a l : F o r R e v i e w O n l y 7 buildingresultsrepository/eurolinkcatpubliccommondatamodels). No individual case data were shared. The registry-based Kaplan-Meier survival estimates were combined centrally in randomeffects meta-analyses of the survival at five ages (1 week, 4 weeks and 1, 5 and 10 years) to estimate the overall survival of children with T13 and T18. The meta-analytic approach applied to these data involved modifying a method proposed by Combescure et al. 20  and is described in detail elsewhere  9  and in Supplemental Box 1.
§Because of the lower linkage success in the earlier years (see Loane et al, 2022 1 ), only birth years with linkage success over 85% for all years were included (i. e. over 95% from 2003 for East Midlands and South Yorkshire, from 2006 for Thames Valley and from 2009 for Emilia Romagna, over 90% from 2006 for Wessex -see Loane et al, 2022 1 ). **The success of registries linking to mortality records only cannot be estimated in a similar way as to vital statistics (see further information in Loane et al, 2022 1 ). MR -registry linked to mortality record database; VS -registry linked to national/vital statistics data; NA -not applicable as linkage was performed with the mortality database only. Given JE, Tan J, et al. Linking a European cohort of children born with congenital anomalies to vital statistics and mortality records: A EUROlinkCAT study.
ACKNOWLEDGEMENTS We are very grateful to the whole EUROlinkCAT Working Group for their contribution to the project (data linkage and standardisation, running syntax scripts):  Dr Joanne Given  ( Ulster University, Belfast, United Kingdom );  Drs L. Renée Lutke  and  Nicole Siemensma-Mühlenberg  ( University Medical Center Groningen, Groningen, The Netherlands );  Dr Oscar Zurriaga ,  Sandra Moreno Marro ,  Laia Barrachina Bonet  and  Laura García Villodre  (Foundation for the  Promotion of Health and Biomedical Research in the Valencian Region, Valencia, Spain );  Dr Sonja Kiuru-Kuhlefelt ,  Anna Heino  and  Tuuli Puroharju  ( THL Finnish Institute for Health and Welfare. Helsinki, Finland );  Drs Alessio Coi  and  Michele Santoro  ( Institute of Clinical Physiology, National Research Council, Pisa, Italy ); ; Drs Gianni Astolfi ,  Aurora Puccini, Annarita Armaroli (Center for Clinical and Epidemiological Research, University of Ferrara, Ferrara, Italy );  Nathalie Bertille  and  Dr Babak Khoshnood  ( INSERM, Paris, France );  Professor Sue Jordan  ( Swansea University, Swansea, Wales, United Kingdom );  Professor Elizabeth Draper  ( University of Leicester, Leicester, United Kingdom ) and  Professor Jenny Kurinczuk  ( University of Oxford, Oxford, United Kingdom ).
Detailed description of the meta-analytic approach used to combine the registry-specific survival data produced by Kaplan-Meier survival analysis run by registries participating in the EUROlinkCAT study (adopted from Glinianaia et al, 20221 ) Page 31 of 32 Archives of Disease in Childhood C o n f i d e n t i a l : F o r R e v i e w O n l y https://mc. manuscriptcentral. com/adc 4 Supplemental Box 1.
Rotational analysis Experimental assignments have been performed using the PGOPHER soware by exploiting Loomis-Wood diagrams. 54 PGOPHER was also used for spectral simulations. The SPFIT/SPCAT suite of programs  55  was used to adjust the rotational constants of all three species using a Watson A-reduced Hamiltonian in the I r representation. For NBD, literature pure rotation data 31 (25 transitions) and ground-state combination differences (GSCD) from rovibrational data  33  (369 GSCD/196 wavenumbers) were tted together allowing for efficient searches at millimetre wavelengths. Both datasets were weighted according to their expected accuracy, i. e. , 1 kHz for data from Vogelsanger and Bauder 31 and 0. 0001 cm -1 to 0. 0003 cm -1 (∼3-9 MHz) for GCSD from Sams and Blake. 33 GCSD are provided in MHz in ref.
33 but we favoured here wavenumber units in order to access individual root mean square values for the two datasets, as conventionally done using SPFIT. To reproduce these datasets at their experimental accuracy, all three rotational constants and ve quartic centrifugal distortion parameters were adjusted. The resulting parameters are reported in Table  1  and are in excellent agreement with those reported by Sams and Blake. 33 The only difference is that we chose not to adjust the sextic centrifugal distortion parameter h K in favour of a more constrained t. All parameters are also in excellent agreement with those predicted from the calculations performed in this study. Using these reliable constants, spectroscopic assignments of the millimetre-wave spectrum of NBD were straightforward, with no notable divergence of the prediction.
Acknowledgements The work at ISMO was performed using HPC resources from the  "Mésocentre" computing center of CentraleSupélec and École Normale Supérieure Paris-Saclay  supported by  CNRS  and  Région Île-de-France  (https:// mesocentre. centralesupelec. fr/). It has also been supported by the  Région Ilede-France , through DIM-ACAV+, from the  Agence Nationale de la Recherche  ( ANR-19-CE30-0017-01 ), and from the  Programme National "Physique et Chimie du Milieu Interstellaire" (PCMI)  of  CNRS/INSU  with  INC/INP  co-funded by  CEA  and  CNES. The work at Chalmers was funded by the  European Research Council (ERC)  under grant agreement  CoG ,  PHOTHERM -101002131 , the  Catalan Institute of Advanced Studies (ICREA) , and the  European Union 's  Horizon 2020 Framework Programme  under grant agreement no.
Finally, the MIRI F2100W and Spitzer/MIPS 24 μm images, which capture flux from the warm dust continuum, are shown for both galaxies. Here, although the relative increase in the angular resolution is similar to that for the previous two sets of images, the improvement in the fidelity of the JWST data is the most dramatic, as the MIPS 24 μm PSF was only 6″, and the majority of emission appeared diffuse. With the MIRI F2100W PSF of 0 67 (30 pc at NGC 628 and 60 pc at NGC 7496), the dust emission is resolved into compact sources, mostly along the spiral arms, and shows the same intricate ISM structure seen in the MIRI F770W image. In terms of surface brightness, the Spitzer images achieve slightly better sensitivities than the JWST data, as might be expected. The NGC 628 images from the Spitzer SINGS program  (Kennicutt, Jr.