dataesr/scientific-paragraphs-categorization huggingface dataset:
Note that recent literature suggests that in some contexts beta bursts can be of much shorter duration than seen in our dataset (e. g. Feingold et al. 2015; Sherman et al. 2016; Lundqvist et al 2016). Since our 300ms windows were aligned to the task timing, i. e. signal occurrences, and beta bursts do not have a fixed temporal relationship with such external events, some windows will overlap with a beta burst, while others will fall in a period with low beta amplitude, and some will partly overlap with a beta burst. Secondly, window duration of 300ms was considered to be a minimal duration needed for meaningful (non-zero) spike counts in a majority of individual windows. However, we additionally restricted our analysis to the subsets of beta-neuron pairs for which the average firing rate of the neuron, across all 300ms windows, was above 3 Hz.
Correlations with p<0. 01 were considered significant, but the complete distributions of rho values across the populations of beta-neuron pairs are always presented, to allow appreciating the magnitude of the different types of correlations. The analysis approach just described resembles as closely as possible for our dataset the approach used by  Canolty et al. (2012). They concatenated LFP and spike data across several recording sessions from implanted multi-electrode arrays, providing between 58-410 minutes of continuous data, including all task epochs. However, in our dataset, there were on average more than twice as many windows available for this task-related correlation analysis approach compared to the number of trials available for the trial-by-trial correlation analysis described in the next section (averages of 117 trials in both short and long for monkey T and 93 and 90 trials in short and long, respectively, for monkey M; see above).
This analysis is more closely comparable to the analysis performed by  Rule et al. (2017) , in which they restricted their analysis to delays considered to entail steady-state movement preparation. However they compared epochs inside and outside of beta bursts, thus at varying moments in their 1 second duration delays considered. As we already described for the current dataset, the neuronal spike rates modulated significantly from the start to the end of the delay (D1) preceding SC, some neurons systematically increasing and others decreasing their rate between TC and SC  (Confais et al. 2012). Thus, in our case, this delay cannot be considered as steady-state in its entirety. To avoid these systematic, task-related modulations in neuronal firing rates influencing our analysis, the window was restricted to the final 300ms prior to the pre-indicated moment of SC onset.
As for the task-related correlation analysis, the analysis included only the subsets of beta-neuron pairs for which the average firing rate of the neuron in the pre-SC epoch was above 3 Hz. The LFPs were filtered to capture the main beta frequency band(s) for each animal as described above. The average beta amplitude (Hilbert envelope) and the spike counts in each trial in this 300ms epoch for analysis (providing one value per signal type per trial window) were then correlated across trials. The trial-by-trial correlation for each betaneuron pair was then quantified as the Spearman's rank order correlation (see example in Figure  2D ; results across all datasets in Table  1  and Figure  3C ), as described above for the task-related correlation analysis. ---Figure  2  near here ---.
Beta phase was extracted from the Hilbert transformation of the beta-filtered LFP, and the phase at each spike time was determined. To quantify the phase locking, we first used Rayleigh's test of non-uniformity of circular data (CircStat Matlab toolbox; Berens 2009). To determine whether the locking was significant for individual neurons, a trial-shuffling method was used. Beta oscillations are typically not phase-reset by external events (but see  Reimer and Hatsopoulos 2010) , and the analyzed pre-SC epoch was sufficiently long after the previous external event (0. 4-1. 7s after TC off), such that any phase-resetting effects should have minimal effect in this epoch. This makes trial-shuffling an efficient method for obtaining a 'baseline' measure of phase locking, destroying the temporal relationship between the two signals, while preserving their individual properties such as rhythmicity.
These examples are representative when it comes to the average beta power and frequency across task epochs in these datasets, as we already described in detail in  Kilavik et al. (2012). Notably monkey T had one dominant beta band, which varied in average frequency between 19-25Hz across task epochs. Monkey M had two dominant beta bands, a low band modulating between 17-21Hz and a high band modulating between 29-34Hz  (Kilavik et al. 2012). For both monkeys and both bands, beta power decreased after SC and during movement execution after GO. Note that even if these trial-averaged spectrograms suggest a prolonged increase in beta amplitude during the delays, as can be seen in the example LFP in Figure  2B  in reality beta oscillations occur in individual bursts of different duration, amplitude and exact timing across trials (see also  Feingold et al.
Trial-by-trial correlations between LFP beta amplitude and neuronal spike counts are rare Figure  2D  shows that in the selected example beta-neuron pair, LFP beta amplitude and neuronal spike count did not correlate trial-by-trial in the pre-SC epoch. This was indeed representative of the populations. Only 3. 4-5. 6% of the pairs had a significant correlation (across both monkeys and bands, short and long delay trials), with similar proportions of negative and positive correlations (see Table  1 ). Figure  3C  shows the distributions of Spearman's rho values for the pre-SC trial-by-trial correlation analysis in short delay trials for the three datasets. The distributions were narrower than for the task-related correlations, and only significantly shifted away from zero for the low beta band in Monkey M in short delay trials, not in long delay trials.
In monkey M, only 2. 0% in short delay trials and 2. 7% in long delay trials of the neurons locked significantly their spikes to both the low and the high bands in this task epoch, such that overall 21. 3% in short delay trials and 19. 6% in long delay trials of the neurons locked their spikes to either the low, high or both LFP beta bands in this monkey. The clear phase-locking found for many neurons in this dataset made us conclude that the observed LFP beta bands were at least partly locally generated, justifying the correlation analyses between beta amplitude and neuronal firing rate. Finally, there was no systematic difference in locking prevalence of the few neurons with, compared to without, a significant trial-by-trial correlation of spike count with beta amplitude in the pre-SC task epoch.
Reconciling these findings -no intrinsic relationship beyond co-modulations driven by task events A direct comparison of the two recent studies  (Canolty et al. 2012; Rule et al. 2017)  suggests that their discrepant conclusions might be due to different analysis approaches, either including data from all trial epochs, or restricting their analysis to steady-state preparatory periods, respectively. The two ways in which the data were analyzed in this study, quantifying both task-related and trial-by-trial correlations in the same dataset, resemble the approaches used by  Canolty et al. (2012)  and  Rule et al. (2017) , respectively. Indeed, we confirm the results of  Canolty et al. (2012)  when including many different task epochs, and we confirm the results of  Rule et al. (2017)  when restricting our analysis to a fixed pre-cue epoch, using data across trials.
Phase-locking of spikes to LFP beta oscillations The lack of an intrinsic relationship between LFP beta amplitude and neuronal activation level (rate) does not exclude other relationships between beta oscillations and neuronal spiking activity. Indeed, as we demonstrate in this dataset, confirming several previous studies  (Murthy and Fetz 1996; Donoghue et al. 1998; Baker et al. 1999; Denker et al. 2011; Canolty et al. 2012; Engelhard et al. 2013; Riehle et al. 2018)  there is significant locking of spike times to LFP beta oscillation phase for many neurons in motor cortex. Such phase locking may result in rhythmic synchronization among populations of neurons thereby increasing their concerted impact on post-synaptic targets without necessary increasing their spike rates  (Destexhe and Paré 1999; Azouz and Gray 2000).
This work was supported by the  Agence Nationale de la Recherche  [grant number  ANR-NEUR-05-045-1 ];  Ministère de l'enseignement supérieur et de la recherche  (PhD grant to J. C. ). The authors wish to thank  Adrian Ponce-Alvarez  for participating in animal training and data recording;  Ivan Balansard  and  Marc Martin  for animal care; and  Joel Baurberg ,  Alain De Moya , and  Xavier Degiovanni  for technical assistance. The current address of JC is Cynbiose, 69280  Marcy l'Étoile, France.
BRN2 loss or low expression correlates with reduced survival and worse prognosis. Although BRN2 has been implicated in melanoma invasiveness, and its expression is highly regulated, whether and how it may contribute to melanoma initiation or incidence is not understood. To evaluate the prevalence of BRN2 loss in human skin cutaneous melanoma (SKCM), we retrieved copy-number alteration (CNA) data for BRN2 in SKCM metastases (stage IV) from the Cancer Genome Atlas (TCGA, https://cancergenome. nih. gov/). The BRN2 locus showed mono-allelic loss in 53% and bi-allelic loss in 2. 7% of all patient samples (n = 367, Figure  1A ). Only a minority (n = 29 of 367, corresponding to 7. 9%) of SKCM samples showed a copy-number gain (n = 27)/amplification (n = 2) for BRN2. We did not further analyze these samples since the expression of BRN2 was slightly increased but not statistically different (p=0.
1C , Supplementary Data 2). From the TCGA, patients carrying the monoallelic loss of BRN2 in metastases displayed a trend to have a shorter overall survival than those with diploid status (Figure  1C ). These results were validated using an independent cohort of 118 regional metastases previously described  31  (Figure  1D ). Moreover, we evaluated the number of BRN2 alleles in nevi and melanoma that arose from these nevi using publically available data  32. It appears that 28% (5 out of 18) or 22% (4 out of 18) of melanomas presented either a mono-allelic loss or a gain of BRN2 respectively compared to nevi (Supplementary Fig. 1D ). The situation is clearly complex, but we may conclude that BRN2 mono-allelic loss can occur during the early steps of melanomagenesis. We next assessed the correlation between BRN2 mRNA levels and overall patient survival to evaluate the effect of BRN2 mono-allelic loss on melanoma progression.
We established "BRN2-high" and "BRN2-low" patient groups based on RNA-seq data available from the TCGA (BRN2 subgroups defined as BRN2-low (≤ 1 transcript per million reads [TPM]) and BRN2 expressed/high [> 1 TPM]). Patients in the "BRN2-low" group displayed significantly shorter overall survival than those of the "BRN2-high" group (Figure  1E ). Overall, the BRN2 locus, frequently associated with a large segmental deletion, is lost (mono-and bi-allelic) in ≈60% of human SKCM metastases and correlates with significantly reduced overall survival. Since CCNC, ROS1 and ARID1B loci are distal to BRN2 on chromosome 6, and are known to be involved in melanomagenesis, we evaluated the overall survival of these patients according to the presence and the level of mRNA expression of the corresponding genes.
Co-occurrence of BRN2 loss with mono-allelic loss of PTEN We next determined whether BRN2 loss co-occurs with melanoma driver mutations by examining the TCGA CNA-data set and human melanoma cell-line panel. There was no significant correlation between BRAF or NRAS mutation and BRN2 loss (mono-or bi-allelic), neither in human melanoma samples nor the human cell-line panel (Supplementary Fig. 2A, B ). We then searched for co-occurring CNAs of other known melanoma-associated genes and found that mono-allelic loss of BRN2 cooccurred with mono-allelic loss of PTEN in approximately 40% of the human melanoma samples in TCGA and in the human cell-line panel (Supplementary Fig. 2C, D ). We next evaluated the concomitant BRN2 locus alterations, BRAF/NRAS mutations, and CDKN2A/PTEN alterations and found the most frequent genetic constellation that co-occurs with BRN2 loss in melanoma to be BRAF V600X mutation together with mono-allelic PTEN loss (Supplementary Fig.
To get a better understanding of melanomagenesis in the various Brn2-WT/het/hom situations, we performed a transcriptomic analysis of the various Brn2 tumors and cell lines (Supplementary Data 3 and 4). The ontology enrichment analysis indicated that the Braf-Pten-Brn2-het tumors were more inflamed than the Braf-Pten-Brn2-WT tumors with increased neutrophil-associated gene expression (Supplementary Fig. 5A ). It also suggests that the extracellular-matrix was actively remodeled and that these Braf-Pten-Brn2-het tumors were more subject to angiogenesis (Supplementary Fig. 5A ). Pathway enrichment analysis supported these results as inflammatory gene expression signatures are enriched from both the WikiPathways and KEGG databases (Supplementary Fig. 5B, C ). Significantly, the PI3K/AKT pathway was enriched in the Braf-Pten-Brn2-het tumors compared to the Braf-Pten-Brn2-WT in both WikiPathways and KEGG databases (Supplementary Fig.
TCGA data All TCGA data for somatic mutations, copy number alterations (CNAs), RNA-seq gene expression, and clinical data for skin cutaneous melanoma were retrieved from the National Cancer Institute (NCI) Genomic Data Commons (GDC) thorough its GDC Application Programming Interface (API) using the TCGAbiolinks package or the CGDS-R package to query the Cancer Genomic Data Server (CGDS) from cBioPortal.
Copy number analysis (CNA) Preprocessed copy number data was obtained from cBioportal. Copy number data sets generated by the GISTIC 2. 0 algorithms, specifically the allthresholded. bygenes. txt of the GISTIC output were used. Samples with GISTIC copy-number values of "-1" were considered as mono-allelic loss (red) and samples with GISTIC copy-number values of "-2" as bi-allelic loss (orange). TCGA dataset CNA-data set (n = 367). BRN2 CNA classified as gain/amplification (GISTIC > "+1" or "+2") are not shown (n = 29, 7. 9%).
Immunohistochemistry of mouse melanoma and inguinal lymph nodes Paraffin-embedded mouse melanomas were sectioned into 7-μm-thick transverse sections and stained with hematoxylin/eosin (H&E), as previously described  64. Antibodies are from Nova-Costra for Ki-67, BD Biosciences for BrdU, from Abcam for SOX10 and Cell signaling for PTEN. Images were captured using a ZEISS Axio Imager 2 with Axiocam 506 color cameras. Image analysis was performed using ZEISS ZEN, Adobe Photoshop, and ImageJ software. Quantifications of Ki-67 and BrdU stainings were determined as a percentage. The percentage of Ki-67 + and BrdU + cells from three fields (1,000-2,000 cells/field) from three independent tumors per genotype was determined and normalized.
Acknowledgements We are grateful to  Dorothy C Bennett ,  Ghanem Ghanem ,  Florence Faure , and  Meenhard Herlyn  for providing cell lines. Hong Wu  for providing Pten flox mice. We thank the  Institut Curie  staff responsible for the animal colony (especially P. Dubreuil), and the histology ( S. Leboucher ),  FACS  ( C. Lasgi ), and  PICT-IBiSA imaging (C. Lovo)  facilities. This work was supported by the  Ligue nationale contre le cancer, INCa ,  ITMO Cancer, Fondation ARC (PGA) , and is under the program «Investissements d'Avenir» launched by the  French Government  and implemented by  ANR Labex CelTisPhyBio  ( ANR-11-LBX-0038  and  ANR-10-IDEX-0001-02 PSL ). MH had a fellowship from  PSL  and  FRM , PS had a fellowship from  INSERM , and MLC had a fellowship from  FRM. CRG was supported by the  Ludwig Institute for Cancer Research.
Sequence collection In order to reconstruct the ancestral sequence of the AhSRK28 and AhSRK03 SRK alleles, we first collected 17 full or partial sequences of the SRK first exon belonging to the haplogroup B/2. Seven allele sequences belonged to A. halleri (AhSRK03, AhSRK08, AhSRK09, AhSRK19, AhSRK23, AhSRK27, AhSRK28), six to A. lyrata (AlSRK06, AlSRK08, AlSRK14, AlSRK18, AlSRK29, AlSRK39) and four to Capsella grandiflora  (CgrSRK1, CgrSRK4, CgrSRK5, CgrSRK6). For the AhSRK19, AhSRK23 and AhSRK27 alleles the SRK exon1 partial sequence was supplemented by Sanger sequencing. We added three sequences from the SRK haplogroup A3/3 as outgroups (AhSRK04, AhSRK10, AhSRK29). Accession numbers for the sequences are reported in Supplementary file 2. After preliminary analyses and in order to obtain a well-supported phylogenetic tree we removed three fast evolving sequences: CgrSRK6, AhSRK08 and AlSRK29.
Ancestral SRK reconstruction The ancestral reconstruction was conducted with the codeml program of the PAML 4. 8 package  (Yang, 2007)  under six different models: M0, M0-FMutSel0, M0-FMutSel, M3, M3-FMutSel0, M3-FMutSel. M0 refers to a one-ratio model, which assumes a single w (d n /d s ) across branches and sites  (Goldman and Yang, 1994) , whereas M3 allows w to vary across sites according to a discrete distribution (with 2 or three categories depending on the models)  (Yang et al. , 2000). The mutationselection models incorporate parameters for mutation bias, with (FMutSel) or without (FMutSel0) selection on synonymous rate  (Yang and Nielsen, 2008). Models were compared using Likelihood Ratio Tests (LRT) and Akaike Information Criteria (AIC). The best fitting-model was found to be M3FMutSel (Supplementary file 3), therefore the ancestral amino acid sequence reconstructed with this model was used to generate transgenic lines (SRKa IA ).
Acknowledgements This research received support through a grant from the  European Research Council  ( NOVEL  project, grant # 648321 ). The authors thank the  French Ministere de l'Enseignement Superieur et de la Recherche , the  Hauts de France Region  and the  European Funds for Regional Economical Development  for their financial support to this project. They also thank  S Billiard ,  I Fobis-Loisy ,  E Durand ,  D Charlesworth ,  M Uyenoyama  and  J Nasrallah  for useful discussions.
La Topographia Palmyrena 8 a repris l'historique des cartes à l'occasion de l'établissement d'un nouveau plan de Palmyre, doublé d'une base de données (pl. 1. 2). Cet ouvrage présente les différentes nécropoles, dont celle du sud-ouest où fut trouvé le tombeau des Trois Frères. Du haut du Jabal Muntar qui la domine s'offre une vue spectaculaire, celle qui est figée dans l'esprit de tous les voyageurs, savants ou non d 'avant 2015  (pl. 1. 3). Le terrain est parsemé de taches d'ombres signalant les hypogées, des tombeaux tours s'élèvent en surface, la route arrivant de Damas marque la limite de l'avancée de l'oasis. Un détail agrandi d'une carte (pl. 1. 4) permet le repérage et le comptage des hypogées avec au centre, le plan en T renversé du tombeau des Trois Frères. Vu du sol, son entrée se remarquait auprès d'un vestige de tombeau tour (pl.
kRaeling 1961-62. 258  the PalmyRa PoRtRait PRoJect and danish aRchaeological ReseaRch in PalmyRa In 2011 the Palmyra collection at Ny Carlsberg Glyptotek laid the ground for exploring the possibilities to apply for a larger research project, which would compile all known palmyrene funerary sculpture in a specially designed database. The Palmyra collection at the Ny Carlsberg Glyptotek is the largest collection of palmyrene funerary sculpture housed in a museum outside of Syria  262. The collection was to a large extent compiled in the 19 th century, when the brewer Carl Jacobsen, who was a keen collector of antiquities and in particular also impressionistic paintings, decided that Palmyrene sculpture along with Greek and Roman sculpture and portraiture also should have a prominent place within his private collections.
In the late 19 th century, the Rabbi Simonsen, on the request of Carl Jacobsen, wrote the first catalogue of the Palmyrene collection housed at the Ny Carlsberg Glyptotek, a monumental building in central Copenhagen, which Jacobsen had constructed for the purpose of making his collections available to the public  263. Within the framework of the Palmyra Portrait Project, the published and unpublished work by Harald Ingholt has been scrutinised and several unpublished parts have been and are being prepared for publication. This includes Ingholt's extensive paper archive of palmyrene sculpture, which is housed at Ny Carlsberg Glyptotek and which has been digitized and concorded with the portrait-database. Furthermore, Ingholt's unpublished excavation diaries are being prepared for publication by Raja and Yon and will appear in the series Studies in Palmyrene Archaeology and History, Brepols, Turnhout.
Le principe de montage sur ordinateur utilise les niveaux de calques et sous-calques du logiciel Adobe Illustrator© pour isoler les différents documents ; dans le calque de la restitution il y a également séparation des « couches » de peinture appliquées et des motifs qui peuvent être assemblés. Un fichier contenant un grand nombre de calques compile les dessins relevés sur place, différentes photographies prises plus ou moins dans le détail, des photographies anciennes etc. (pl. 99. 3 et 4). Il permet in fine de faire apparaître la proposition de restitution finale. Le « jeu » de vision, toujours sur ordinateur, consiste à afficher ou non un ou plusieurs documents (avec effet de transparence) afin de pouvoir apposer le plus justement possible un tracé vectoriel ; celui-ci doit constituer une surface fermée correspondant le plus précisément possible aux surfaces de couleurs.
Le dessin élaboré dans un fichier numérique n'est donc pas un document fixe : il se présente comme une base de données cumulant différents niveaux d'information affichés selon l'optique de travail et la représentation recherchée. Le dessin archéologique est depuis toujours un outil d'analyse et constitue une représentation essentielle de l'objet étudié avec un objectif d'utilisation différent de celui de la prise de vue photographique  63. Il permet entre autres de faire abstraction des informations visibles sur la photographie, non indispensables pour étayer un discours scientifique, et de faire ressortir des éléments techniques. Par extension le dessin de restitution infographique -par travail de compilation des données graphiques trouvées sur l'objet archéologique puis de dessin -peut présenter des informations qui ne sont plus visibles sur des prises de vue récentes.
Inscriptions La vectorisation des inscriptions peintes a suivi le même processus et j'étais, là aussi, à la disposition des chercheurs jusqu'à la phase de rédaction. Ainsi, à la demande de 64. pascha 1918 (pl. 9. 2). l'épigraphiste, il a été facile d'extraire du fichier « base de données » infographique des vues montrant comment j'avais procédé pour suggérer une restitution à partir d'une vue ancienne (pl. 100. 3). En retour, le travail de lecture et de transcription de l'épigraphiste permet quant à lui d'ajuster certains tracés susceptibles de n'être pas correctement restitués.