dataesr/scientific-paragraphs-categorization huggingface dataset:
General Methods, Analytical and Physical Measurements The crystal evaluation and intensity data collection for 1 were performed with a Bruker-Nonius Kappa CCD single-crystal diffractometer with Mo-Kα radiation (λ = 0. 71073 Å) at 293  (2). Crystallographic data and selected bond lengths and angles are listed in Table  S1. Microanalyses were done by the Microanalytical Service of the University of Pannonia. Infrared spectra were recorded on an Avatar 330 FT-IR Thermo Nicolet instrument (Thermo Nicolet Corporation, Madison, WI, USA) using samples mulled in KBr pellets. UV-Vis spectra were recorded on a Cary 60 spectrophotometer (Agilent Technologies, Penang, Malaysia) equipped with a fiber-optic probe with 1 cm path length. NMR spectrum was recorded on a Bruker Avance 400 spectrometer (Bruker Biospin AG, Fällanden, Switzerland).
Acknowledgements 10 D. C. F. gratefully acknowledges support from the  Brazilian agencies CAPES  and CNPQ. M. A. C. and M. N-R. acknowledge support from the program Capes-Cofecub Ph664/10. MN-R acknowledges  A. Cano  for discussions. S. Pairis ,  B. Fernandez ,  P. Plaindoux  and  Th. Fournier  have provided essential technical help.
These were left at room temperature in the dark overnight and then assessed for root hair deformation. The NGR234 Nod factors were analysed by high-pressure liquid chromatography coupled to a Shimadzu IT-ToF mass spectrometer. Nod factors were separated on a 50 9 2. 1 mm 2. 7 l Kinetex XB-C18 column (Phenomenex, Macclesfield, UK) using the following gradient of acetonitrile (B) vs 0. 1% formic acid in water (A), run at 600 ll min À1 and 40°C: 0 min, 5% B; 11. 67 min, 95% B; 14. 58 min, 95% B; 15. 17 min, 5% B; 18. 08 min, 5% B. Products were detected by positive and negative mode electrospray, with automatic data-dependent collection of MS2 data at an isolation width of m/z 3. 0, 50% collision energy and 50% collision gas. Spray chamber conditions were 250°C curved desorbation line, 300°C heat block, 1.
Parasponia andersonii is a tropical tree that can be propagated vegetatively (Op den Camp et al. , 2011b) and plantlets from vegetative propagation were used in this study. P. andersonii showed Ca 2+ oscillations in root hair cells in response to NGR234 Nod factor following microinjection (Fig. 3a ; Table  1 ). However, microinjection of P. andersonii root hairs was extremely challenging and this made it difficult to gather data from a sufficient number of cells. We therefore used A. rhizogenes to introduce the Ca 2+ reporter cameleon (NupYC2. 1; Sieberer et al. , 2009)  into P. andersonii roots. When challenged with NGR234 Nod factor, these cameleon-transformed roots revealed Ca 2+ oscillations (Table  1 ). Plant species of the sister genus of Parasponia, Trema, do not nodulate and to assess Nod factor-induced Ca 2+ oscillations in this close relative, we transformed T.
Acknowledgements Giulia Morieri  helped with the purification of the NGR234 Nod factors. We thank  Kew Gardens Millenium Seed Bank  and  Milagros Le on Barrios  for providing seeds. Thanks also to  Janet Sprent  and  Euan James  for advice early in the project. This work was supported by the  BBSRC  as  BB/J004553/1  and by the  European Research Council  as SYMBIOSIS. E. G. was funded by the  John Innes Foundation  and R. G. by  NWO   VICI 865. 13. 001. Thanks are also expressed to the  French ANR  ( Sesam ,  ANR-10-BLAN-1708 ).
Acknowledgement JCB aknowledges the financial support from the  European Research Council (ERC)  under the European Union's  Seventh Framework Program  ( FP7/2007-2013)/ERC Grant  agreement  306385-SofI , from the  SFB-755 , from the  IdEx Bordeaux  and the  'Région Aquitaine '. PG and BR also aknowledge the support of the GGNB doctoral school.
Prevention of groin injuries in athletes A new systematic review with a meta-analysis of randomised controlled trials on the prevention of groin injuries in sports was performed. 11 Seven trials, with six on football and one on handball, were identified. Two studies used an adductor strengthening programme, two studied the FIFA '11' preventive programme and two looked at balance training. The final study used a presentation to educate players. In total, there were 4191 participants included in the prevention studies and they sustained 157 injuries. After data pooling, no significant groin injury prevention effect was found (relative risk 0. 81; 95% CI 0. 60 to 1. 09). A potentially clinically relevant, but not statistically significant, reduction of 19% was found on meta-analysis. Future studies should focus on high-risk sports such as football or ice hockey and be adequately powered.
However, already at 120/s, the loading speed oscillations are very significant oscillating between 0 and 240/s at a frequency of about 6. 4kHz. At very high speeds, i. e. if the duration of the experiment is shorter than the round-trip travel within the puller bar, the set-up of the FW system is conceptually the same as an Split Hopkinson Tensile Bar system and the observed phenomenon is no longer relevant. The first author is grateful for the partial financial support through the French National Research Agency (Grant ANR-11-BS09-0008, LOTERIE).
20 In addition, EGF is among the topranked genes of a signature highly correlated with HCC development in HCV cirrhosis. 21 An early clinical chemoprevention trial is currently evaluating whether erlotinib is able to revert this high-risk HCC signature into a low risk (NCT02273362). To date, no drug, including sorafenib, has been able to decrease HCC incidence in high-risk patients, or prevent tumor recurrence after curative treatments. 22 ost of the polymorphisms associated with HCC development on chronic liver disease are related to specific risk factors. This observation highlights the close relationships among the nature of the exposure, the genetic background, and the mechanism of hepatocyte transformation/proliferation. 23 The association between aflatoxin B1 (AFB1), hepatitis B virus (HBV), and SNP of GTSM1 and GSTT1 is the prototype of a strong interplay between specific exposure to genotoxic contaminant together with viral infection and common polymorphisms to dramatically increase HCC risk.
NRAS/KRAS/HRAS are mutated in <3% of HCC. 49, 65, 66 reliminary data from a phase 2 trial (ie, BASIL [(Assessing BAY86-9766 Plus Sorafenib for the Treatment of Liver Cancer) NCT01204177]) in patients with advanced HCC receiving a combination of MEK inhibitor refametinib (BAY86-9766) plus sorafenib found mutations in approximately 6% of patients (4 of 69)  143  ; analysis was conducted on circulating DNA. Three of these four patients had confirmed partial responses. Inactivating mutations in RAS inhibitor RP6SKA3 are more prevalent (2%À9%)  49, 62, 65  and could also predict response to RAS inhibition. A phase 2 study testing the combination of refametinib and sorafenib in RAS mutant HCCs is ongoing. JAK1 mutation frequency has been described up to 9% based on wholegenome sequencing data in HBV-HCC.
66 This has not been confirmed in subsequent studies. 45, 49, 64, 65 Experimental evidence suggests that its blockage could have antitumor activity. 66 gnaling Pathways or Immune Checkpoints MET. Overexpression at the messenger RNA and protein levels has been described in at least 40%À50% of HCC samples. 144 A subanalysis of the phase 2b trial testing tivantinib vs placebo in second line suggested that the drug was particularly effective in those patients with high expression of MET on immunohistochemistry. 145  There has been some concerns about tivantinib's specificity as an MET inhibitor,  146  but a phase 3 RCT enrolling patients with high MET is currently evaluating its role in second line (NCT02029157). IGF2. Enrichment of high transcript levels of IGF2 (>20-fold) in approximately 10% of HCC samples suggest that it could act as a tumor driver.
Methods We conducted a systematic review of literature on BRCA1 mutation spectrum and frequencies in MENA cases published on scientific databases up to March 2014. Search terms included breast cancer, heredity breast/ovarian cancer families, BRCA genes, BRCA1 gene, Middle East, and North Africa. Original articles were identified from Cyprus, Egypt, Jordan, Lebanon, Morocco, Algeria, and Tunisia. The included studies had to meet the following criteria: the study must relate to the role of BRCA1 gene in BC, it should analyze all the coding regions, test specific mutations, or select exons of BRCA1 gene; the study must provide sufficient information on the deleterious BRCA1 mutations frequencies. Thirteen relevant references were identified (Table  1 ), including 10 which used DNA sequencing of all coding axons and flanking intron sequences of the BRCA1 gene.
The c. 5266dupC (5382insC) mutation was described among Egyptian  [17]  and Tunisian families  [26] [27] [28]. It is the second most frequently reported mutation in the BIC database. Though being often referred to as a Jewish founder mutation  [38] , c. 5266dupC is common in Central and Eastern Europe with a high frequency among different ethnic populations  [39]. It is thought that this mutation probably originated in the Baltic area 38 generations ago, with a gradual decrease in the prevalence going from east to west regions in Europe. A haplotype analysis indicates the likelihood of a single founder both in Europe and in North America for c. 5266dupC mutations  [40]. The c. 5062 5064delGTT mutation was detected in early onset Moroccan BC case with a strong family history of HBOC  [22]. It represents the most frequent mutation in Northeast Italy and has been confirmed to be pathogenic using a number of independent approaches  [41].
The c. 1016dupA mutation was detected in Moroccan families  [23]. It has previously been described as one of four founder mutations originating from the Eastern population of Norway  [42]. In contrast to other Norwegian founder mutations, the c. 1016dupA has also been reported in other ethnic groups. In the BIC database, the c. 1016dupA mutation is the 12th most common frame-shift mutation occurring in BRCA1. It has been reported that it occurs in populations throughout Europe including Spain, the Netherlands, Austria, and Italy, as well as in Latin America and North America; however, allelotyping results indicated an independent origin of this mutation. The c. 1016dupA is a frame-shift mutation due to the insertion of an A at nucleotide acid 1135 of codon 340 in exon 11, which is predicted to lead to a premature stop codon 345 and a truncated protein.
The c. 5095C>T mutation was identified in two Moroccan families  [23]. It has been described previously in BC families  [43] [44] [45]  and is classified as clinically significant in the BIC database. The amino acid substitution leads to a folding defect in the BRCT domain of the BRCA1 gene and reduces the proteolytic stability of this domain that interacts with numerous proteins involved in transcription and DNA repair  [46]. Functional data and cosegregation suggest that the c. 5095C>T mutation is deleterious and predisposes carriers to family history of breast and/or ovarian cancer  [46] [47] [48] [49]. Interestingly, the c. 211dupA mutation was identified among four early onset BC families (27-40 years) originated from the same geographical area in Tunisia  [28]. c. 211dupA was reported for the first time in two Tunisian families  [26]  and has never been previously reported in any other population, suggesting that this mutation may therefore be specific for the Tunisian population  [28].
Methods IHCA are defined by presence of chest compression and/ or external electrical shock (EES). All IHCA witnessed by an anesthesiologist in the OR or ICU are analyzed. All IHCA are recorded on a database including : demographic data, medical history, location of IHCA, event time sequence of CPR, initial cardiac rhythm (VF, VT, PEA, Asystole), first treatment attempt, number of EES, type of IV treatment, immediate survival rate (ISR). For Survivors : SAPS II score, duration of ICU stay, treatments and hospital survival rate (HSR) are recorded. Two groups defined by presence (group V) or absence (Group NV) of MV prior to IHCA were compared.
Data The data were collected from medical records and included civil status, date of diagnosis, topography and morphology of the cancer coded by ICD-O 3, the staging performed, the date of the EIC dedicated to the sarcoma, the characteristics of the tumour and the treatment (date, type and location). We defined "expert teams" as those that were (a) trained in interdisciplinary sarcoma management and (b) organised weekly interdisciplinary committees dedicated to sarcoma management. Later (2010), these teams were labelled by the French Cancer Institute (INCa) for the management of sarcoma patients.
Key performance indicators We collected data regarding the key-indicators of the initial examination and diagnosis of sarcoma  [6]  to evaluate the compliance of expert teams to the procedures described in the EBG for the initial check-up. This included biopsy before planned curative-intent surgery, appropriate primary tumour imaging and appropriate chest imaging. Some key-indicators related to the management process were also collected: rate of incident cases discussed by an EIC dedicated to sarcoma, rate of incident cases discussed within the three months following the diagnosis, the rate of incident cases discussed before the first treatment (pre-biopsy EIC) and the rate of R0 resection among operated patients  [7].
Microscopic examination of the colony showed dark brown septate hyphae with branching and cladosporium-type conidiation suggestive of F. pedrosoi. The patient was then given terbinafin 250 mg daily during six months allowing a complete clinical recovery after three months with pigmented sequelae (Fig. 3 ). Finally, molecular identification of the isolate was obtained by sequencing the ITS1-5. 8S-ITS2 region of rDNA with primers V9D and LS266  [2]. Comparison of the nucleotide sequences (568 bp) with the GenBank database revealed 99. 3% similarity with Fonsecaea nubica type strain CBS 269. 64 (accession number EU938592).
Lineage + cells were primarily phenotypic GR1 + /CD11B + myeloid for all co-culture conditions (data not shown). To quantify progenitor activity, total CD45 + cells were sorted from BMEC-Akt1 and BMS-Akt1 co-cultures, plated in methylcellulose, and scored for colony-forming units (CFUs). All conditions maintained appreciable levels of progenitor activity, while BMEC-Akt1 co-cultured CD45 + cells possessed significantly higher levels of CFU-E and CFU-G activity (Figures  3D  and 3E ). To assess the long-term, multi-lineage engraftment capacity of our ex vivo co-cultured HSPCs, 10 5 total CD45. 2 + sorted cells were transplanted into lethally irradiated (950 Rads) CD45. 1 + recipients with 5 3 10 5 CD45. 1 + whole BM (WBM) cells as a competitive dose. BMEC-Akt1 cocultured CD45 + cells show stable engraftment in recipient   3D  and 3F ), with BMS-Akt1 and feeder-free controls producing diminutive levels of CD45.
HSPC Co-culture Modulates BMEC-Akt1 Gene Expression In the BM microenvironment, HSCs are found in close proximity to the vasculature  (Kiel et al. , 2005; Kunisaki et al. , 2013) , suggesting that direct cellular contact may be necessary for the maintenance of resident stem cells. However, little is known about the cross-talk between HSCs and cells that composes the supportive environment. To explore this reciprocal cross-talk, we co-cultured BMEC-Akt1 and BMS-Akt1 with HSPCs (Figure  3A ), sorted (CD45 À DAPI À ) to collect purified feeders (Figure  S4 ), and analyzed via RNA sequencing. Feeders grown in co-culture media without HSPCs were used as baseline controls. Principal component analysis (PCA) and hierarchical clustering of RNA-sequencing data from cultured BMEC-Akt1 and BMS-Akt1 cells alone or following co-culture demonstrated a strong segregation into four distinct groups, accounting for 90% of the variance in the dataset (Figures  5A  and S4B ).
To assess tissue-specific BMEC-Akt1 engraftment, transplanted mice were intravitally labeled with Isolectin-B 4 prior to sacrifice and assayed by immunohistochemistry (IHC) at short-and long-term time points. mCherry + BMEC-Akt1 were present within the BM at early time points, but were absent at 16-weeks post-irradiation (Figure  S6E ). mCherry + BMEC-Akt1 cells were not observed in the spleen at either short-or long-term time points (Figure  S6F ). mCherry + BMEC-Akt1 cells were also undetectable within the BM microenvironment by flow cytometry at 16 weeks (data not shown). Therefore, BMEC-Akt1 are transiently present following myeloablative injury, but do not engraft tissues long-term, consistent with other reports  (Chute et al. , 2007; Li et al. , 2010; Salter et al. , 2009). These data suggest that transplanted BMEC-Akt1 exerts its pro-regenerative effects rapidly and transiently.
ACKNOWLEDGMENTS We thank the  Starr Foundation Tri-Institutional Core Facilities  and the  Weill Cornell Medical College's Genomics Core. J. M. B. is supported by the  Ansary Stem Cell Institute ;  Tri-Institutional Stem Cell Initiative ,  American Society of   Hematology Scholar Award , and  American Federation of Aging Research Award. M. G. P. is supported by a  Postdoctoral Tri-Institutional Stem Cell Initiative Fellowship (New York , NY). J. M. B. and M. G. P. are supported by a  Sponsored Research Agreement from Angiocrine Bioscience.
ACKNOWLEDGMENTS We thank the MSPC-affected family members and their relatives for their contribution and availability. We thank  L Bouzir  for helping with sample collection and  A Msakni ,  S Sassi , and  M Gaussen  for their technical support. We thank  B Lane ,  I Szeverenyi ,  L Lacina ,  SH Tan , and  X Lim  for their constructive feedback. O Mamaı  ¨is a PhD student at the  University of Monastir in Tunisia  and is funded by an  A*STAR   Research Attachment Program. B Reversade  is a fellow of the  Branco Weiss Foundation , an A*STAR Investigator, and  Young EMBO Investigator. This work was partly funded by the  Ministry of Higher Education and Scientific Research of Tunisia , the  Skin Research Institute of Singapore , and a  Strategic Positioning Fund on Genetic Orphan Diseases from A*STAR, Singapore.
Acknowledgements Financial support from  CNRS, University Claude-Bernard Lyon  1 and the  French Agence Nationale de Recherche  (support of the  ANR  project  GPdia   ANR-08-BLAN-0305 ) is gratefully acknowledged. Dr. R. Simon ,  C. Duchamp  and  N. Henriques  are gratefully acknowledged for mass spectrometry analyses. Tibor Docsa  is a recipient of the  Bolyai Fellowship  from the  Hungarian Academy of Sciences.
Such publications were triggered by the possibility to perform a direct comparison with experimental data obtained by scanning tunneling microscopy (STM), a technique well suited for probing the surface LDOS modulations at the atomic scale  [27, 28]. In this article, we shall present some key STM results performed on graphene monolayer and bilayer grown on a SiC surface, focusing on the LDOS modulations around impurities. Our approach will mostly be based on the analysis of 2D Fourier transform of the STM data. Following our previous work (Refs. [29, 30] ), we will especially emphasize how this technique can be pushed up to unravel the electronic pseudospin of the Dirac quasiparticles in graphene. Finally, recent unpublished data obtained on twisted bilayer graphene on Cu(100) will also be discussed.
6 nm -1. Thus the FS of ML and BL graphene on SiC(0001) are mostly similar, and correspond to the schematic in Fig. 2c. However, the pseudospin texture is different between ML and BL: for the latter, states in a single valley with opposite momentums + q andq have the same pseudospin orientation (Fig. 2e ). BL graphene should hence behave more like a conventional 2D system, with no particular quenching of the backscattering processes on smooth defects. The experimental STM data taken at 5 K and at small sample bias are presented in Fig. 3. At sufficiently low bias, STM images mostly reflect the LDOS maps at the Fermi energy. Although severals group have undertaken similar experiments to evidence QPIs in graphene on SiC  [54] [55] [56] [57] , no pseudospin-related fine structures in the 2D FT LDOS maps were reported, except by our work  [29, 30].
Measured data have been corrected for the spectral and polarization dependence of the optical set-up using a calibrated quartz tungsten halogen lamp (Newport, Oriel 63355). For energy-momentum spectroscopy, a 100-mm Bertrand lens was used to image the back focal plane of the objective and thus project the radiation pattern of emission onto the entrance slit of the spectrograph. Using a rotatable polarizer, s-and p-polarized back focal plane spectra were then obtained by imaging the energy-and momentum-resolved photoluminescence on the 2D NIR camera. The all-optical modulation experiment was performed by focusing a 1,064-nm laser on the sample through the same Â 100 objective. The laser line was filtered out by a 1,064-nm dichroic mirror and a 1,064-nm long pass filter. Precise coalignment of the 532 nm and the 1,064-nm lasers was enabled by using an eyepiece camera to monitor the position of their respective foci.
Acknowledgements The authors acknowledge fruitful discussion with  S. Karaveli ,  C. M. Dodson  and  M. Jiang. Financial support was provided by the  Air Force Office of Scientific Research  ( FA9550-10-1-0026  and  FA9550-12-1-0189 ),  Army Research Office  ( W911NF-14-1-0669 ),  Department of Education  ( P200A090076 ) and  National Science Foundation  ( EECS-0846466  and  EECS-1408009 ).
ACKNOWLEDGMENTS We thank  Mickael Ploquin  and  Rob Klose  for help with protein expression and purification,  Graham Kay  for the gift of the Smchd1 cDNA, and members of the  Brockdorff, Klose, and Nasmyth laboratories  for discussion and advice. This work was funded by  Wellcome Trust  grants  081385  and  103768. The OPIC electron microscopy facility was founded by a  Wellcome Trust   JIF award  ( 060208/Z/00/Z ) and is supported by a  Wellcome Trust  equipment grant ( 093305/Z/10/Z ). N. J. B. , A. -V. G. , and T. B. N. generated plasmids and cell lines; N. J. B. , H. C. , and A. -V. G. performed gel filtration and sucrose gradient sedimen-tation; A. -V. G. , K. B. , J. D. , and R. A. P. performed mass spectrometry; C. A. S performed electron microscopy; N. J. B. performed protein expression, purification, and biochemical assays; N.
Search Strategy and Search Terms The medical literature searches on the WEB device were undertaken up to September 2015 by using the MEDLINE, EMBASE, Cochrane Library, ClinicalTrials. gov, Database of Abstracts of Reviews of Effectiveness, and Health Technology Assessment data bases. The following key words were used in combination (by using "AND" and "OR"): "WEB," "Woven EndoBridge," "intracranial aneurysm (aneurysms)," "brain aneurysm (aneurysms). ".
28 d the WEB Clinical Assessment of Intrasaccular Aneurysm Therapy [WEBCAST] study26). No comparative data (either historical or prospective) are available to accurately determine the clinical and anatomic benefit of the WEB device in comparison with existing strategies. To our knowledge, no randomized clinical trial is either ongoing or planned to compare the WEB device with standard treatment, including endovascular coiling or surgical clipping. A prospective, multicenter, singlearm, cohort study (The WEB Intrasaccular Therapy Study [WEB-IT], ClinicalTrials. govIdentifier: NCT02191618) is being conducted in the United States to finally obtain FDA clearance. 28.