10 research outputs found

    Spectral algorithm modifications for (alpha,N) reactions on beryllium in the SOURCES computer code

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    This work represents a new tool to predict neutron energy spectra in the lower energy regime and, upon submission to the Radiation Safety Information Computational Center, the code distributor, will ultimately upgrade SOURCES from version 4C to 5A --Abstract, page iv

    A New ā¹Be(A,n) Cross-Section Evaluation for Use in the SOURCES Computer Code

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    Experimental breakup reaction data was the basis for choosing a set of Ī± optical potential parameters for calculating the cross section from the 9Be(Ī±,Ī±ā€²n) reaction with the GNASH code. Although not in complete agreement with experimental values, the promising results suggest additional work and continued research for optimal parameters. Accommodating modifications in the SOURCES code system required improved data and an approximation for the three-body reaction branching fractions is presented as a temporary solution. Experimental spectra from AcBe, CmBe, and simulated AmBe neutron sources are compared to SOURCES calculations using the new branching fractions and serve as benchmarks for this new version of the code

    Comprehensive genomic characterization of head and neck squamous cell carcinomas

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    The Cancer Genome Atlas profiled 279 head and neck squamous cell carcinomas (HNSCCs) to provide a comprehensive landscape of somatic genomic alterations. Here we show that human-papillomavirus-associated tumours are dominated by helical domain mutations of the oncogene PIK3CA, novel alterations involving loss of TRAF3, and amplification of the cell cycle gene E2F1. Smoking-related HNSCCs demonstrate near universal loss-of-function TP53 mutations and CDKN2A inactivation with frequent copy number alterations including amplification of 3q26/28 and 11q13/22. A subgroup of oral cavity tumours with favourable clinical outcomes displayed infrequent copy number alterations in conjunction with activating mutations of HRAS or PIK3CA, coupled with inactivating mutations of CASP8, NOTCH1 and TP53. Other distinct subgroups contained loss-of-function alterations of the chromatin modifier NSD1, WNT pathway genes AJUBA and FAT1, and activation of oxidative stress factor NFE2L2, mainly in laryngeal tumours. Therapeutic candidate alterations were identified in most HNSCCsclose9
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