The Glitch That Stole Christmas From The Pac-10

The Bowl Championship Series (BCS) employs a multi-criteria decision model (MCDM) to determine eligibility to play in the most elite college football bowls at the end of the season.  MCDM’s are widely used in business and government to make important decisions, including those with tremendous financial impacts.  The BCS college bowls have the biggest payouts involving several million dollars.  This year, the PAC-10 could have been the first football conference to place two teams in the BCS bowl.  What a Merry Christmas that would have been!  The payout would have been $2.75 million or$275 thousand per team.  Unfortunately, due to the use of a faulty MCDM that distorts the relationship between those football programs considered, a glitch in the BCS formula stole the Rose Bowl prestige and the money from the PAC-10 during the Christmas holidays.  Using appropriate multipliers, the economic impact in PAC-10 communities could have been very significant.   The implication for future competition through enhanced athletic facilities, for example, could have a sustained economic impact for several years in those communities.  It will be demonstrated in this paper that had the BCS employed a valid and consistent algorithm for determining a final score, even with the BCS’s own data, the University of California would have a higher score than the University of Texas and the PAC-10 would have benefited by $2.75 Million, and they would have a much merrier Christmas than they had from playing in the Holiday Bowl

Poster 156 Musculoskeletal Injuries in Dancers

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/147106/1/pmr2s223.pd

ESR Spectrum of the 9‐Molybdomanganate(IV) Ion in Dilute Single Crystal

The ESR spectrum of a single crystal of (NH4)6[NI(IV)O6Mo9O26]⋅8H2O containing 1% (NH4)6‐[Mn(IV)O6Mo9O26]⋅8H2O has been investigated. This is the first ESR report on quadrivalent manganese in a chemically well‐characterized environment. The site symmetry is D3D3, and anisotropic gg values, hyperfine splittings, and zero‐field splitting values were obtained by fitting the spectrum with an axial spin Hamiltonian.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71351/2/JCPSA6-50-9-3647-1.pd

Hearing dysfunction in heterozygous M itf Mi‐wh /+ mice, a model for W aardenburg syndrome type 2 and T ietz syndrome

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95364/1/pcmr12030.pd

Tests of electron flavor conservation with the Sudbury Neutrino Observatory

We analyze tests of electron flavor conservation that can be performed at the Sudbury Neutrino Observatory (SNO). These tests, which utilize $^8$B solar neutrinos interacting with deuterium, measure: 1) the shape of the recoil electron spectrum in charged-current (CC) interactions (the CC spectrum shape); and 2) the ratio of the number of charged current to neutral current (NC) events (the CC/NC ratio). We determine standard model predictions for the CC spectral shape and for the CC/NC ratio, together with realistic estimates of their errors and the correlations between errors. We consider systematic uncertainties in the standard neutrino spectrum and in the charged-current and neutral current cross-sections, the SNO energy resolution and absolute energy scale, and the SNO detection efficiencies. Assuming that either matter-enhanced or vacuum neutrino oscillations solve the solar neutrino problems, we calculate the confidence levels with which electron flavor non-conservation can be detected using either the CC spectrum shape or the CC/NC ratio, or both. If the SNO detector works as expected, the neutrino oscillation solutions that best-fit the results of the four operating solar neutrino experiments can be distinguished unambiguously from the standard predictions of electron flavor conservation.Comment: 31 pages (RevTeX) + 10 figures (postscript). Requires epsfig.sty. Gzipped figures also available at ftp://ftp.sns.ias.edu/pub/lisi/snopaper . To appear in Phys. Rev.

Is poetry therapy an appropriate intervention for clients recovering from anorexia? A critical review of the literature and client report

© 2017 Informa UK Limited, trading as Taylor & Francis Group. Poetry therapy is an arts-based psychotherapeutic intervention, often delivered in groups. This paper argues that the process and benefits of poetry therapy may be particularly suited to clients recovering from anorexia, as an adjunct to other treatments. Poetry therapy and its history are described briefly, and the relevance of poetry therapy for clients recovering from anorexia is outlined. After one client contributes her experience of this treatment for illustration, the paper offers a review of the evidence base for poetry therapy for eating disorders, and argues that, while research is limited, further research is warranted. Finally, a description of one form of clinical application is offered, to enable replication

Mode of action of DNA-competitive small molecule inhibitors of tyrosyl DNA phosphodiesterase 2

TDP2 is a 5’-tyrosyl DNA phosphodiesterase important for the repair of DNA adducts generated by non-productive (abortive) activity of topoisomerase II. TDP2 facilitates therapeutic resistance to topoisomerase poisons, which are widely used in the treatment of a range of cancer types. Consequently, TDP2 is an interesting target for the development of small molecule inhibitors that could restore sensitivity to topoisomerase-directed therapies. Previous studies identified a class of deazaflavin-based molecules that showed inhibitory activity against TDP2 at therapeutically useful concentrations, but their mode of action was uncertain. We have confirmed that the deazaflavin series inhibits TDP2 enzyme activity in a fluorescence-based assay, suitable for HTS-screening. We have gone on to determine crystal structures of these compounds bound to a ‘humanised’ form of murine TDP2. The structures reveal their novel mode of action as competitive ligands for the binding site of an incoming DNA substrate, and point the way to generating novel and potent inhibitors of TDP2

XRCC1 mutation is associated with PARP1 hyperactivation and cerebellar ataxia

XRCC1 is a molecular scaffold protein that assembles multi-protein complexes involved in DNA single-strand break repair1,2. Here we show that biallelic mutations in the human XRCC1 gene are associated with ocular motor apraxia, axonal neuropathy, and progressive cerebellar ataxia. Cells from a patient with mutations in XRCC1 exhibited not only reduced rates of single-strand break repair but also elevated levels of protein ADP-ribosylation. This latter phenotype is recapitulated in a related syndrome caused by mutations in the XRCC1 partner protein PNKP3,4,5 and implicates hyperactivation of poly(ADP-ribose) polymerase/s as a cause of cerebellar ataxia. Indeed, remarkably, genetic deletion of Parp1 rescued normal cerebellar ADP-ribose levels and reduced the loss of cerebellar neurons and ataxia in Xrcc1-defective mice, identifying a molecular mechanism by which endogenous single-strand breaks trigger neuropathology. Collectively, these data establish the importance of XRCC1 protein complexes for normal neurological function and identify PARP1 as a therapeutic target in DNA strand break repair-defective disease

Identification of novel risk loci for restless legs syndrome in genome-wide association studies in individuals of European ancestry : a meta-analysis

Background Restless legs syndrome is a prevalent chronic neurological disorder with potentially severe mental and physical health consequences. Clearer understanding of the underlying pathophysiology is needed to improve treatment options. We did a meta-analysis of genome-wide association studies (GWASs) to identify potential molecular targets. Methods In the discovery stage, we combined three GWAS datasets (EU-RLS GENE, INTERVAL, and 23andMe) with diagnosis data collected from 2003 to 2017, in face-to-face interviews or via questionnaires, and involving 15126 cases and 95 725 controls of European ancestry. We identified common variants by fixed-effect inverse-variance meta-analysis. Significant genome-wide signals (p Findings We identified and replicated 13 new risk loci for restless legs syndrome and confirmed the previously identified six risk loci. MEIS1 was confirmed as the strongest genetic risk factor for restless legs syndrome (odds ratio 1.92, 95% CI 1 85-1.99). Gene prioritisation, enrichment, and genetic correlation analyses showed that identified pathways were related to neurodevelopment and highlighted genes linked to axon guidance (associated with SEMA6D), synapse formation (NTNG1), and neuronal specification (HOXB cluster family and MYT1). Interpretation Identification of new candidate genes and associated pathways will inform future functional research. Advances in understanding of the molecular mechanisms that underlie restless legs syndrome could lead to new treatment options. We focused on common variants; thus, additional studies are needed to dissect the roles of rare and structural variations.Peer reviewe