Fit to Moments of Inclusive B->Xc lv and B-> Xs gamma Decay Distributions using Heavy Quark Expansions in the Kinetic Scheme

We present a fit to measured moments of inclusive distributions in B->Xc lv and B-> Xs gamma decays to extract values for the CKM matrix element |Vcb|, the b- and c-quark masses, and higher order parameters that appear in the Heavy Quark Expansion. The fit is carried out using theoretical calculations in the kinetic scheme and includes moment measurements of the Babar, Belle, CDF, CLEO and DELPHI collaborations for which correlation matrices have been published. We find |Vcb| = (41.96 +- 0.23(exp) +- 0.35(HQE) +- 0.59(Gamma_SL)) 10^-3 and m_b = 4.590 +- 0.025(exp) +- 0.30(HQE) GeV where errors are experimental and theoretical respectively. We also derive values for the heavy quark distribution function parameters m_b and \mu_\pi^2 in different theoretical schemes that can be used as input for the determination of |Vub|.Comment: 13 pages, 6 figures. v3: Fig 1+2 show absolute values for moments and fit rather than the difference. Updated some references. v2: Updated to include Belle photon moments and PDG 2005 lifetime. Included extrapolation factors for the BR(B->Xs gamma) to 1.6 Gev based on the HQE parameters from the fit and added an updated OPE expression for |Vub

Second Order Perturbation Theory for Improved Gluon and Staggered Quark Actions

We present the results of our perturbative calculations of the static quark potential, small Wilson loops, the static quark self energy, and the mean link in Landau gauge. These calculations are done for the one loop Symanzik improved gluon action, and the improved staggered quark action.Comment: 3 pages, LaTeX, Lattice2001(improvement

Highly Improved Naive and Staggered Fermions

We present a new action for highly improved staggered fermions. We show that perturbative calculations for the new action are well-behaved where those of the conventional staggered action are badly behaved. We discuss the effects of the new terms in controlling flavor mixing, and discuss the design of operators for the action.Comment: Contribution to Lattice2001(improvement); 3 page

Wdpcp, a PCP Protein Required for Ciliogenesis, Regulates Directional Cell Migration and Cell Polarity by Direct Modulation of the Actin Cytoskeleton

Planar cell polarity (PCP) regulates cell alignment required for collective cell movement during embryonic development. This requires PCP/PCP effector proteins, some of which also play essential roles in ciliogenesis, highlighting the long-standing question of the role of the cilium in PCP. Wdpcp, a PCP effector, was recently shown to regulate both ciliogenesis and collective cell movement, but the underlying mechanism is unknown. Here we show Wdpcp can regulate PCP by direct modulation of the actin cytoskeleton. These studies were made possible by recovery of a Wdpcp mutant mouse model. Wdpcp-deficient mice exhibit phenotypes reminiscent of Bardet-Biedl/Meckel-Gruber ciliopathy syndromes, including cardiac outflow tract and cochlea defects associated with PCP perturbation. We observed Wdpcp is localized to the transition zone, and in Wdpcp-deficient cells, Sept2, Nphp1, and Mks1 were lost from the transition zone, indicating Wdpcp is required for recruitment of proteins essential for ciliogenesis. Wdpcp is also found in the cytoplasm, where it is localized in the actin cytoskeleton and in focal adhesions. Wdpcp interacts with Sept2 and is colocalized with Sept2 in actin filaments, but in Wdpcp-deficient cells, Sept2 was lost from the actin cytoskeleton, suggesting Wdpcp is required for Sept2 recruitment to actin filaments. Significantly, organization of the actin filaments and focal contacts were markedly changed in Wdpcp-deficient cells. This was associated with decreased membrane ruffling, failure to establish cell polarity, and loss of directional cell migration. These results suggest the PCP defects in Wdpcp mutants are not caused by loss of cilia, but by direct disruption of the actin cytoskeleton. Consistent with this, Wdpcp mutant cochlea has normal kinocilia and yet exhibits PCP defects. Together, these findings provide the first evidence, to our knowledge, that a PCP component required for ciliogenesis can directly modulate the actin cytoskeleton to regulate cell polarity and directional cell migration

Surveillance of Sentinel Node-Positive Melanoma Patients with Reasons for Exclusion from MSLT-II:Multi-Institutional Propensity Score Matched Analysis

BACKGROUND: In sentinel lymph node (SLN)-positive melanoma, two randomized trials demonstrated equivalent melanoma-specific survival with nodal surveillance vs completion lymph node dissection (CLND). Patients with microsatellites, extranodal extension (ENE) in the SLN, or >3 positive SLNs constitute a high-risk group largely excluded from the randomized trials, for whom appropriate management remains unknown. STUDY DESIGN: SLN-positive patients with any of the three high-risk features were identified from an international cohort. CLND patients were matched 1:1 with surveillance patients using propensity scores. Risk of any-site recurrence, SLN-basin-only recurrence, and melanoma-specific mortality were compared. RESULTS: Among 1,154 SLN-positive patients, 166 had ENE, microsatellites, and/or >3 positive SLN. At 18.5 months median follow-up, 49% had recurrence (vs 26% in patients without high-risk features, p 3 positive SLN constitute a high-risk group with a 2-fold greater recurrence risk. For those managed with nodal surveillance, SLN-basin recurrences were more frequent, but all-site recurrence and melanoma-specific mortality were comparable to patients treated with CLND. Most recurrences were outside the SLN-basin, supporting use of nodal surveillance for SLN-positive patients with microsatellites, ENE, and/ or >3 positive SLN

Active surveillance of patients who have sentinel node positive melanoma:An international, multi-institution evaluation of adoption and early outcomes after the Multicenter Selective Lymphadenectomy trial II (MSLT-2)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/168248/1/cncr33483.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/168248/2/cncr33483_am.pd