Mixing of pseudoscalar mesons and isospin symmetry breaking

Mixing of the pseudoscalar mesons is discussed in the quark-flavor basis with the hypothesis that the basis decay constants follow the pattern of particle state mixing. The divergences of the axial vector currents which embody the axial vector anomaly, combined with this hypothesis provide a calculational scheme for the parameters describing the mixing of the pion, eta and eta' mesons. Phenomenological applications of this mixing scheme are presented with particular interest focussed on isospin symmetry breaking in QCD estimated as eta and eta' admixtures to the pion. In contrast to previous work a possible difference in the basis decay constants f_u and f_d is considered and consequences of this potentially large effect on the strength of isospin symmetry breaking is discussed.Comment: 10 pages, (using LATEX with w-ijmpa.sty), invited talk presented at MESON 2004, 8th Intern. Workshop on Meson Production, Properties and Interaction

Acquiring and Maintaining Premium Seat Customers in the “Big Four” Leagues

The sports industry in the United States will bring in an estimated $400 to$425 billion in 2011 (Plunkett Research, Ltd, 2011). Of the overall revenue, $10 billion is derived from premium seating. Unlike general admission and television revenue, income from premium seats is not usually shared with other teams in the league (Miller & Washington, 2010). Premium seating revenue makes a significant contribution to the overall revenue stream of sports organizations. In the 2010-2011 seasons, there were a total of 12,527 luxury suites across all the professional sports venues within the National Football League (NFL), National Basketball Association (NBA), Major League Baseball (MLB) and National Hockey League (NHL) (ALSD, 2010). Premium seats also benefit the teams because most seats are purchased through a multi- year contract where the team receives payment upfront, which is crucial where the end product (a win) cannot be guaranteed (Casselman, 2009)

Comment on “Effects of Arsenite during Fetal Development on Energy Metabolism and Susceptibility to Diet-Induced Fatty Liver Diseases in Male Mice” and “Mechanisms Underlying Latent Disease Risk Associated with Early-Life Arsenic Exposure: Current Trends and Scientific Gaps”

Peer reviewedPublisher PD

Sorafenib inhibits therapeutic induction of necroptosis in acute leukemia cells

Induction of necroptosis has emerged as an alternative approach to trigger programmed cell death, in particular in apoptosis-resistant cancer cells. Recent evidence suggests that kinase inhibitors targeting oncogenic B-RAF can also affect Receptor-interacting serine/threonine-protein kinase (RIP) 1 and RIP3. Sorafenib, a multi-targeting kinase inhibitor with activity against B-RAF, is used for the treatment of acute leukemia. In the present study, we therefore investigated whether Sorafenib interferes with therapeutic induction of necroptosis in acute leukemia. Here, we report that Sorafenib inhibits necroptotic signaling and cell death in two models of necroptosis in acute leukemia. Sorafenib significantly reduces Second mitochondria-derived activator of caspases (Smac) mimetic-induced necroptosis in apoptosis-resistant acute myeloid leukemia (AML) cells as well as Smac mimetic/Tumor Necrosis Factor (TNF)alpha-induced necroptosis in FADD-deficient acute lymphoblastic leukemia (ALL) cells. Sub- to low micromolar concentrations of Sorafenib corresponding to its plasma levels reported in cancer patients are sufficient to inhibit necroptosis, emphasizing the clinical relevance of our findings. Furthermore, Sorafenib blocks Smac mimetic-mediated phosphorylation of mixed-lineage kinase domain-like protein (MLKL) that marks its activation, indicating that Sorafenib targets components upstream of MLKL such as RIP1 and RIP3. Intriguingly, Sorafenib reduces the Smac mimetic/TNF alpha-stimulated interaction of RIP1 with RIP3 and MLKL, demonstrating that it interferes with the assembly of the necrosome complex. Importantly, Sorafenib significantly protects primary, patient-derived AML blasts from Smac mimetic-induced necroptosis. By demonstrating that Sorafenib limits the anti-leukemic activity of necroptosisinducing drugs in acute leukemia cells, our study has important implications for the use of Sorafenib in the treatment of acute leukemia

Recovering Fine Details for Neural Implicit Surface Reconstruction

Recent works on implicit neural representations have made significant strides. Learning implicit neural surfaces using volume rendering has gained popularity in multi-view reconstruction without 3D supervision. However, accurately recovering fine details is still challenging, due to the underlying ambiguity of geometry and appearance representation. In this paper, we present D-NeuS, a volume rendering-base neural implicit surface reconstruction method capable to recover fine geometry details, which extends NeuS by two additional loss functions targeting enhanced reconstruction quality. First, we encourage the rendered surface points from alpha compositing to have zero signed distance values, alleviating the geometry bias arising from transforming SDF to density for volume rendering. Second, we impose multi-view feature consistency on the surface points, derived by interpolating SDF zero-crossings from sampled points along rays. Extensive quantitative and qualitative results demonstrate that our method reconstructs high-accuracy surfaces with details, and outperforms the state of the art