Relativistic description of nuclear matrix elements in neutrinoless double-β\beta decay

Neutrinoless double-$\beta$ ($0\nu\beta\beta$) decay is related to many fundamental concepts in nuclear and particle physics beyond the standard model. Currently there are many experiments searching for this weak process. An accurate knowledge of the nuclear matrix element for the $0\nu\beta\beta$ decay is essential for determining the effective neutrino mass once this process is eventually measured. We report the first full relativistic description of the $0\nu\beta\beta$ decay matrix element based on a state-of-the-art nuclear structure model. We adopt the full relativistic transition operators which are derived with the charge-changing nucleonic currents composed of the vector coupling, axial-vector coupling, pseudoscalar coupling, and weak-magnetism coupling terms. The wave functions for the initial and final nuclei are determined by the multireference covariant density functional theory (MR-CDFT) based on the point-coupling functional PC-PK1. The low-energy spectra and electric quadrupole transitions in ${}^{150}$Nd and its daughter nucleus ${}^{150}$Sm are well reproduced by the MR-CDFT calculations. The $0\nu\beta\beta$ decay matrix elements for both the $0_1^+\rightarrow 0_1^+$ and $0_1^+\rightarrow 0_2^+$ decays of ${}^{150}$Nd are evaluated. The effects of particle number projection, static and dynamic deformations, and the full relativistic structure of the transition operators on the matrix elements are studied in detail. The resulting $0\nu\beta\beta$ decay matrix element for the $0_1^+\rightarrow 0_1^+$ transition is $5.60$, which gives the most optimistic prediction for the next generation of experiments searching for the $0\nu\beta\beta$ decay in ${}^{150}$Nd.Comment: 17 pages, 9 figures; table adde

Distributed Clustering in Cognitive Radio Ad Hoc Networks Using Soft-Constraint Affinity Propagation

Absence of network infrastructure and heterogeneous spectrum availability in cognitive radio ad hoc networks (CRAHNs) necessitate the self-organization of cognitive radio users (CRs) for efficient spectrum coordination. The cluster-based structure is known to be effective in both guaranteeing system performance and reducing communication overhead in variable network environment. In this paper, we propose a distributed clustering algorithm based on soft-constraint affinity propagation message passing model (DCSCAP). Without dependence on predefined common control channel (CCC), DCSCAP relies on the distributed message passing among CRs through their available channels, making the algorithm applicable for large scale networks. Different from original soft-constraint affinity propagation algorithm, the maximal iterations of message passing is controlled to a relatively small number to accommodate to the dynamic environment of CRAHNs. Based on the accumulated evidence for clustering from the message passing process, clusters are formed with the objective of grouping the CRs with similar spectrum availability into smaller number of clusters while guaranteeing at least one CCC in each cluster. Extensive simulation results demonstrate the preference of DCSCAP compared with existing algorithms in both efficiency and robustness of the clusters

Nonlinear Aggregation-Diffusion Equations: Radial Symmetry and Long Time Asymptotics

We analyze under which conditions equilibration between two competing effects, repulsion modeled by nonlinear diffusion and attraction modeled by nonlocal interaction, occurs. This balance leads to continuous compactly supported radially decreasing equilibrium configurations for all masses. All stationary states with suitable regularity are shown to be radially symmetric by means of continuous Steiner symmetrization techniques. Calculus of variations tools allow us to show the existence of global minimizers among these equilibria. Finally, in the particular case of Newtonian interaction in two dimensions they lead to uniqueness of equilibria for any given mass up to translation and to the convergence of solutions of the associated nonlinear aggregation-diffusion equations towards this unique equilibrium profile up to translations as $t\to\infty$

Systematic study of nuclear matrix elements in neutrinoless double-beta decay with a beyond mean-field covariant density functional theory

We report a systematic study of nuclear matrix elements (NMEs) in neutrinoless double-beta decays with a state-of-the-art beyond mean-field covariant density functional theory. The dynamic effects of particle-number and angular-momentum conservations as well as quadrupole shape fluctuations are taken into account with projections and generator coordinate method for both initial and final nuclei. The full relativistic transition operator is adopted to calculate the NMEs. The present systematic studies show that in most of the cases there is a much better agreement with the previous non-relativistic calculation based on the Gogny force than in the case of the nucleus $^{150}$Nd found in Song et al. [Phys. Rev. C 90, 054309 (2014)]. In particular, we find that the total NMEs can be well approximated by the pure axial-vector coupling term with a considerable reduction of the computational effort.Comment: 9 pages with 7 figures and 3 table

Radiative penguin Bs decays at Belle

We report searches for the radiative penguin decays Bs to phi gamma and Bs to gamma gamma based on a 23.6 fb-1 data sample collected with the Belle detector at the KEKB e+e- energy-asymmetric collider operating at the Upsilon(5S) resonance.Comment: On behalf of the Belle Collaboration. To appear in the proceedings of the International Europhysics Conference on High Energy Physics (EPS-HEP2007), Manchester, England, 19-25 July 2007. 3 pages, 2 figure

Numerical simulation of solid tumor blood perfusion and drug delivery during the “vascular normalization window” with antiangiogenic therapy

This Article is provided by the Brunel Open Access Publishing Fund - Copyright @ 2011 Hindawi PublishingTo investigate the influence of vascular normalization on solid tumor blood perfusion and drug delivery, we used the generated blood vessel network for simulations. Considering the hemodynamic parameters changing after antiangiogenic therapies, the results show that the interstitial fluid pressure (IFP) in tumor tissue domain decreases while the pressure gradient increases during the normalization window. The decreased IFP results in more efficient delivery of conventional drugs to the targeted cancer cells. The outcome of therapies will improve if the antiangiogenic therapies and conventional therapies are carefully scheduled

Local anaesthetic bupivacaine induced ovarian and prostate cancer apoptotic cell death and underlying mechanisms in vitro

Retrospective studies indicate that the use of regional anesthesia can reduce cancer recurrence after surgery which could be due to ranging from immune function preservation to direct molecular mechanisms. This study was to investigate the effects of bupivacaine on ovarian and prostate cancer cell biology and the underlying molecular mechanisms. Cell viability, proliferation and migration of ovarian carcinoma (SKOV-3) and prostate carcinoma (PC-3) were examined following treatment with bupivacaine. Cleaved caspase 3, 8 and 9, and GSK-3β, pGSK-3β(tyr216) and pGSK-3β(ser9) expression were assessed by immunofluorescence. FAS ligand neutralization, caspase and GSK-3 inhibitors and GSK-3β siRNA were applied to further explore underlying mechanisms. Clinically relevant concentrations of bupivacaine reduced cell viability and inhibited cellular proliferation and migration in both cell lines. Caspase 8 and 9 inhibition generated partial cell death reversal in SKOV-3, whilst only caspase 9 was effective in PC-3. Bupivacaine increased the phosphorylation of GSK-3β(Tyr216) in SKOV-3 but without measurable effect in PC3. GSK-3β inhibition and siRNA gene knockdown decreased bupivacaine induced cell death in SKOV-3 but not in PC3. Our data suggests that bupivacaine has direct ‘anti-cancer’ properties through the activation of intrinsic and extrinsic apoptotic pathways in ovarian cancer but only the intrinsic pathway in prostate cancer