The puzzles in B→ππB\to \pi\pi and πK \pi K decays: possible implications for R-parity violating supersymmetry

Recent experiments suggest that certain data of $B \to \pi\pi,\pi K$ decays are inconsistent with the standard model expectations. We try to explain the discrepancies with R-parity violating suppersymmetry. By employing the QCD factorization approach, we study these decays in the minimal supersymmetric standard model with R-parity violation. We show that R-parity violation can resolve the discrepancies in both $B \to \pi\pi$ and $B \to \pi K$ decays, and find that in some regions of parameter spaces all these requirements, including the CP averaged branching ratios and the direct CP asymmetries, can be satisfied. Furthermore, we have derived stringent bounds on relevant R-parity violating couplings from the latest experimental data, and some of these constraints are stronger than the existing bounds.Comment: 24 pages, 6 figures and 5 tables. Text revised. Final version to appear in PR

Polarizations in decays B_{u,d}\to VV and possible implications for R-parity violating SUSY

Recently BABAR and Belle have measured anomalous large transverse polarizations in some pure penguin $B \to VV$ decays, which might be inconsistent with the Standard Model expectations. We try to explore its implications for R-parity violating (RPV) supersymmetry. The QCD factorization approach is employed for the hadronic dynamics of B decays. We find that it is possible to have parameter spaces solving the anomaly. Furthermore, we have derived stringent bounds on relevant RPV couplings from the experimental data, which is useful for further studies of RPV phenomena.Comment: 26 pages, 12 eps figures. Typos corrected and references added. Final version to appear in PR

Paxillin facilitates timely neurite initiation on soft-substrate environments by interacting with the endocytic machinery.

Neurite initiation is the first step in neuronal development and occurs spontaneously in soft tissue environments. Although the mechanisms regulating the morphology of migratory cells on rigid substrates in cell culture are widely known, how soft environments modulate neurite initiation remains elusive. Using hydrogel cultures, pharmacologic inhibition, and genetic approaches, we reveal that paxillin-linked endocytosis and adhesion are components of a bistable switch controlling neurite initiation in a substrate modulus-dependent manner. On soft substrates, most paxillin binds to endocytic factors and facilitates vesicle invagination, elevating neuritogenic Rac1 activity and expression of genes encoding the endocytic machinery. By contrast, on rigid substrates, cells develop extensive adhesions, increase RhoA activity and sequester paxillin from the endocytic machinery, thereby delaying neurite initiation. Our results highlight paxillin as a core molecule in substrate modulus-controlled morphogenesis and define a mechanism whereby neuronal cells respond to environments exhibiting varying mechanical properties

Lifshitz Scaling Effects on Holographic Superconductors

Via numerical and analytical methods, the effects of the Lifshitz dynamical exponent $z$ on holographic superconductors are studied in some detail, including $s$ wave and $p$ wave models. Working in the probe limit, we find that the behaviors of holographic models indeed depend on concrete value of $z$. We obtain the condensation and conductivity in both Lifshitz black hole and soliton backgrounds with general $z$. For both $s$ wave and $p$ wave models in the black hole backgrounds, as $z$ increases, the phase transition becomes more difficult and the growth of conductivity is suppressed. For the Lifshitz soliton backgrounds, when $z$ increases ($z=1,~2,~3$), the critical chemical potential decreases in the $s$ wave cases but increases in the $p$ wave cases. For $p$ wave models in both Lifshitz black hole and soliton backgrounds, the anisotropy between the AC conductivity in different spatial directions is suppressed when $z$ increases. The analytical results uphold the numerical results.Comment: Typos corrected; Footnote added; References added; To be published in Nuclear Physics

Five-dimensional generalized f(R)f(R) gravity with curvature-matter coupling

The generalized $f(R)$ gravity with curvature-matter coupling in five-dimensional (5D) spacetime can be established by assuming a hypersurface-orthogonal spacelike Killing vector field of 5D spacetime, and it can be reduced to the 4D formulism of FRW universe. This theory is quite general and can give the corresponding results to the Einstein gravity, $f(R)$ gravity with both no-coupling and non-minimal coupling in 5D spacetime as special cases, that is, we would give the some new results besides previous ones given by Ref.\cite{60}. Furthermore, in order to get some insight into the effects of this theory on the 4D spacetime, by considering a specific type of models with $f_{1}(R)=f_{2}(R)=\alpha R^{m}$ and $B(L_{m})=L_{m}=-\rho$, we not only discuss the constraints on the model parameters $m$, $n$, but also illustrate the evolutionary trajectories of the scale factor $a(t)$, the deceleration parameter $q(t)$ and the scalar field $\epsilon(t)$, $\phi(t)$ in the reduced 4D spacetime. The research results show that this type of $f(R)$ gravity models given by us could explain the current accelerated expansion of our universe without introducing dark energy.Comment: arXiv admin note: text overlap with arXiv:0912.4581, arXiv:gr-qc/0411066 by other author

The MAPK Pathway-Based Drug Therapeutic Targets in Pituitary Adenomas

Mitogen-activated protein kinases (MAPKs) include ERK, p38, and JNK MAPK subfamilies, which are crucial regulators of cellular physiology, cell pathology, and many diseases including cancers. For the MAPK signaling system in pituitary adenomas (PAs), the activation of ERK signaling is generally thought to promote cell proliferation and growth; whereas the activations of p38 and JNK signaling are generally thought to promote cell apoptosis. The role of MAPK in treatment of PAs is demonstrated through the effects of currently used medications such as somatostatin analogs such as SOM230 and OCT, dopamine agonists such as cabergoline and bromocriptine, and retinoic acid which inhibit the MAPK pathway. Further, there are potential novel therapies based on putative molecular targets of the MAPK pathway, including 18beta-glycyrrhetinic acid (GA), dopamine-somatostatin chimeric compound (BIM-23A760), ursolic acid (UA), fulvestrant, Raf kinase inhibitory protein (RKIP), epidermal growth factor pathway substrate number 8 (Eps8), transmembrane protein with EGF-like and two follistatin-like domains (TMEFF2), cold inducible RNA-binding protein (CIRP), miR-16, and mammaliansterile-20-like kinase (MST4). The combined use of ERK inhibitor (e.g., SOM230, OCT, or dopamine) plus p38 activator (e.g., cabergoline, bromocriptine, and fulvestrant) and/or JNK activator (e.g., UA), or the development of single drug (e.g., BIM-23A760) to target both ERK and p38 or JNK pathways, might produce better anti-tumor effects on PAs. This article reviews the advances in understanding the role of MAPK signaling in pituitary tumorigenesis, and the MAPK pathway-based potential therapeutic drugs for PAs