Search for C=+C=+ charmonium and bottomonium states in e+e−→γ+Xe^+e^-\to \gamma+ X at B factories

We study the production of $C=+$ charmonium states $X$ in $e^+e^-\to \gamma + X$ at B factories with $X=\eta_c(nS)$ (n=1,2,3), $\chi_{cJ}(mP)$ (m=1,2), and $^1D_2(1D)$. In the S and P wave case, contributions of tree-QED with one-loop QCD corrections are calculated within the framework of nonrelativistic QCD(NRQCD) and in the D-wave case only the tree-QED contribution are considered. We find that in most cases the QCD corrections are negative and moderate, in contrast to the case of double charmonium production $e^+e^-\to J/\psi + X$, where QCD corrections are positive and large in most cases. We also find that the production cross sections of some of these states in $e^+e^-\to \gamma + X$ are larger than that in $e^+e^-\to J/\psi + X$ by an order of magnitude even after the negative QCD corrections are included. So we argue that search for the X(3872), X(3940), Y(3940), and X(4160) in $e^+e^-\to \gamma + X$ at B factories may be helpful to clarify the nature of these states. For completeness, the production of bottomonium states in $e^+e^-$ annihilation is also discussed.Comment: 13pages, 4 figure

The Role of c-Kit Receptor Tyrosine Kinase in Beta-Cell Proliferation, Function and Survival

c-Kit, a receptor tyrosine kinase, interacts with Stem Cell Factor (SCF), mediating cell differentiation, function, and survival. c-Kit is critical for the development and maintenance of beta-cell function in both rodents and humans. The mutation of c-Kit at W locus (c-KitWv/+) in mice results in an early onset of diabetes. However, the underlying mechanisms by which c-Kit deficiency leads to beta-cell failure are unknown. Therefore, studying SCF/c-Kit downstream signaling pathways is essential to understanding the precise mechanism by which c-Kit regulates beta-cell survival and function in vivo. We identified that dysregulated Akt/Glycogen synthase kinase 3β (Gsk3β)/cyclin D1 pathway, downstream of c-Kit, is responsible for reduced beta-cell proliferation, leading to a severe loss of beta-cell mass in c-KitWv/+ mice. An up-regulation of Fas-mediated caspase-dependent apoptotic machinery is also associated with beta-cell death in c-KitWv/+ mouse islets. The loss of functional Fas (lpr mutation) reversed beta-cell apoptosis and dysfunction in c-KitWv/+;Faslpr/lpr double mutant mice, demonstrating that a balance between c-Kit and Fas signaling is critical for beta-cell survival and function. To further delineate the primary functional role of c-Kit in beta-cells, we developed a transgenic (c-KitβTg) mouse model with beta-cell specific c-KIT overexpression. c-KitβTg mice exhibited increased beta-cell mass with improved insulin secretion, which is mediated by up-regulation of Akt/Gsk3β/cyclin D1 pathway. c-KIT overexpression in beta-cells not only protected islet function from 4 weeks of high-fat-diet (HFD) challenge, but also recused the onset of diabetes observed in c-KitWv/+ mice. We also found that c-Kit signaling plays a critical role in islet vascularization. c-Kit mediates VEGF-A production via the Akt/mTOR pathway in vivo. c-KIT overexpression in beta-cells rescued the islet vascular defects in c-KitWv/+ mice. However, under long-term HFD challenge, c-KitβTg mouse islets displayed dilated vessels with reduced beta-cell mass and increased beta-cell apoptosis. The observed beta-cell failure was likely associate with expanded islet vasculature causing increased islet inflammatory response. In conclusion, this series of studies represent an integrated in vitro and in vivo approach aimed at unraveling the cellular mechanisms by which SCF/c-Kit regulates beta-cell survival and function