Form Factors from Light-Cone Sum Rules with B-Meson Distribution Amplitudes

New sum rules for $B\to \pi,K$ and $B\to \rho,K^*$ form factors are derived from the correlation functions expanded near the light-cone in terms of B-meson distribution amplitudes. The contributions of quark-antiquark and quark-antiquark-gluon components in the B meson are taken into account. Models for the B-meson three-particle distribution amplitudes are suggested, based on QCD sum rules in HQET. Employing the new light-cone sum rules we calculate the form factors at small momentum transfers, including $SU(3)_{fl}$ violation effects. The results agree with the predictions of the conventional light-cone sum rules.Comment: 32 pages, 7 figures, the discussion of numerical results extended, two references added, version to be published in Phys.Rev.

Zebrafish mutants in vegfab can affect endothelial cell proliferation without altering ERK phosphorylation and are phenocopied by loss of PI3K signaling.

The formation of appropriately patterned blood vessel networks requires endothelial cell migration and proliferation. Signaling through the Vascular Endothelial Growth Factor A (VEGFA) pathway is instrumental in coordinating these processes. mRNA splicing generates short (diffusible) and long (extracellular matrix bound) Vegfa isoforms. The differences between these isoforms in controlling cellular functions are not understood. In zebrafish, vegfaa generates short and long isoforms, while vegfab only generates long isoforms. We found that mutations in vegfaa had an impact on endothelial cell (EC) migration and proliferation. Surprisingly, mutations in vegfab more strongly affected EC proliferation in distinct blood vessels, such as intersegmental blood vessels in the zebrafish trunk and central arteries in the head. Analysis of downstream signaling pathways revealed no change in MAPK (ERK) activation, while inhibiting PI3 kinase signaling phenocopied vegfab mutant phenotypes in affected blood vessels. Together, these results suggest that extracellular matrix bound Vegfa might act through PI3K signaling to control EC proliferation in a distinct set of blood vessels during angiogenesis.We would like to thank Reinhild Bussmann, Mona Finch Stephen, Nadine Greer and Bill Vought for excellent fish care. In addition, we would like to thank Roman Tsaryk and Zeenat Diwan for critically reading of the manuscript and Caitlyn Parker for excellent technical assistance. We are grateful to Federica Lunella for help with the mouse retina dissection and immunohistochemistry. We would like to thank William Jones and Mary Mullins for providing the pCS2þ β-galactosidase plasmid. This work was funded by the Max-Planck-Society (A.F.S.), the Deutsche Forschungsgemeinschaft (DFG SI-1374/4-1, DFG SI-1374/5-1 and DFG SI-1374/6-1; A.F.S.) and start-up funds from the Cardiovascular Institute and the Department of Cell and Developmental Biology of the University of Pennsylvania Perelman School of Medicine (A.F.S.). We further acknowledge support from the NIH R01HL152086 (A.F.S.). Work in R.B.’s lab was funded by the Ministerio de Economía, Industría y Competitividad (MEIC: SAF2017-89299-P and RYC-2013-13209) and the European Research Council (ERC-2014-StG – 638028 AngioGenesHD).S

Einführung in das Schwerpunktthema

Einführung in das Schwerpunktthem

BB-Meson Distribution Amplitude from the B→πB\to \pi Form Factor

Employing the light-cone sum rule approach in QCD, we relate the $B$-meson distribution amplitude to the $B\to \pi$ form factor at zero momentum transfer. In leading order, the sum rule is converted into a simple expression for the inverse moment $\lambda_B$ of the distribution amplitude $\phi_{+}^B$. Using as an input the $B\to\pi$ form factor calculated from the light-cone sum rule in terms of pion distribution amplitudes, we obtain an estimate: $\lambda_B =460 \pm 160$ MeV. We investigate how this result is modified by the $B$-meson three-particle distribution amplitudes.Comment: 11 pages, 1 figure, version to appear in Phys.Lett.