One-loop Reggeon-Reggeon-gluon vertex at arbitrary space-time dimension

In order to check the compatibility of the gluon Reggeization in QCD with the $s$-channel unitarity, the one-loop correction to the Reggeon-Reggeon-gluon vertex must be known at arbitrary space-time dimension $D$. We obtain this correction from the gluon production amplitude in the multi-Regge kinematics and present an explicit expression for it in terms of a few integrals over the transverse momenta of virtual particles. The one-gluon contribution to the non-forward BFKL kernel at arbitrary $D$ is also obtained.Comment: 22 pages, LaTe

ALICE diffractive physics in p-p and Pb-Pb collisions at the LHC

The ALICE detector is introduced and a double gap trigger is presented. The interest in studying double pomeron induced events both in proton-proton and in lead-lead reactions is discussed.Comment: 5 pages, 5 figures, to appear in proceedings conference Diffraction 2008, La Londe-les-Maures, France, sep 9-14, 200

Finite-size scaling and deconfinement transition: the case of 4D SU(2) pure gauge theory

A recently introduced method for determining the critical indices of the deconfinement transition in gauge theories, already tested for the case of 3D SU(3) pure gauge theory, is applied here to 4D SU(2) pure gauge theory. The method is inspired by universality and based on the finite size scaling behavior of the expectation value of simple lattice operators, such as the plaquette. We obtain an accurate determination of the critical index $\nu$, in agreement with the prediction of the Svetitsky-Yaffe conjecture.Comment: 11 pages, 3 eps figure

Endoplasmic reticulum stress, degeneration of pancreatic islet β-cells, and therapeutic modulation of the unfolded protein response in diabetes.

BackgroundMyriad challenges to the proper folding and structural maturation of secretory pathway client proteins in the endoplasmic reticulum (ER) - a condition referred to as "ER stress" - activate intracellular signaling pathways termed the unfolded protein response (UPR).Scope of reviewThrough executing transcriptional and translational programs the UPR restores homeostasis in those cells experiencing manageable levels of ER stress. But the UPR also actively triggers cell degeneration and apoptosis in those cells that are encountering ER stress levels that exceed irremediable thresholds. Thus, UPR outputs are "double-edged". In pancreatic islet β-cells, numerous genetic mutations affecting the balance between these opposing UPR functions cause diabetes mellitus in both rodents and humans, amply demonstrating the principle that the UPR is critical for the proper functioning and survival of the cell.Major conclusionsSpecifically, we have found that the UPR master regulator IRE1α kinase/endoribonuclease (RNase) triggers apoptosis, β-cell degeneration, and diabetes, when ER stress reaches critical levels. Based on these mechanistic findings, we find that novel small molecule compounds that inhibit IRE1α during such "terminal" UPR signaling can spare ER stressed β-cells from death, perhaps affording future opportunities to test new drug candidates for disease modification in patients suffering from diabetes