The \bar{B} \to X_s γγdecay: NLL QCD contribution of the Electromagnetic Dipole operator O_7

We calculate the set of O(\alpha_s) corrections to the double differential decay width d\Gamma_{77}/(ds_1 \, ds_2) for the process \bar{B} \to X_s \gamma \gamma originating from diagrams involving the electromagnetic dipole operator O_7. The kinematical variables s_1 and s_2 are defined as s_i=(p_b - q_i)^2/m_b^2, where p_b, q_1, q_2 are the momenta of b-quark and two photons. While the (renormalized) virtual corrections are worked out exactly for a certain range of s_1 and s_2, we retain in the gluon bremsstrahlung process only the leading power w.r.t. the (normalized) hadronic mass s_3=(p_b-q_1-q_2)^2/m_b^2 in the underlying triple differential decay width d\Gamma_{77}/(ds_1 ds_2 ds_3). The double differential decay width, based on this approximation, is free of infrared- and collinear singularities when combining virtual- and bremsstrahlung corrections. The corresponding results are obtained analytically. When retaining all powers in s_3, the sum of virtual- and bremstrahlung corrections contains uncanceled 1/\epsilon singularities (which are due to collinear photon emission from the s-quark) and other concepts, which go beyond perturbation theory, like parton fragmentation functions of a quark or a gluon into a photon, are needed which is beyond the scope of our paper.

[Hyperinsulinemia as a consequence of systemic venous drainage in patients with pancreas transplantation]

To evaluate the metabolic consequences of pancreatic transplantation with systemic venous drainage on beta cell function, we examined insulin and C-peptide responses to arginine and secretin in type I diabetic recipients of pancreas transplantation (n = 16), and normal controls (n = 28). Basal insulin levels were 24 +/- 3 microU/l in pancreas recipients, and 7 +/- 1 microU/l in controls (p less than 0.001). Stimulated insulin levels following arginine (MANOVA, p less than 0.001), and secretin (MANOVA, p less than 0.001) were 1.5 to 3 fold elevated compared to controls. In contrast, integrated C-peptide responses following stimulation with arginine or secretin did not differ significantly between the two groups. We conclude that recipients of pancreas allografts with systemic venous drainage have elevated basal and stimulated insulin levels and that these alterations are primarily due to alterations of first pass hepatic insulin clearance although insulin resistance secondary to immunosuppressive therapy (including prednisone) may also play a contributing role. To avoid hyperinsulinemia and its possible long term adverse consequences, transplantation of pancreas allografts in sites with portal rather than systemic venous drainage may be preferable.

[Intolerance as consequence of hyperreactivity]

Many patients complain about hyperreactivity of the skin or mucosal membranes, whereby rather harmless "triggers" lead to exaggerated reactions like running nose, bronchospasm, urticaria, etc. Most of these hyperreactivities have an underlying inflammation. It is important not to focus only on the triggers, but to look for the agent causing the inflammation and to avoid/treat it: elimination of the cause also eliminates the hyperreactivity. Four examples are presented where this cause--trigger model of hyperreactivity is illustrated (exercise induced asthma, pollen associated food allergy, flare-up reactions in drug allergy and hyperreactivity in chronic urticaria).