Semileptonic and rare B meson decays into a light pseudoscalar meson

In the framework of a QCD relativistic potential model we evaluate the form factors describing the exclusive decays B => \pi l nu and B => K l+ l-. The present calculation extends a previous analysis of B meson decays into light vector mesons. We find results in agreement with the data, when available, and with the theoretical constraints imposed by the Callan-Treiman relation and the infinite heavy quark mass limit.Comment: 11 pages LaTeX + 2 figure

Semileptonic and Rare BB-meson transitions in a QCD relativistic potential model

Using a QCD relativistic potential model, previously applied to the calculation of the heavy meson leptonic constants, we evaluate the form factors governing the exclusive decays $B\to\rho\ell\nu$, $B\to K^*\gamma$ and $B\to K^*\ell^+\ell^-$. In our approach the heavy meson is described as a $Q\bar q$ bound state, whose wave function is solution of the relativistic Salpeter equation, with an instantaneous potential displaying Coulombic behaviour at small distances and linear behaviour at large distances. The light vector meson is described by using a vector current interpolating field, according to the Vector Meson Dominance assumption. A Pauli-Villars regularized propagator is assumed for the quarks not constituting the heavy meson. Our procedure allows to avoid the description of the light meson in terms of wave function and constituent quarks, and consequently the problem of boosting the light meson wave function. Assuming as an input the experimental results on $B\to K^*\gamma$, we evaluate all the form factors describing the $B\to \rho, K^*$ semileptonic and rare transitions. The overall comparison with the data, whenever available, is satisfactory.Comment: Latex, 19 pages, 3 figure

B => \pi \pi \ell \nu decays in a QCD relativistic potential model

In the framework of a QCD relativistic potential model we evaluate the form factors describing the exclusive decay B => \pi\pi \ell \nu. The calculation is performed in a phase space region far away from the resonances and therefore is complementary to other decay mechanisms where the pions are produced by intermediate particles, e.g. in the chiral approach. We give an estimate of the contribution of the non resonant channel of the order of BR(B- => \pi+ \pi- \ell \nu) \approx 2.2 x 10^(-4).Comment: 14 pages LaTeX2e + 3 figures, Napoli Preprint DSF 99/3

Semileptonic and nonleptonic B decays to three charm quarks: B->J/psi (eta_c) D l nu and J/psi (eta_c) D pi

We evaluate the form factors describing the semileptonic decays $\bar{B^0}\to J/\psi (\eta_c) D^+ \ell^- \bar \nu_\ell$, within the framework of a QCD relativistic potential model. This decay is complementary to $\bar{B^0}\to J/\psi (\eta_c) D^+ \pi^-$ in a phase space region where a pion factors out.We estimate the branching ratio for these semileptonic and nonleptonic channels, finding $\mathcal{BR}(\bar{B^0} \to J/\psi (\eta_c) D^+ \ell \nu_\ell) \simeq 10^{-13}$, $\mathcal{BR}(\bar{B^0} \to J/\psi D^+ \pi^-) = 3.1 \times 10^{-8}$ and $\mathcal{BR}(\bar{B^0} \to \eta_c D^+ \pi^-) = 3.5 \times 10^{-8}$.Comment: 14 pages, 4 figure

B and B_s decays into three pseudoscalar mesons and the determination of the angle gamma of the unitarity triangle

We reconsider two classical proposals for the determination of the angle gamma of the unitarity triangle: B^\pm => chi_{c0} \pi^\pm => \pi^+\pi^-\pi^\pm and B_s => rho^0 K_S => \pi^+ \pi^- K_S. We point out the relevance, in both cases, of non resonant amplitudes, where the \pi^+ \pi^- pair is produced by weak decay of a B^* (J^P=1^-) or B_0 (J^P=0^+) off-shell meson. In particular, for the B decay channel, the inclusion of the B_0 pole completes some previous analyses and confirms their conclusions, provided a suitable cut in the Dalitz plot is performed; for the B_s decay the inclusion of the B^*, B_0 amplitudes enhances the role of the tree diagrams as compared to penguin amplitudes, which makes the theoretical uncertainty related to the B_s => rho^0 K_S decay process less significant. While the first method is affected by theoretical uncertainties, the second one is cleaner, but its usefulness will depend on the available number of events to perform the analysis.Comment: 8 pages LATEX, 4 figures, 1 tabl

Axial stent strut angle influences wall shear stress after stent implantation: analysis using 3D computational fluid dynamics models of stent foreshortening

INTRODUCTION: The success of vascular stents in the restoration of blood flow is limited by restenosis. Recent data generated from computational fluid dynamics (CFD) models suggest that the vascular geometry created by an implanted stent causes local alterations in wall shear stress (WSS) that are associated with neointimal hyperplasia (NH). Foreshortening is a potential limitation of stent design that may affect stent performance and the rate of restenosis. The angle created between axially aligned stent struts and the principal direction of blood flow varies with the degree to which the stent foreshortens after implantation. METHODS: In the current investigation, we tested the hypothesis that stent foreshortening adversely influences the distribution of WSS and WSS gradients using time-dependent 3D CFD simulations of normal arteries based on canine coronary artery measurements of diameter and blood flow. WSS and WSS gradients were calculated using conventional techniques in ideal (16 mm) and progressively foreshortened (14 and 12 mm) stented computational vessels. RESULTS: Stent foreshortening increased the intrastrut area of the luminal surface exposed to low WSS and elevated spatial WSS gradients. Progressive degrees of stent foreshortening were also associated with strut misalignment relative to the direction of blood flow as indicated by analysis of near-wall velocity vectors. CONCLUSION: The current results suggest that foreshortening may predispose the stented vessel to a higher risk of neointimal hyperplasia

Cardioprotection by Glucose-Insulin-Potassium: Dependence on K\u3csub\u3eATP\u3c/sub\u3e Channel Opening and Blood Glucose Concentration Before Ischemia

We tested the hypothesis that glucose-insulin-potassium (GIK)-induced protection against myocardial infarction depends on ATP-dependent K+ (KATP) channel activation and is abolished by hyperglycemia before the ischemia. Dogs were subjected to a 60-min coronary artery occlusion and 3-h reperfusion in the absence or presence of GIK (25% dextrose; 50 IU insulin/l; 80 mM/l KCl infused at 1.5 ml·kg−1·h−1) beginning 75 min before coronary artery occlusion or 5 min before reperfusion. The role of KATP channels was evaluated by pretreatment with glyburide (0.1 mg/kg). The efficacy of GIK was investigated with increases in blood glucose (BG) concentrations to 300 or 600 mg/dl or experimental diabetes (alloxan/streptozotocin). Infarct size (IS) was 29 ± 2% of the area at risk in control experiments. GIK decreased (P \u3c 0.05) IS when administered beginning 5 min before reperfusion. This protective action was independent of BG (13 ± 2 and 12 ± 2% of area at risk; BG = 80 or 600 mg/dl, respectively) but was abolished in dogs receiving glyburide (30 ± 4%), hyperglycemia before ischemia (27 ± 4%), or diabetes (25 ± 3%). IS was unchanged by GIK when administered before ischemia independent of BG (31 ± 3, 27 ± 2, and 35 ± 3%; BG = 80, 300, and 600 mg/dl, respectively). The insulin component of GIK promotes cardioprotection by KATP channel activation. However, glucose decreases KATP channel activity, and this effect predominates when hyperglycemia is present before ischemia

Adenosine Type 1 (A ) Receptors Mediate Protection Against Myocardial 1 Infarction Produced by Chronic, Intermittent Ingestion of Ethanol in Dogs

Background: Chronic consumption of small amounts of ethanol protects myocardium from ischemic injury. We tested the hypothesis that adenosine type 1 (A1) receptors mediate these beneficial effects. Methods: Dogs (n=37) were fed with ethanol (1.5 g/kg) or water mixed with dry food twice per day for 12 weeks, fasted overnight before experimentation, and instrumented for measurement of hemodynamics. Dogs received intravenous drug vehicle (50% polyethylene glycol in 0.1 N sodium hydroxide and 0.9% saline over 15 min) or the selective A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 0.8 mg/kg over 15 min) and were subjected to a 60 min coronary artery occlusion followed by 3 h of reperfusion. Myocardial infarct size and transmural coronary collateral blood flow were measured with triphenyltetrazolium chloride staining and radioactive microspheres, respectively. Results: The area at risk (AAR) for infarction was similar between groups. Pretreatment with ethanol significantly reduced infarct size to 13±2% (n=7) of the AAR as compared to control experiments (26±2%; n=7). DPCPX abolished the protective effects of ethanol pretreatment (30±3%; n=7) but had no effect in dogs that did not receive ethanol (25±2%; n=7). No differences in transmural coronary collateral blood flow were observed between groups. Conclusions: The present findings indicate that chronic ingestion of small amounts of ethanol produces myocardial protection that persists after the discontinuation of ethanol. The results indicate that A1 receptors mediate ethanol-induced preconditioning in dogs independent of alterations in systemic hemodynamics or coronary collateral blood flow