Decay Constants and Semileptonic Form Factors of Pseudoscalar Mesons

A relativistic constituent quark model is adopted to give an unified description of the leptonic and semileptonic decays of pseudoscalar mesons (\pi, K, D, D_s, B, B_s). The calculated leptonic decay constants and form factors are found to be in good agreement with available experimental data and the results of other approaches. Eventually, the model is found to reproduce the scaling behaviours of spin-flavor symmetry in the heavy-quark limit.Comment: 5 pages LaTeX; based on talk given at the "QFTHEP '99 Workshop", Moscow, May 27- June 2, 199

The semileptonic form factors of B and D mesons in the Quark Confinement Model

The form factors of the weak currents, which appear in the semileptonic decays of the heavy pseudoscalar mesons, are calculated within the quark confinement model by taking into account, for the first time, the structure of heavy meson vertex and the finite quark mass contribution in the heavy quark propagators. The results are in quite good agreement with the experimental data.Comment: 12 pages LaTeX (elsart.sty) + 3 figure

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

Phenomenological Bounds on B to Light Semileptonic Form Factors

The form factors for the weak currents between B and light mesons are studied by relating them to the corresponding D form factors at q^2_{max} according to HQET, by evaluating them at q^2=0 by QCD sum rules, and by assuming a polar q^2 dependence. The results found are consistent with the information obtained from exclusive non-leptonic two-body decays and, with the only exception of A_1, with lattice calculations.Comment: 8 LaTeX pages + 2 figures. Will appear in Mod. Phys. Lett.

A Matrix Approach to Numerical Solution of the DGLAP Evolution Equations

A matrix-based approach to numerical integration of the DGLAP evolution equations is presented. The method arises naturally on discretisation of the Bjorken x variable, a necessary procedure for numerical integration. Owing to peculiar properties of the matrices involved, the resulting equations take on a particularly simple form and may be solved in closed analytical form in the variable t=ln(alpha_0/alpha). Such an approach affords parametrisation via data x bins, rather than fixed functional forms. Thus, with the aid of the full correlation matrix, appraisal of the behaviour in different x regions is rendered more transparent and free of pollution from unphysical cross-correlations inherent to functional parametrisations. Computationally, the entire programme results in greater speed and stability; the matrix representation developed is extremely compact. Moreover, since the parameter dependence is linear, fitting is very stable and may be performed analytically in a single pass over the data values.Comment: 13 pages, no figures, typeset with revtex4 and uses packages: acromake, amssym

Tackling dysfunction of mitochondrial bioenergetics in the brain

Oxidative phosphorylation (OxPhos) is the basic function of mitochondria, although the landscape of mitochondrial functions is continuously growing to include more aspects of cellular homeostasis. Thanks to the application of -omics technologies to the study of the OxPhos system, novel features emerge from the cataloging of novel proteins as mitochondrial thus adding details to the mitochondrial proteome and defining novel metabolic cellular interrelations, especially in the human brain. We focussed on the diversity of bioenergetics demand and different aspects of mitochondrial structure, functions, and dysfunction in the brain. Definition such as ‘mitoexome’, ‘mitoproteome’ and ‘mitointeractome’ have entered the field of ‘mitochondrial medicine’. In this context, we reviewed several genetic defects that hamper the last step of aerobic metabolism, mostly involving the nervous tissue as one of the most prominent energy-dependent tissues and, as consequence, as a primary target of mitochondrial dysfunction. The dual genetic origin of the OxPhos complexes is one of the reasons for the complexity of the genotype-phenotype correlation when facing human diseases associated with mitochondrial defects. Such complexity clinically manifests with extremely heterogeneous symptoms, ranging from organ-specific to multisystemic dysfunction with different clinical courses. Finally, we briefly discuss the future directions of the multi-omics study of human brain disorders

Quantitative Characterization of α-Synuclein Aggregation in Living Cells through Automated Microfluidics Feedback Control

Aggregation of α-synuclein and formation of inclusions are hallmarks of Parkinson's disease (PD). Aggregate formation is affected by cellular environment, but it has been studied almost exclusively in cell-free systems. We quantitatively analyzed α-synuclein inclusion formation and clearance in a yeast cell model of PD expressing either wild-type (WT) α-synuclein or the disease-associated A53T mutant from the galactose (Gal)-inducible promoter. A computer-controlled microfluidics device regulated α-synuclein in cells by means of closed-loop feedback control. We demonstrated that inclusion formation is strictly concentration dependent and that the aggregation threshold of the A53T mutant is about half of the WT α-synuclein (56%). We chemically modulated the proteasomal and autophagic pathways and demonstrated that autophagy is the main determinant of A53T α-synuclein inclusions’ clearance. In addition to proposing a technology to overcome current limitations in dynamically regulating protein expression levels, our results contribute to the biology of PD and have relevance for therapeutic applications