Why quarks cannot be fundamental particles

Many reasons why quarks should be considered composite particles are found in the book Preons by D'Souza and Kalman. One reason not found in the book is that all the quarks except for the u quark decay. The electron and the electron neutrino do not decay. A model of fundamental particles based upon the weak charge is presented.Comment: 3 pages - PDF file. to be published Proceedings of the 6th International Conference Hyperons, Charm and Beauty Hadron

The Kalman-Tran-D'Souza Model and the Semileptonic Decay Rates of Heavy Baryons

We present an investigation of the inclusive semileptonic decay widths of the heavy baryons Lambda_Q and Xi_Q, (Q=b,c) performed within a relativistic constituent quark model, formulated on the light-front. In a way conceptually similar to the deep-inelastic scattering case, the H_Q baryon inclusive width is expressed as the integral of the free Q-quark partial width multiplied by a bound-state factor related to the Q-quark distribution function in the H_Q. The non-perturbative meson structure is described through the quark-model wave functions, constructed via the Hamiltonian light-front formalism using as input the Kalman-Tran-D'Souza equal time wave functions. A link between spectroscopic quark models and the H_Q decay physics is obtained in this way. It is shown that the bound-state effects and the Fermi motion of the b-quark remarkably reduce the decay rate with respect to the free-quark result. Our predictions for the BR(Lambda_c ->X_s e nu_e) and BR(Lambda_b->X_c e nu_e) decays are in good agreement with existing data.Comment: 6 pages, latex, espcrc2.sty (included), 3 figures. The invited talk presented by C.S.K. at the 4-th International Conference on Hyperons, Charm and Beauty Hadrons, Valencia, June 27-30, 200

Hyperons, Charm and Beauty Hadrons

editor del volume dei proceedings. della conferenza (v. titolo) tenuta a Genova in giugno 199

Atrial fFibrillation and obesity: reverse remodeling of atrial substrate with weight reduction

Objectives This study sought to evaluate the effect of weight loss on the atrial substrate for atrial fibrillation (AF). Background Whether weight loss can reverse the atrial substrate of obesity is not known. Methods Thirty sheep had sustained obesity induced by ad libitum calorie-dense diet over 72 weeks. Animals were randomized to 3 groups: sustained obesity and 15% and 30% weight loss. The animals randomized to weight loss underwent weight reduction by reducing the quantity of hay over 32 weeks. Eight lean animals served as controls. All were subjected to the following: dual-energy x-ray absorptiometry, echocardiogram, cardiac magnetic resonance, electrophysiological study, and histological and molecular analyses (fatty infiltration, fibrosis, transforming growth factor β1, and connexin 43). Results Sustained obesity was associated with increased left atrium (LA) pressure (p < 0.001), inflammation (p < 0.001), atrial transforming growth factor β1 protein (p < 0.001), endothelin-B receptor expression (p = 0.04), atrial fibrosis (p = 0.01), epicardial fat infiltration (p < 0.001), electrophysiological abnormalities, and AF burden (p = 0.04). Connexin 43 expression was decreased in the obese group (p = 0.03). In this obese ovine model, 30% weight reduction was associated with reduction in total body fat (p < 0.001), LA pressure (p = 0.007), inflammation (p < 0.001), endothelin-B receptor expression (p = 0.01), atrial fibrosis (p = 0.01), increase in atrial effective refractory period (cycle length: 400 and 300 ms; p < 0.001), improved conduction velocity (cycle length: 400 and 300 ms; p = 0.01), decreased conduction heterogeneity (p < 0.001), and decreased AF inducibility (p = 0.03). Weight loss was associated with a nonsignificant reduction in epicardial fat infiltration in posterior LA (p = 0.34). Conclusions Weight loss in an obese ovine model is associated with structural and electrophysiological reverse remodeling and a reduced propensity for AF. This provides evidence for the direct role of obesity in AF substrate and the role of weight reduction in patients with AF.Rajiv Mahajan, Dennis H. Lau, Anthony G.Brooks, Nicholas J. Shipp, John P.M.Wood, Jim Manavis ... et al

Um sistema de controle da produção para a manufatura celular parte I: sistema de apoio à decisão para a elaboração do programa mestre de produção A production control system to the cellular manufacturing part I: decision support system for elaborating the master production scheduling

Este artigo e mais o artigo Parte II (Emissão de Ordens e Programação de Operações) fazem parte de um trabalho que visa integrar todas as atividades de programação da produção dentro do contexto de um Sistema de Controle da Produção, concebido para operar na manufatura celular semi-repetitiva. Para deixarmos claro o que entendemos por manufatura celular semi-repetitiva fazemos uma classificação dos sistemas de produção e uma taxonomia da manufatura celular. O sistema proposto foi concebido e implementado computacionalmente em 3 módulos (nível de produto final, de componentes e de operações). O primeiro é tratado neste artigo (Parte I), enquanto que outros dois módulos são tratados no outro artigo (Parte II).<br>This paper and that of Part II (ordering system and operations scheduling) aims to integrate all production scheduling activities in a semi-repetitive cellular manufacturing environment. With the aim of clarifying what we mean by semi-repetitive cellular manufacturing, we have made a production systems classification and a cellular manufacturing taxonomy. The proposed system was conceptualized and computationally implemented in three modules (product, component and operation levels). The first level is treated in this paper and the other two are treated in the Part II