Salmonella enterica in Alberta Slaughter Hogs

Cecal samples were collected and cultured to determine the occurrence of Salmonella spp. in Alberta slaughter hogs. Salmonella enterica subsp. enterica was recovered from 211/602 samples yielding 282 individual isolates distributed among 37 serotypes. The 5 most common serotypes (California, lnfantis, Derby, Mbandanka and Worthington) comprised 68.4% of all isolates. Resistance to tetracycline, streptomycin, and sulfamethoxazole, were commonly identified. Resistance to 5 or more antibiotics was noted in 9.6% of all isolates, and only in serotypes Agona, California, Derby, Typhimurium var. Copenhagen DTl 04, and Worthington. This study has shown that 35% of Alberta slaughter hogs carry S. enterica subsp. enterica. Resistance by Salmonella spp. isolates to streptomycin, sulfamethoxazole and tetracycline, singly or in combination, was relatively frequent but multi-resistant isolates were less common

Infinite Nuclear Matter on the Light Front: Nucleon-Nucleon Correlations

A relativistic light front formulation of nuclear dynamics is developed and applied to treating infinite nuclear matter in a method which includes the correlations of pairs of nucleons: this is light front Brueckner theory. We start with a hadronic meson-baryon Lagrangian that is consistent with chiral symmetry. This is used to obtain a light front version of a one-boson-exchange nucleon-nucleon potential (OBEP). The accuracy of our description of the nucleon-nucleon (NN) data is good, and similar to that of other relativistic OBEP models. We derive, within the light front formalism, the Hartree-Fock and Brueckner Hartree-Fock equations. Applying our light front OBEP, the nuclear matter saturation properties are reasonably well reproduced. We obtain a value of the compressibility, 180 MeV, that is smaller than that of alternative relativistic approaches to nuclear matter in which the compressibility usually comes out too large. Because the derivation starts from a meson-baryon Lagrangian, we are able to show that replacing the meson degrees of freedom by a NN interaction is a consistent approximation, and the formalism allows one to calculate corrections to this approximation in a well-organized manner. The simplicity of the vacuum in our light front approach is an important feature in allowing the derivations to proceed. The mesonic Fock space components of the nuclear wave function are obtained also, and aspects of the meson and nucleon plus-momentum distribution functions are computed. We find that there are about 0.05 excess pions per nucleon.Comment: 39 pages, RevTex, two figure

Light-Front Bethe-Salpeter Equation

A three-dimensional reduction of the two-particle Bethe-Salpeter equation is proposed. The proposed reduction is in the framework of light-front dynamics. It yields auxiliary quantities for the transition matrix and the bound state. The arising effective interaction can be perturbatively expanded according to the number of particles exchanged at a given light-front time. An example suggests that the convergence of the expansion is rapid. This result is particular for light-front dynamics. The covariant results of the Bethe-Salpeter equation can be recovered from the corresponding auxiliary three-dimensional ones. The technical procedure is developed for a two-boson case; the idea for an extension to fermions is given. The technical procedure appears quite practicable, possibly allowing one to go beyond the ladder approximation for the solution of the Bethe-Salpeter equation. The relation between the three-dimensional light-front reduction of the field-theoretic Bethe-Salpeter equation and a corresponding quantum-mechanical description is discussed.Comment: 42 pages, 5 figure

Teleparallel formalism of galilean gravity

A pseudo-Riemannian manifold is introduced, with light-cone coordinates in (4+1) dimensional space-time, to describe a Galilei covariant gravity. The notion of 5-bein and torsion are developed and a galilean version of teleparallelism is constructed in this manifold. The formalism is applied to two spherically symmetric configurations. The first one is an ansatz which is inferred by following the Schwarzschild solution in general relativity. The second one is a solution of galilean covariant equations. In addition, this Galilei teleparallel approach provides a prescription to couple the 5-bein field to the galilean covariant Dirac field.Comment: 10 page

Defective complex I assembly due to C20orf7 mutations as a new cause of Leigh syndrome

Background: Leigh syndrome is an early onset, progressive, neurodegenerative disorder with developmental and motor skills regression. Characteristic magnetic resonance imaging abnormalities consist of focal bilateral lesions in the basal ganglia and/or the brainstem. The main cause is a deficiency in oxidative phosphorylation due to mutations in an mtDNA or nuclear oxidative phosphorylation gene. Methods and results: A consanguineous Moroccan family with Leigh syndrome comprise 11 children, three of which are affected. Marker analysis revealed a homozygous region of 11.5 Mb on chromosome 20, containing 111 genes. Eight possible mitochondrial candidate genes were sequenced. Patients were homozygous for an unclassified variant (p.P193L) in the cardiolipin synthase gene (CRLS1). As this variant was present in 20% of a Moroccan control population and enzyme activity was only reduced to 50%, this could not explain the rare clinical phenotype in our family. Patients were also homozygous for an amino acid substitution (p.L159F) in C20orf7, a new complex I assembly factor. Parents were heterozygous and unaffected sibs heterozygous or homozygous wild type. The mutation affects the predicted S-adenosylmethionine (SAM) dependent methyltransferase domain of C20orf7, possibly involved in methylation of NDUFB3 during the assembly process. Blue native gel electrophoresis showed an altered complex I assembly with only 30-40% of mature complex I present in patients and 70-90% in carriers. Conclusions: A new cause of Leigh syndrome can be a defect in early complex I assembly due to C20orf7 mutations

Prediction of ventricular arrhythmia in phospholamban p.Arg14del mutation carriers–reaching the frontiers of individual risk prediction

Aims: This study aims to improve risk stratification for primary prevention implantable cardioverter defibrillator (ICD) implantation by developing a new mutation-specific prediction model for malignant ventricular arrhythmia (VA) in phospholamban (PLN) p.Arg14del mutation carriers. The proposed model is compared to an existing PLN risk model. / Methods and results: Data were collected from PLN p.Arg14del mutation carriers with no history of malignant VA at baseline, identified between 2009 and 2020. Malignant VA was defined as sustained VA, appropriate ICD intervention, or (aborted) sudden cardiac death. A prediction model was developed using Cox regression. The study cohort consisted of 679 PLN p.Arg14del mutation carriers, with a minority of index patients (17%) and male sex (43%), and a median age of 42 years [interquartile range (IQR) 27-55]. During a median follow-up of 4.3 years (IQR 1.7-7.4), 72 (10.6%) carriers experienced malignant VA. Significant predictors were left ventricular ejection fraction, premature ventricular contraction count/24 h, amount of negative T waves, and presence of low-voltage electrocardiogram. The multivariable model had an excellent discriminative ability {C-statistic 0.83 [95% confidence interval (CI) 0.78-0.88]}. Applying the existing PLN risk model to the complete cohort yielded a C-statistic of 0.68 (95% CI 0.61-0.75). / Conclusion: This new mutation-specific prediction model for individual VA risk in PLN p.Arg14del mutation carriers is superior to the existing PLN risk model, suggesting that risk prediction using mutation-specific phenotypic features can improve accuracy compared to a more generic approach

Hexb enzyme deficiency leads to lysosomal abnormalities in radial glia and microglia in zebrafish brain development

Sphingolipidoses are severe, mostly infantile lysosomal storage disorders (LSDs) caused by defective glycosphingolipid degradation. Two of these sphingolipidoses, Tay Sachs and Sandhoff diseases, are caused by β-Hexosaminidase (HEXB) enzyme deficiency, resulting in ganglioside (GM2) accumulation and neuronal loss. The precise sequence of cellular events preceding, and leading to, neuropathology remains unclear, but likely involves inflammation and lysosomal accumulation of GM2 in multiple cell types. We aimed to determine the consequences of Hexb activity loss for different brain cell types using zebrafish. Hexb deficient zebrafish (hexb−/− ) showed lysosomal abnormalities already early in development both in radial glia, which are the neuronal and glial progenitors, and in microglia. Additionally, at 5 days postfertilization, hexb−/− zebrafish showed reduced locomotor activity. Although specific oligosaccharides accumulate in the adult brain, hexb−/− ) zebrafish are viable and apparently resistant to Hexb deficiency. In all, we identified cellular consequences of loss of Hexb enzyme activity during embryonic brain development, showing early effects on glia, which possibly underlie the behavioral aberrations. Hereby, we identified clues into the contribution of non-neuronal lysosomal abnormalities in LSDs affecting the brain and provide a tool to further study what underlies the relative resistance to Hexb deficiency in vivo