Duality for symmetric second rank tensors. II. The linearized gravitational field

The construction of dual theories for linearized gravity in four dimensions is considered. Our approach is based on the parent Lagrangian method previously developed for the massive spin-two case, but now considered for the zero mass case. This leads to a dual theory described in terms of a rank two symmetric tensor, analogous to the usual gravitational field, and an auxiliary antisymmetric field. This theory has an enlarged gauge symmetry, but with an adequate partial gauge fixing it can be reduced to a gauge symmetry similar to the standard one of linearized gravitation. We present examples illustrating the general procedure and the physical interpretation of the dual fields. The zero mass case of the massive theory dual to the massive spin-two theory is also examined, but we show that it only contains a spin-zero excitation.Comment: 20 pages, no figure

Multi-omics profiling of the impact of an Angiotensin (1-7)-expressing probiotic combined with exercise training in aged male rats

   Angiotensin (1-7) [Ang (1-7)] is an active heptapeptide of the non-canonical arm of the renin-angiotensin system that modulates molecular signaling pathways associated with vascular and cellular inflammation, vasoconstriction, hyperplasia and fibrosis. Pre-clinical evidence suggests that Ang (1-7) is a promising therapeutic target that may ameliorate physical and cognitive decline in prevalent age-related diseases, but its short half-life and low oral bioavailability reduce its applicability in clinical care. This study evaluated a genetically modified probiotic (GMP) that expresses Ang (1-7) as a potential approach to overcome these barriers. We gave this GMP with and without moderate exercise training and evaluated cross-tissue (prefrontal cortex, hippocampus, colon, liver and skeletal muscle) multi-omics responses in aged male rats. After 12-weeks of intervention, the GMP and exercise training distinctly altered fecal microbiome composition. The GMP altered 3 generas while exercise training enhanced beta-diversity. Exercise training also significantly altered neuro-remodeling, inflammation and circadian rhythm gene expression on relevant regulatory tissues. </p

N-terminal amino acid sequences of the major outer membrane proteins from a Neisseria meningitidis group B strain isolated in Brazil

The four dominant outer membrane proteins (46, 38, 33 and 28 kDa) were detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) in a semi-purified preparation of vesicle membranes of a Neisseria meningitidis (N44/89, B:4:P1.15:P5.5,7) strain isolated in Brazil. The N-terminal amino acid sequence for the 46 kDa and 28 kDa proteins matched that reported by others for class 1 and 5 proteins respectively, whereas the sequence (25 amino acids) for the 38 kDa (class 3) protein was similar to class 1 meningococcal proteins. The sequence for the 33 kDa (class 4) was unique and not homologous to any known protein

Molecular and cellular events in alcohol-induced muscle disease

Alcohol consumption induces a dose-dependent noxious effect on skeletal muscle, leading to progressive functional and structural damage of myocytes, with concomitant reductions in lean body mass. Nearly half of high-dose chronic alcohol consumers develop alcoholic skeletal myopathy. The pathogenic mechanisms that lie between alcohol intake and loss of muscle tissue involve multiple pathways, making the elucidation of the disease somewhat difficult. This review discusses the recent advances in basic and clinical research on the molecular and cellular events involved in the development of alcohol-induced muscle disease. The main areas of recent research interest on this field are as follows: (i) molecular mechanisms in alcohol exposed muscle in the rat model; (ii) gene expression changes in alcohol exposed muscle; (iii) the role of trace elements and oxidative stress in alcoholic myopathy; and (iv) the role of apoptosis and preapoptotic pathways in alcoholic myopathy. These aforementioned areas are crucial in understanding the pathogenesis of this disease. For example, there is overwhelming evidence that both chronic alcohol ingestion and acute alcohol intoxication impair the rate of protein synthesis of myofibrillar proteins, in particular, under both postabsorptive and postprandial conditions. Perturbations in gene expression are contributory factors to the development of alcoholic myopathy, as ethanol-induced alterations are detected in over 400 genes and the protein profile (i.e., the proteome) of muscle is also affected. There is supportive evidence that oxidative damage is involved in the pathogenesis of alcoholic myopathy. Increased lipid peroxidation is related to muscle fibre atrophy, and reduced serum levels of some antioxidants may be related to loss of muscle mass and muscle strength. Finally, ethanol induces skeletal muscle apoptosis and increases both pro- and antiapoptotic regulatory mechanisms