Oxidative stress and muscle homeostasis

Purpose of review The term oxidative stress is often used to indicate a condition in which the accumulation of reactive oxygen species is considered just damaging. We will discuss both the physiological and pathological role of oxidative stress on skeletal muscle homeostasis and function, and how oxidative stress can activates opposite signaling molecule to regulate gene and protein expression to guarantee muscle adaptation and to trigger a pathological condition. Recent findings Emerging evidences have assigned a critical role to oxidative stress in muscle homeostasis and in the physiopathology of skeletal muscle, suggesting that reactive oxygen species are not merely damaging agent inflicting random destruction to the cell structure and function, but useful signaling molecules to regulate growth, proliferation, differentiation, and adaptation, at least within physiological concentration. Summary The role of oxidative stress on muscle homeostasis is quite complex. It is clear that transiently increased levels of oxidative stress might reflect a potentially health promoting process, whereas an uncontrolled accumulation of oxidative stress might have pathological implication. Additional work is, therefore, necessary to understand and define precisely whether the manipulation of the redox balance represents a useful approach in the design of therapeutic strategies for muscle diseases.PURPOSE OF REVIEW: The term oxidative stress is often used to indicate a condition in which the accumulation of reactive oxygen species is considered just damaging. We will discuss both the physiological and pathological role of oxidative stress on skeletal muscle homeostasis and function, and how oxidative stress can activates opposite signaling molecule to regulate gene and protein expression to guarantee muscle adaptation and to trigger a pathological condition. RECENT FINDINGS: Emerging evidences have assigned a critical role to oxidative stress in muscle homeostasis and in the physiopathology of skeletal muscle, suggesting that reactive oxygen species are not merely damaging agent inflicting random destruction to the cell structure and function, but useful signaling molecules to regulate growth, proliferation, differentiation, and adaptation, at least within physiological concentration. SUMMARY: The role of oxidative stress on muscle homeostasis is quite complex. It is clear that transiently increased levels of oxidative stress might reflect a potentially health promoting process, whereas an uncontrolled accumulation of oxidative stress might have pathological implication. Additional work is, therefore, necessary to understand and define precisely whether the manipulation of the redox balance represents a useful approach in the design of therapeutic strategies for muscle diseases

Hunting for heavy composite Majorana neutrinos at the LHC

We investigate the search for heavy Majorana neutrinos stemming from a composite model scenario at the upcoming LHC Run II at a center of mass energy of 13 TeV. While previous studies of the composite Majorana neutrino were focussed on gauge interactions via magnetic type transition coupling between ordinary and heavy fermions (with mass $m^*$) here we complement the composite model with contact interactions at the energy scale $\Lambda$ and we find that the production cross sections are dominated by such contact interactions by roughly two/three orders of magnitude. This mechanism provides therefore very interesting rates at the prospected luminosities. We study the same sign di-lepton and di-jet signature ($pp \to \ell\ell jj$) and perform a fast detector simulation based on Delphes. We compute 3$\sigma$ and 5$\sigma$ contour plots of the statistical significance in the parameter space ($\Lambda,m^*$). We find that the potentially excluded regions at $\sqrt{s} =13$ TeV are quite larger than those excluded so far at Run I considering searches with other signatures.Comment: 14 pages, 9 figures, Minor comments and few references added. Version accepted by the European Physical Journal C (EPJC

Searching Doubly Charged Leptons at Present and Future Colliders

The production at the LHC of exotic excited leptons of charge $Q = +2e$ is considered. Such states are predicted in composite models with extended isospin multiplets ($I_{W}=1$ and $I_{W}=3/2$). The coupling among these doubly charged leptons and Standard Model fermions may occurs either via gauge or contact interactions. In the former case the decay channels are more constrained. We study the production cross section at the LHC of $L^{++}$ ($pp \rightarrow L^{++} \, \ell^{-}$) and focus on the leptonic signature deriving from the subsequent decays $L^{++} \rightarrow W^{+} \ell^{+} \rightarrow \ell^{+} \ \ell^{+} \, \nu_l $. The invariant mass distribution of the like-sign dilepton exhibits a sharp end-point corresponding to excited doubly charged lepton mass$m^{*}$. A preliminary study for the production of doubly charged leptons at the future linear colliders, by considering the process$e^{-} e^{-} \rightarrow L_{e}^{--} \, \nu_{e}$, is carried out. Both the contact and gauge interaction mechanisms are investigated and compared.Comment: 8 pages, 4 figures, submitted as a proceeding for the LC13 Conference (ECT*, Trento), updated bibliograph

Return to competition in a chronic low back pain runner: beyond a therapeutic exercise approach, a case report

Chronic low back pain (CLBP) is a disabling condition affecting both quality of life and performance in athletes. Several approaches have been proposed in the field of physiotherapy, manual therapy, physical exercise and counseling. None apparently is outdoing the other with the exception of trunk stability exercises in specific conditions. The present paper describes a clinical success in managing a CLBP runner affected by MRI documented disk herniation via dietary change. Dietary changes allowed our patient that had failed with previous standard therapeutic approaches, to regain an optimal pain-free condition. We advance the hypothesis that a visceral-autonomic concomitant or primary disturbance possibly generating mild gastrointestinal discomfort in CLBP patients should be ruled out as a possible cause of pain and disability at the somato-motor level

S-100a0 protein stimulates Ca2+ -induced Ca2+ release from isolated sarcoplasmic reticulum vesicles

AbstractS-100a0 protein, the αα-isoform of the S-100 family, stimulates Ca2+ -induced Ca2+ release from terminal cisternae isolated from rat skeletal muscle cells. The stimulatory effect of S-100a0 is maximal at ∼5 μM S-100a0 and half maximal at ∼0.1 μM S-100a0, at 1.8 μM free Ca2+ in the presence of 5 mM Mg2+ plus 0.1 M KCl. The effect of the protein on Ca2+ -induced Ca2+ release is completely inhibted by the calcium release blocker, ruthenium red

Transcription profile analysis of vastus lateralis muscle from patients with chronic fatigue syndrome.

Chronic fatigue syndrome (CFS) is a disabling condition characterized by unexplained chronic fatigue that impairs normal activities. Many body systems are affected and etiology has not yet been identified. In addition to immunological and psychological aspects, skeletal muscle symptoms are prominent in CFS patients. In an effort to establish which pathways might be involved in the onset and development of muscle symptoms, we used global transcriptome analysis to identify genes that were differentially expressed in vastus lateralis muscle of female and male CFS patients. We found that the expression of genes that play key roles in mitochondrial function and oxidative balance, including superoxide dismutase 2, were altered, as were genes involved in energy production, muscular trophism and fiber phenotype determination. Importantly, the expression of a gene encoding a component of the nicotinic cholinergic receptor binding site was reduced, suggesting impaired neuromuscular transmission. We argue that these major biological processes could be involved in and/or responsible for the muscle symptoms of CFS

Effects of acute and chronic low frequency electromagnetic field exposure on PC12 cells during neuronal differentiation.

The purpose of this study was to provide information about the in vitro neuritogenesis during cell exposure to extremely low frequency electromagnetic fields (ELF-EMFs) of different intensities and durations using pheochromocytoma-derived cell line (PC12 cells) as neuronal model.Proliferative rates and neuritogenesis were tested by colorimetric assay and morphological analysis, respectively; reactive oxygen species (ROS) levels and intracellular Ca(2+) variations monitored using single cell videomicroscopy.The long-lasting ELF-EMF exposure (0.1-1.0 mT) did not appear to significantly affect the biological response (proliferation and neuritogenesis). However, during the acute ELF-EMF exposure (30 min), in undifferentiated PC12 cells, there were increased ROS levels and decreased catalase activity, that, conversely, resulted increased after chronic exposure (7 days) at 1.0 mT. Acute exposure (0.1-1.0 mT) affected the spontaneous intracellular Ca(2+) variations in undifferentiated cells, in which basal intracellular Ca(2+) resulted increased after chronic exposure. In addition acute exposure affected cell response to a depolarizing agent, while basal membrane potential was not changed.Even if further studies remain necessary to identify the ROS/intracellular Ca(2+)cross-talking pathway activated by ELF-EMF exposure, we support the hypothesis that ROS and Ca(2+) could be the cellular "primum movens" of the ELF-EMF induced effects on biological systems