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Infectious diseases caused by bacteria, viruses, or parasites are the major causes of mortality and economic losses in commercial aquaculture. Some pathologies, especially those of bacterial origin, can be treated with commercially available drugs, while others are poorly managed. In fact, despite having been recognized as a useful preventive measure, no effective vaccination against many economically relevant diseases exist yet, such as for viral and parasitic infections.
Muscle dystrophy is a muscle disease that leads to a progressive loss of muscle mass and a weakened musculoskeletal system in accordance with age of onset, severity, and the group of muscles affected.
Magnesium (Mg) is a mineral acting as cofactor of more than 300 enzymes. Mg in farm animals’ is recommended to avoid Mg deficiency, ensure adequate growth and health maintenance. Further, Mg supplementation above the estimated minimum requirements is the best practice to improve farm animals’ performances (fertility and yield) and food products’ quality. In human nutrition, sub-optimal Mg intake has several implications in bone development, muscle function and health maintenance.
Transient receptor potential (TRP) channels have emerged as key molecular identities in the sensory transduction of pain-producing stimuli. The ability of nociceptors to behave as noxious stimuli detectors relies on the presence of specialized transducing molecules at their peripheral nerve terminals capable of transforming the harmful physical (thermal and mechanical) and chemical stimuli into generator potentials. Upon nerve terminal stimulation, the output signal conveying to the central nervous system depends on the properties of transducer channels which produce generator potentials. Voltage-gated channels subsequently translate it into action potential firing. Nociceptive TRP channels are among the most studied transducer channels expressed in nociceptors and play a pivotal role in the study of pain.
Protease-activated receptors (PARs) are a class of G protein-coupled receptors (GPCRs) with a unique mechanism of activation, prompted by a proteolytic cleavage in their N-terminal domain that uncovers a tethered ligand, which binds and stimulates the same receptor.
Aquaporins (AQPs) are a family of membrane water channel proteins that control osmotically-driven water transport across cell membranes. Recent studies have focused on the assessment of fluid flux regulation in relation to the biological processes that maintain mesenchymal stem cell (MSC) physiology. In particular, AQPs seem to regulate MSC proliferation through rapid regulation of the cell volume. Furthermore, several reports have shown that AQPs play a crucial role in modulating MSC attachment to the extracellular matrix, their spread, and migration. This review aims to describe the recent findings on AQPs role in MSCs physiology taking into account their reflex for potential applicatio in regenerative medicine.
Over the last decade, many regular physical activity studies with large prospective cohorts have been conducted. Taken together, more than a million subjects have been included in these exercise studies. The risk of morbidity and mortality has been reduced by 30% to 40% as a result of exercise. These risk reductions hold true for many diseases, as well as for prevention and rehabilitation. Physical activity has also been in the treatment of many diseases, such as cardiopulmonary, metabolic or neurologic/psychiatric diseases, all with positive results.
Intracellular calcium (Ca2+) is an important second messenger that regulates multiple cellular functions, such as synaptic plasticity, action potentials, and learning and memory. Ca2+ dyshomeostasis, on the other hand, contributes to detrimental mechanisms such as necrosis, apoptosis, autophagy deficits, and neurodegeneration. Perturbations in intracellular Ca2+ are involved in many neurodegenerative diseases including Alzheimer's disease (AD), Parkinson’s disease, and Huntington’s disease. Ca2+ dyshomeostasis is an early event in the AD timeline. Ca2+ dysregulation in AD comes as a result of hyperactivity of Ca2+ channels in the plasma membrane and intracellular compartments. It does not seem to be restricted to neurons, but rather is a global phenomenon that affects many cell types in the brain.
Inflammatory bowel disease (IBD) is a chronic inflammation of the gastrointestinal tract (GIT), including Crohn’s disease (CD) and ulcerative colitis (UC), which differ in the location and lesion extensions. Both diseases are associated with microbiota dysbiosis, with a reduced population of butyrate-producing species, abnormal inflammatory response, and micronutrient deficiency (e.g., vitamin D hypovitaminosis). Vitamin D (VitD) is involved in immune cell differentiation, gut microbiota modulation, gene transcription, and barrier integrity. Vitamin D receptor (VDR) regulates the biological actions of the active VitD (1α,25-dihydroxyvitamin D3), and is involved in the genetic, environmental, immune, and microbial aspects of IBD. VitD deficiency is correlated with disease activity and its administration targeting a concentration of 30 ng/mL may have the potential to reduce disease activity. Moreover, VDR regulates functions of T cells and Paneth cells and modulates release of antimicrobial peptides in gut microbiota-host interactions. Meanwhile, beneficial microbial metabolites, e.g., butyrate, upregulate the VDR signaling.