Magnesium (Mg) is involved in the regulation of metabolism and in the maintenance of the homeostasis of all the tissues, including the brain, where it harmonizes nerve signal transmission and preserves the integrity of the blood–brain barrier. Mg deficiency contributes to systemic low-grade inflammation, the common denominator of most diseases. In particular, neuroinflammation is the hallmark of neurodegenerative disorders. Starting from a rapid overview on the role of magnesium in the brain, this narrative review provides evidences linking the derangement of magnesium balance with multiple sclerosis, Alzheimer’s, and Parkinson’s diseases.

Beyond their fundamental role in hemostasis, platelets importantly contribute to other processes aimed at maintaining homeostasis. Indeed, platelets are a natural source of growth factors and also release many other substances—such as fibronectin, vitronectin, sphingosine 1-phosphate—that are important in maintaining healthy tissues, and ensuring regeneration and repair. Despite rare thrombotic events have been documented in astronauts, somein vivoandin vitrostudies demonstrate that microgravity affects platelet’s number and function, thus increasing the risk of hemorrhages and contributing to retard wound healing. Here we provide an overview about events linking platelets to the impairment of wound healing in space, also considering, besides weightlessness, exposure to radiation and psychological stress. In the end we discuss the possibility of utilizing platelet rich plasma as a tool to treat skin injuries eventually occurring during space missions.

Infections of orthopedic implants are associated with high morbidity. The emergence of antibiotic resistant strains and the tendency of microbes to form biofilms on orthopedic devices prompt the individuation of novel antimicrobial agents. Silver nanoparticles represent an interesting alternative, but their effects on bone cells need to be clarified. We focused on osteoblast-like cells and on bone marrow-mesenchymal stem cells and found that these cells are rather resistant to the cytotoxic effects of silver nanoparticles, with a half maximal inhibitory concentration around 25 µg/mL as detected by MTT assay. Within a month of treatment, osteoblast-like cells adapt to the presence of the nanoparticles by upregulating hsp70 as shown by western blot. Hsp70 overexpression correlates with the restoration of normal cell proliferation. No alterations in the extent and time requirements were detected in mesenchymal stem cell induced to differentiate in osteoblasts in the presence of silver nanoparticles. Because the concentrations of silver nanoparticles which show antimicrobial activity are lower than those exerting toxic effects on bone-forming cells in vitro, we suggest that silver nanoparticles might represent a challenging tool to fight infections in orthopedic implants.

Reduced blood flow, as occurring in ischemia or resulting from exposure to microgravity such as encountered in space flights, induces a decrease in the level of shear stress sensed by endothelial cells forming the inner part of blood vessels. In the present study, we use a microvasculature-on-a-chip device in order to investigate in vitro the effect of such a reduction in shear stress on shear-adapted endothelial cells. We find that, within 1 h of exposition to reduced wall shear stress, human umbilical vein endothelial cells undergo reorganization of their actin skeleton with a decrease in the number of stress fibers and actin being recruited into the cells’ peripheral band, indicating a fairly fast change in the cells’ phenotype due to altered flow.

Background: Magnesium deficiency contributes to atherogenesis partly by promoting the dysfunction of endothelial cells, which are critical in vascular homeostasis and diseases. Since EDF-1 and PPARγ regulate crucial endothelial activities, we investigated the modulation of these proteins involved in lipogenesis as well the deposition of lipids in human endothelial cells cultured in different concentrations of magnesium. Methods: Human endothelial cells from the umbilical vein were cultured in medium containing from 0.1 to 5 mM magnesium for 24 h. The levels of EDF-1 and PPARγ were visualized by Western blot. Reactive oxygen species (ROS) were measured by DCFDA. Lipids were detected after O Red Oil staining. Results: Magnesium deficiency leads to the accumulation of ROS which upregulate EDF-1. Further, PPARγ is increased after culture in low magnesium, but independently from ROS. Moreover, lipids accumulate in magnesium-deficient cells. Conclusions: Our results suggest that magnesium deficiency leads to the deposition of lipids by inducing EDF-1 and PPARγ. The increase in intracellular lipids might be interpreted as an adaptive response of endothelial cells to magnesium deficiency.