Mg(OH)2 Recovery from Real Bitterns: a Proof of Concept at Pilot Scale

Water, energy, and minerals are fundamental pillars for the future of humankind. Sustainable and renewable productive processes and resources are the only possibility to face the continuously growing global population and high living standards requirements. The present work introduces a proof of concept for the pilot scale production of magnesium hydroxide, Mg(OH)2, from waste saltworks bitterns located in the district of Trapani, Italy. Mg(OH)2 was produced by adopting a proprietary “Magnesium Crystals Granulometry Controlled Reactor”, Mg-CGCR. The influence of several parameters was investigated on Mg(OH)2 suspensions and powders characteristics: (i) the bittern flow rate, (ii) alkaline sodium hydroxide, NaOH, concentrations solutions (adopted as the precipitant agent) and (iii) the final suspension pH value (stoichiometric or OH- excess amounts). A Mg2+ recovery >99 % can be achieved thanks to the adoption of a product recycling strategy in the reactor. Furthermore, highly pure Mg(OH)2 powders, addressed by cationic purity, were synthesized. Results demonstrate the possibility of producing highly pure Mg(OH)2 products from waste-concentrated saline solutions, thus turning waste into valuable compounds

Redox regulation of cellular stress response in multiple sclerosis

Multiple sclerosis (MS) is an autoimmune-mediated neurodegenerative disease with characteristic foci of inflammatory demyelination in the brain, spinal cord, and optic nerves. Recent studies have demonstrated not only that axonal damage and neuronal loss are significant pathologic components of MS, but that this neuronal damage is thought to cause the permanent neurologic disability often seen in MS patients. Emerging finding suggests that altered redox homeostasis and increased oxidative stress, primarily implicated in the pathogenesis of MS, are a trigger for activation of a brain stress response. Relevant to maintenance of redox homeostasis, integrated mechanisms controlled by vitagenes operate in brain in preserving neuronal survival during stressful conditions. Vitagenes encode for heat shock proteins (Hsp) Hsp32, Hsp70, the thioredoxin and the sirtuin protein systems. In the present study we assess stress response mechanisms in the CSF, plasma and lymphocytes of control patients compared to MS patients. We found that the levels of vitagenes Hsp72, Hsc70, HO-1, as well as oxidative stress markers carbonyls and hydroxynonenals were significantly higher in the blood and CSF of MS patients than in control patients. In addition, an increased expression of Trx and sirtuin 1, together with a decrease in the expression of TrxR were observed. Our data strongly support a pivotal role for redox homeostasis disruption in the pathogenesis of MS and, consistently with the notion that new therapies that prevent neurodegeneration through nonimmunomodulatory mechanisms can have a tremendous potential to work synergistically with current MS therapies, unravel important targets for new cytoprotective strategies