Copper Recovery From Ammonia Solutions Through Electro-Electrodialysis (EED).

Alkaline leaching with highly selective ammoniacal complexing agents is an interesting alternative for the treatment of copper concentrates. This treatment is beneficial for copper recovery because it allows the formation of soluble amines complexes, with cupric tetramine (  Cu ( NH 3 ) 4 2 + ) being the most stable. In order to suppress the unit operation of solvent extraction (SX) and move directly to the electrochemical process, an electro-electrodialysis (EED) process using ion exchange membranes to obtain copper is proposed. The study contemplates the operation with synthetic ammonia solutions containing copper at different concentrations and current density under standard conditions of pressure and temperature. The presented data demonstrate that the concentration of copper in the solution and the excess of ammonia are inversely related to the efficiency of the current and the voltage of the cell, whereas an increase in current density causes an increase in current efficiency, contrary to what happens in sulfuric systems.

Teriflunomide treatment for multiple sclerosis modulates T cell mitochondrial respiration with affinity-dependent effects.

Interference with immune cell proliferation represents a successful treatment strategy in T cell-mediated autoimmune diseases such as rheumatoid arthritis and multiple sclerosis (MS). One prominent example is pharmacological inhibition of dihydroorotate dehydrogenase (DHODH), which mediates de novo pyrimidine synthesis in actively proliferating T and B lymphocytes. Within the TERIDYNAMIC clinical study, we observed that the DHODH inhibitor teriflunomide caused selective changes in T cell subset composition and T cell receptor repertoire diversity in patients with relapsing-remitting MS (RRMS). In a preclinical antigen-specific setup, DHODH inhibition preferentially suppressed the proliferation of high-affinity T cells. Mechanistically, DHODH inhibition interferes with oxidative phosphorylation (OXPHOS) and aerobic glycolysis in activated T cells via functional inhibition of complex III of the respiratory chain. The affinity-dependent effects of DHODH inhibition were closely linked to differences in T cell metabolism. High-affinity T cells preferentially use OXPHOS during early activation, which explains their increased susceptibility toward DHODH inhibition. In a mouse model of MS, DHODH inhibitory treatment resulted in preferential inhibition of high-affinity autoreactive T cell clones. Compared to T cells from healthy controls, T cells from patients with RRMS exhibited increased OXPHOS and glycolysis, which were reduced with teriflunomide treatment. Together, these data point to a mechanism of action where DHODH inhibition corrects metabolic disturbances in T cells, which primarily affects profoundly metabolically active high-affinity T cell clones. Hence, DHODH inhibition may promote recovery of an altered T cell receptor repertoire in autoimmunity.