Selective removal and recovery of gallium and germanium from synthetic zinc refinery residues using biosorption and bioprecipitation.

The depletion of primary ores, the environmental concerns related to mining activities, and the need to promote circular economy has drawn attention to the recycling of metallic compounds. Bio-based technologies are suitable for metal recovery, as they operate under mild conditions (ambient temperature and pressure) and are ideal for treating low-concentration waters. This study compared the effectiveness of adsorption and precipitation for the removal and recovery of gallium, germanium and zinc. Adsorption of the metallic ions on elemental forms of sulfur (S0), selenium (Se0) and tellurium (Te0), both of chemical and biological sources, was tested. Biosorption onto elemental forms of S0bio, Se0bio and Te0bio effectively removed Ga and Zn. The highest removal efficiency (Õ²) was obtained for Ga onto the adsorbent Te0bio (69 ± 0.4%), with an adsorption capacity (q) of 74 mg Ga (g Te0bio)-1, followed by Zn (Õ² = 40 ± 0.7%) with 43 mg Zn (g Te0bio)-1. Precipitation with chemical and biogenic sulfide at different metal to sulfide (Me/S) ratios was also assessed. Biologically produced sulfide was more efficient for Ga and Zn compared to chemical sulfide. Precipitation with biogenic sulfide was efficient for the removal of Ga (Õ² = 59.9 ± 2.6%) and Zn (Õ² = 44.2 ± 3.0%). The lowest ratio between metal to sulfide (Me/S = 0.2) achieved higher zinc removal efficiencies, whereas gallium removal was more efficient at Me/S = 1.5. None of the tested methods allowed for recovery of Ge. Biosorption and bioprecipitation gave nevertheless high removal and recovery of Ga and Zn.

Inflammation-induced mTORC2-Akt-mTORC1 signaling promotes macrophage foam cell formation.

The transformation of macrophages into lipid-loaded foam cells is a critical and early event in the pathogenesis of atherosclerosis. Several recent reports highlighted that induction of TLR4 signaling promotes macrophage foam cell formation; however, the underlying molecular mechanisms have not been clearly elucidated. Here, we found that the TLR4 mediated inflammatory signaling communicated with mTORC2-Akt-mTORC1 metabolic cascade in macrophage and thereby promoting lipid uptake and foam cell formation. Mechanistically, LPS treatment markedly upregulates TLR4 mediated inflammatory pathway which by activating mTORC2 induces Akt phosphorylation at serine 473 and that aggravate mTORC1 dependent scavenger receptors expression and consequent lipid accumulation in THP-1 macrophages. Inhibition of mTORC2 either by silencing Rictor expression or inhibiting its association with mTOR notably prevents LPS induced Akt activation, scavenger receptors expression, and macrophage lipid accumulation. Although suppression of mTORC1 expression by genetic knockdown of Raptor did not produce any significant change in Akt S473 phosphorylation, however, incubation with Akt activator in Rictor silenced cells failed to promote scavenger receptors expression and macrophage foam cell formation. Thus, present research explored the signaling pathway involved in inflammation-induced macrophage foam cells formation and therefore, targeting this pathway might be useful for preventing macrophage foam cell formation.