A coupled electrochemical process for schwertmannite recovery from acid mine drainage: Important roles of anodic reactive oxygen species and cathodic alkaline.

The increasing need for sustainable acid mine drainage (AMD) treatment has spurred much attention to strategic development of resource recovery. Along this line, we envisage that a coupled electrochemical system involving anodic Fe(II) oxidation and cathodic alkaline production will facilitate in situ synthesis of schwertmannite from AMD. Multiple physicochemical studies showed the successful formation of electrochemistry-induced schwertmannite, with its surface structure and chemical composition closely related to the applied current. A low current (e.g., 50 mA) led to the formation of schwertmannite having a small specific surface area (SSA) of 122.8 m2 g-1 and containing small amounts of -OH groups (formula Fe8O8(OH)4.49(SO4)1.76), whereas a large current (e.g., 200 mA) led to schwertmannite high in SSA (169.5 m2 g-1) and amounts of -OH groups (formula Fe8O8(OH)5.16(SO4)1.42). Mechanistic studies revealed that the reactive oxygen species (ROS)-mediated pathway, rather than the direct oxidation pathway, plays a dominant role in accelerating Fe(II) oxidation, especially at high currents. The abundance of •OH in the bulk solution, along with the cathodic production of OH-, were the key to obtaining schwertmannite with desirable properties. It was also found to function as a powerful sorbent in removal of arsenic species from the aqueous phase.

In Situ Reconstruction of Metal Oxide Cathodes for Ammonium Generation from High-Strength Nitrate Wastewater: Elucidating the Role of the Substrate in the Performance of Co3O4-x.

In situ electrochemical reconstruction is important for transition metal oxides explored as electrocatalysts for electrochemical nitrate reduction reactions (ENRRs). Herein, we report substantial performance enhancement of ammonium generation on Co, Fe, Ni, Cu, Ti, and W oxide-based cathodes upon reconstruction. Among them, the performance of a freestanding ER-Co3O4-x/CF (Co3O4 grown on Co foil subjected to electrochemical reduction) cathode was superior to its unreconstructed counterpart and other cathodes; e.g., an ammonium yield of 0.46 mmol h-1 cm-2, an ammonium selectivity of 100%, and a Faradaic efficiency of 99.9% were attained at -1.3 V in a 1400 mg L-1 NO3--N solution. The reconstruction behaviors were found to vary with the underlying substrate. The inert carbon cloth only acted as a supporting matrix for immobilizing Co3O4, without appreciable electronic interactions between them. A combination of physicochemical characterizations and theoretical modeling provided compelling evidence that the CF-promoted self-reconstruction of Co3O4 induced the evolution of metallic Co and the creation of oxygen vacancies, which promoted and optimized interfacial nitrate adsorption and water dissociation, thus boosting the ENRR performance. The ER-Co3O4-x/CF cathode performed well over wide ranges of pH and applied current and at high nitrate loadings, ensuring its high efficacy in treating high-strength real wastewater.

Photoinduced transformation of ferrihydrite in the presence of aqueous sulfite and its influence on the repartitioning of Cd.

The photoinduced transformation of ferrihydrite is an important process that can predict the geochemical cycle of Fe in anoxic environments as well as the fate of trace elements bonded to Fe minerals. We report that the photooxidation of sulfite by UV irradiation produces hydrated electrons (super-reductants), which significantly promote ferrihydrite reduction to Fe(II), and SO3•- (a moderate oxidant), enabling its further oxidation to more crystalline Fe(III) products. The experimental results show that the concentration of sulfite was key in influencing the rate and extent of surface-bound Fe(II) formation, which ultimately determined the distribution of individual products. For example, fitting of the Mössbauer spectroscopy data revealed that the relative abundances of mineral species after 8 h of treatment in the UV/sulfite systems were 41.9% lepidocrocite and 58.1% ferrihydrite at 2 mM SO32-; 41.8% goethite, 28.2% lepidocrocite, and 29.1% ferrihydrite at 5 mM SO32-; and 100% goethite at 10 mM SO32-. The combined results of the chemical speciation analysis and the Cd K-edge EXAFS characterization provided compelling evidence that Cd was firmly incorporated into the structure of newly formed minerals, particularly at high sulfite concentrations. These findings provide an understanding of the role of UV/sulfite in facilitating ferrihydrite transformation and promoting Cd stabilization in oxygen-deficit soils and aquatic environments.

Boosting the oxidative capacity of the Fe(0)/O2 system via an air-breathing cathode.

The corrosion of Fe(0) in the presence of O2 in nature can lead to the oxidation of organic compounds, but the efficiency is very limited. Herein, attempts were made to establish a galvanic system that separates the anodic Fe(0) oxidation reaction and the cathodic O2 reduction reaction using an air-breathing cathode. Compared with the chemical Fe(0)/O2 system, it exhibited a substantially higher capability of destroying a variety of pollutants, such as organic dyes (12 types), phenol, nitrobenzene, acetaminophen, phenol, and ethylenediaminetetraacetic acid. The degradation rate constant of a model dye (i.e., Rhodamine B) increased from 0.047 min-1 (chemical) to 1.412 min-1 (galvanic) under the passive air-breathing condition. The electric circuit design promoted Fe(0) dissolution to Fe(II) and triggered electron transfer that drives O2 reduction to H2O2, two important species responsible for the generation of HO• at high abundance. In addition, the galvanic Fe(0)/O2 system produces electricity while destroying pollutants. Tests with real Ni plating wastewater further demonstrated the capability of the system to oxidize complexed organics and phosphite. This study provides a new strategy for boosting the oxidative capacity of the Fe(0)/O2 system, which shows promise for acid wastewater treatment.

FTY720 induces ferroptosis and autophagy via PP2A/AMPK pathway in multiple myeloma cells.

AIMS: Multiple myeloma (MM) is the second hematological plasma cell malignany and sensitive to fingolimod (FTY720), a novel immunosuppressant. Previous study shows FTY720-induced apoptosis and autophagy can cause cell death in MM cells, however, the high death rate cannot fully be explained. The study aims to investigate further mechanism of how FTY720 kills MM cells. MATERIALS AND METHODS: Experiments are performed on 25 human primary cell samples and two MM cell lines by flow cytometry, fluorescence microscopy, and transmission electron microscopy. Expressions of relative factors are tested by qRT-PCR or western blot. KEY FINDINGS: Ferroptosis-specific inhibitors, deferoxamine mesylate (DFOM) and ferropstatin-1 (Fer-1), reverse FTY720-induced cell death in MM cells. Glutathione peroxidase 4 (GPX4) and soluble carrier family 7 member 11 (SLC7A11), key regulators of ferroptosis, are highly expressed in primary MM cells and can be decreased by FTY720 at the mRNA and protein level in MM cells. In addition, FTY720 induces other characteristic changes of ferroptosis. Furthermore, FTY720 can dephosphorylate AMP-activated protein kinase subunit ɑ (AMPKɑ) at the Thr172 site by activating protein phosphatase 2A (PP2A) and reduce the expression of phosphorylated eukaryotic elongation factor 2 (eEF2), finally cause MM cell death. Using LB-100, a PP2A inhibitor, AICAR, an agonist of AMPK, and bafilomycin A1 (Baf-A1), an autophagy inhibitor, we discover that FTY720 induces ferroptosis and autophagy through the PP2A/AMPK pathway, and ferroptosis and autophagy can reinforce each other. SIGNIFICANCE: These results provide a new perspective on the treatment of MM.

miR­144­3p inhibits the proliferation, migration and angiogenesis of multiple myeloma cells by targeting myocyte enhancer factor 2A.

Multiple myelomas (MM) are the second most common haematological malignancy, for which no curative treatments have been reported to date. MicroRNAs (miRNAs or miRs) have recently been shown to be involved in the proliferation of MM cells. However, the molecular mechanisms through which miRNAs regulate migration and angiogenesis in MM are poorly understood. Accordingly, the present study evaluated the role of miR­144­3p in MM. miR­144­3p exhibited a lower expression in patients with MM and in MM cell lines compared with normal cells (mononuclear cells derived from bone marrow). The transfection of miR­144­3p into MM cells inhibited proliferation, migration and angiogenesis, and induced cell cycle arrest and apoptosis compared to the control cells. Furthermore, miR­144­3p suppressed the transcription and translation of the myocyte enhancer factor 2A (MEF2A) gene and disrupted the expression of vascular endothelial growth factor. The knockdown of MEF2A significantly inhibited the proliferation, migration and angiogenesis of MM cells. However, the overexpression of MEF2A reversed these effects. On the whole, the findings of the present study demonstrate that miR­144­3p exerts antitumour effects by downregulating MEF2A to inhibit the proliferation, migration and angiogenesis of MM cells. This suggests that the miR­144­3p/MEF2A interaction may prove to be a potential therapeutic target for MM.

PIWI-Interacting RNA-004800 Is Regulated by S1P Receptor Signaling Pathway to Keep Myeloma Cell Survival.

PIWI-interacting RNA (piRNA) is a kind of non-coding single stranded RNA which plays major roles in epigenetic expressions, genome rearrangement, and regulation of gene and protein. Because piRNAs are abnormally expressed in various cancers, they can be used as novel biomarkers and therapeutic targets. However, the roles of piRNAs in cancer cell growth and survival are not well-known. Here, we are the first to provide evidence that PIWI-interacting RNA-004800 (piR-004800) is overexpressed in both exosomes from multiple myeloma (MM) patients' bone marrow supernatant and primary MM cells. The expression level of piR-004800 is positively correlated with the stages of MM, according to the international staging system (ISS). In MM cell lines, downregulation of piR-004800 induced apoptosis and autophagic cell death. This was accompanied by in vitro and in vivo inhibition of cell proliferation. Our previous study shows that sphingosine-1-phosphate receptor (S1PR) signaling pathway plays a crucial part in MM cell proliferation. In this study, we find that S1PR signaling pathway can regulate the PI3K/Akt/mTOR pathway through control of piR-004800 expressions. Taken together our data supports an oncogenic role for piR-004800 in MM, which sheds insight into a new mechanism that may lead to therapeutic targets in MM, an incurable plasma cell neoplasm.

Is complement C1q a potential marker for tumor burden and immunodeficiency in multiple myeloma?

Multiple myeloma (MM) patients are immunodeficient. Complement C1q is an important cofactor of both nonspecific and humoral immunity, and it participates in the immunomodulation of multiple tumors. Thus, this study aimed to determine the risk factors and clinical significance of C1q expression in MM patients. In total, 193 MM patients were examined. The mean value of C1q in the patient group (130.46 ± 36.17 mg/L), was lower than that in the control group (anemia and nonmalignant hematologic disease). C1q dynamically changed with different MM stages and was recovered to normal levels when the disease was in remission; however, it decreased again after disease progression. The risk factors of C1q reduction included Durie-Salmon stage and the immunoglobulin type of the disease. In conclusion, C1q appears to be a useful biomarker of tumor burden and a prognostic factor of disease relapse. C1q is a potential marker of the immunodeficiency status in MM patients.