Fluoride and Arsenite Removal by Adsorption on La2O3-CeO2/Laterite

In the present article, the adsorbent prepared from laterite with lanthanum and cerium oxides (La2O3-CeO2/laterite (LCL)) was efficiently employed for the removal of arsenite and fluoride from an aqueous environment. The obtained materials were characterized by XRD, SEM, and nitrogen adsorption/desorption. The synthesized LCL exhibited a high adsorption capacity towards arsenite (As(III)) and fluoride. The adsorption of both analytes on LCL, which was well-fitted to a pseudo-second-order equation, was found to be kinetically fast in the first 20 minutes and reached equilibrium at around 180 minutes. Weber’s intraparticle diffusion model in multilinearity using the piecewise linear regression combined with Akaike’s criteria was addressed. The adsorption capacities of LCL calculated from Langmuir’s isotherm model were found to be 67.08 mg·g-1 for arsenite and 58.02 mg·g-1 for fluoride. Thermodynamic parameters presented an endothermic nature of arsenite adsorption but an exothermic nature for fluoride and a negative Gibbs free energy for the spontaneous process of arsenite or fluoride adsorption at the studied temperature range. The excellent adsorption performance and stability make the composite of laterite and La-Ce binary oxides an alternative efficient and cheap adsorbent for the removal of arsenite and fluoride in an aqueous solution.

TDP-43 Mutation Affects Stress Granule Dynamics in Differentiated NSC-34 Motoneuron-Like Cells

Amyotrophic Lateral Sclerosis (ALS) is characterized by degeneration of motor neurons in the brain and spinal cord. Cytoplasmic inclusions of TDP-43 are frequently reported in motor neurons of ALS patients. TDP-43 has also been shown to associate with stress granules (SGs), a complex of proteins and mRNAs formed in response to stress stimuli that temporarily sequester mRNA translation. The effect of pathogenic TDP-43 mutations within glycine-rich regions (where the majority of ALS-causing TDP-43 mutations occur) on SG dynamics in motor neurons is poorly understood. To address this issue, we generated murine NSC-34 cell lines that stably over-express wild type TDP-43 (TDP-43WT) or mutant forms (ALS-causing TDP-43 mutations TDP-43A315T or TDP-43M337V). We then differentiated these NSC-34 lines into motoneuron-like cells and evaluated SG formation and disassembly kinetics in response to oxidative or osmotic stress treatment. Wild type and mutant TDP-43 appeared to be largely retained in the nucleus following exposure to arsenite-induced oxidative stress. Upon arsenite removal, mutant TDP-43 clearly accumulated within HuR positive SGs in the cytoplasm, whereas TDP-43WT remained mostly within the nucleus. 24 h following arsenite removal, all SGs were disassembled in both wild type and mutant TDP-43 expressing cells. By contrast, we observed significant differences in the dynamics of mutant TDP-43 association with SGs in response to hyperosmotic stress. Specifically, in response to sorbitol treatment, TDP-43WT remained in the nucleus, whereas mutant TDP-43 relocalized to HuR positive SGs in the cytoplasm following exposure to sorbitol stress, resulting in a significant increase in TDP-43 SG numbers. These SGs remained assembled for 24 h following removal of sorbitol. Our data reveal that under certain stress conditions the rates of SG formation and disassembly is modulated by TDP-43 mutations associated with ALS, and suggest that this may be an early event in the seeding of insoluble cytoplasmic inclusions observed in ALS.