Green application of trimetallic nickel-cobalt-molybdenum nanocomposites on 3D graphene oxide as a powerful electrocatalyst for hydrogen evolution reaction.

In-situ designing of multiple metals electrocatalysts with high active sites and performance is the main challenge for hydrogen evolution reaction (HER). So in this work, 3D-rGO was easily obtained from 2D-graphene by a simple one-step hydrothermal method to create the interspace sites and active surface area. The Ni-Co-Mo tri-metallic@3D-rGO was synthesized and fully characterized by different techniques, e.g., FT-IR, XRD, Raman, FE-SEM, TEM, EDS, mapping, ICP-OES, AFM, voltammetry, and electrochemical impedance spectroscopy. According to the FE-SEM and TEM images, the Ni-Co-Mo tri-metallic@3D-rGO has a crumpled-formed structure. The as-prepared nanocomposite has high HER performance with a low potential of -0.11 (vs. RHE) to deliver 10 mA cm-2 and Tafel slope of 68 mV dec-1 for Pt and -0.25 V (vs. RHE) to deliver 10 mA cm-2 and Tafel slope of 110 mV dec-1 for graphite counter electrode. Furthermore, the 3D structure illustrates high long-term durability in the HER process for 1000 continuous cycles and 12 h operation at -0.42 V (vs. RHE) for Pt and graphite counter electrode. It's noticeable HER performance has the synergetic effect between 3D-rGO and tri-metallic structure with high porosity and electrical conductivity, enhancing HER kinetic.

Nod-like receptor protein 3 and nod-like receptor protein 1 inflammasome activation in the hippocampal region of postmortem methamphetamine chronic user.

OBJECTIVE AND BACKGROUND: Methamphetamine (Meth) is one of the most important central nervous system (CNS) stimulant abuse drugs that cause long-term or permanent damage to different regions of the brain, particularly hippocampus, by neuronal apoptosis and inflammation. In this study, we evaluated Nod-like Receptor Protein 3(NLRP3) and Nod-like Receptor Protein1 (NLRP1) Inflammasome Activation in the Hippocampal Region of postmortem Meth Chronic User. METHODS: Molecular and histological analyses were conducted on the brain of 14 non-addicted and 11 Meth users separately. The expression level of NLRP1, NLRP3 was measured using western blotting and immunohistochemistry (IHC) techniques. Histopathological assessment was performed with stereological Cell Counting of hippocampal cells stained with hematoxylin and eosin (H et E). Moreover, Tunel staining was carried out in order to detect any kind of DNA damage. RESULTS: Based on our findings using western blotting and immunohistochemistry assay, overexpression of NLRP1 and NLRP3 proteins in the hippocampal region of Meth addicts was observed. The stereological analysis in the hippocampus of the human brain revealed increased neurodegeneration. Furthermore, the increased rate of apoptosis and cell death were significant and confirmed by Tunel assay in the hippocampus of Meth groups. CONCLUSION: Chronic Meth abuse could result in increases of NLRP1 and NLRP3 and induction of inflammation and apoptosis in the hippocampus in Meth groups (Tab. 1, Fig. 9, Ref. 40).

Deferoxamine promotes mesenchymal stem cell homing in noise-induced injured cochlea through PI3K/AKT pathway.

OBJECTIVE: Over 5% of the world's population suffers from disabling hearing loss. Stem cell homing in target tissue is an important aspect of cell-based therapy, which its augmentation increases cell therapy efficiency. Deferoxamine (DFO) can induce the Akt activation, and phosphorylation status of AKT (p-AKT) upregulates CXC chemokine receptor-4 (CXCR4) expression. We examined whether DFO can enhance mesenchymal stem cells (MSCs) homing in noise-induced damaged cochlea by PI3K/AKT dependent mechanism. MATERIALS AND METHODS: Mesenchymal stem cells were treated with DFO. AKT, p-AKT protein and hypoxia inducible factor 1- α (HIF-1α) and CXCR4 gene and protein expression was evaluated by RT- PCR and Western blot analysis. For in vivo assay, rats were assigned to control, sham, noise exposure groups without any treatment or receiving normal, DFO-treated and DFO +LY294002 (The PI3K inhibitor)-treated MSCs. Following chronic exposure to 115 dB white noise, MSCs were injected into the rat cochlea through the round window. Number of Hoechst- labelled cells was determined in the endolymph after 24 hours. RESULTS: Deferoxamine increased P-AKT, HIF-1α and CXCR4 expression in MSCs compared to non-treated cells. DFO pre-conditioning significantly increased the homing ability of MSCs into injured ear compared to normal MSCs. These effects of DFO were blocked by LY294002. CONCLUSIONS: Pre-conditioning of MSCs by DFO before transplantation can improve stem cell homing in the damaged cochlea through PI3K/AKT pathway activation.