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A room-temperature electrodeposition method with an organic electrolyte was developed to fabricate a HNO 3 -pretreated graphene paper Cu (GP′–Cu) composite. To improve the interfacial bonding of GP′–Cu composite, magnetron sputtering technology was used to create a “sandwich” structural gradient GP′–Cu composite. The selection of the intermediate transition layer metal was based on two-dimensional disregistry. Scanning electron microscopy, X-ray photoelectron spectroscopy, and other analytical methods confirmed that the addition of an intermediate transition metal (Cr, Ni) layer reduced the gap distance and enhanced the interfacial bonding of the GP′ and Cu deposited layers. The GP′–Ni–Cu composite exhibited the largest increase in tensile strength and conductivity. In addition, it had the highest thermal diffusivity and elongation at break among the GP′–Cu, GP′–Cr–Cu and GP′–Ni–Cu composites.

The comprehensive recovery of small amounts of valuable minerals such as gold and base-metal sulfide minerals from a low-grade refractory ore was investigated. The following treatment strategy was applied to a sample of this ore： gold flotation-gold concen- trate leaching-lead and zinc flotation from the gold concentrate leaching residue. Closed-circuit trials of gold flotation yielded a gold concen- trate that assayed at 40.23 g·t-1 Au with a recovery of 86.25%. The gold concentrate leaching rate was 98.76%. Two variants of lead-zinc flotation from the residue--preferential flotation of lead and zinc and bulk flotation of lead and zinc--were tested using the middling processing method. Foam from the reflotation was returned to the lead rougher flotation or lead-zinc bulk flotation, whereas middlings from reflotation were discarded. Sulfur concentrate was a byproduct. The combined strategy of flotation, leaching, and flotation is recommended for the treatment of this kind of ore.

Background. Systemic lupus erythematosus (SLE) is a multisystem disease that is characterized by the appearance of serum autoantibodies. No effective treatment for SLE currently exists. Methods. We used human umbilical cord mesenchymal stem cell (H-UC-MSC) transplantation to treat B6.Fas mice. Results. After four rounds of cell transplantation, we observed a statistically significant decrease in the levels of mouse anti-nuclear, anti-histone, and anti-double-stranded DNA antibodies in transplanted mice compared with controls. The percentage of CD4+CD25+Foxp3+ T cells in mouse peripheral blood significantly increased after H-UC-MSC transplantation. Conclusions. The results showed that H-UC-MSCs could repair lesions in B6.Fas mice such that all of the relevant disease indicators in B6.Fas mice were restored to the levels observed in normal C57BL/6 mice.

Ginsenoside Rb1 has been reported to exert anti-aging and anti-neurodegenerative effects. In the present study, we investigate whether ginsenoside Rb1 is involved in neurite outgrowth and neuroprotection against damage induced by amyloid beta（25–35） in cultured hippocampal neurons, and explore the underlying mechanisms. Ginsenoside Rb1 significantly increased neurite outgrowth in hippocampal neurons, and increased the expression of phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2. These effects were abrogated by API-2 and PD98059, inhibitors of the signaling proteins Akt and MEK. Additionally, cultured hippocampal neurons were exposed to amyloid beta（25–35） for 30 minutes; ginsenoside Rb1 prevented apoptosis induced by amyloid beta（25–35）, and this effect was blocked by API-2 and PD98059. Furthermore, ginsenoside Rb1 significantly reversed the reduction in phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2 levels induced by amyloid beta（25–35）, and API-2 neutralized the effect of ginsenoside Rb1. The present results indicate that ginsenoside Rb1 enhances neurite outgrowth and protects against neurotoxicity induced by amyloid beta（25–35） via a mechanism involving Akt and extracellular signal-regulated kinase 1/2 signaling.