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In an effort to examine signaling pathway of inflammation of the mouse liver caused by intragastric administration of titanium dioxide nanoparticles (NPs), we assessed Toll-like receptor-2 (TLR2), TLR-4, IκB kinase (IKK-α, IKK-β), IκB nucleic factor-κB (NF-κB), NF-κBP52, NF-κBP65, tumor necrosis factor-α (TNF-α), NF-κB-inducible kinase (NIK), interleukin-2 (IL-2), biochemical parameters of liver functions, and histopathological changes and liver ultrastructure in the TiO(2) NPs-treated mice. The results showed the titanium accumulation in liver, histopathological changes and hepatocytes apoptosis of mice liver, and the liver function damaged by TiO(2) NPs. The real-time quantitative reverse transcriptase polymerase chain reaction and enzyme-linked immunosorbent assay analyses showed that TiO(2) NPs can significantly increase the mRNA and protein expression of TLR2 and TLR4 and several inflammatory cytokines, including IKK1, IKK2, NF-κB, NF-κBP52, NF-κBP65, TNF-α, and NIK, and TiO(2) NPs can significantly decrease the mRNA and protein expression of IκB and IL-2. The results of this study added to our understanding of TiO(2) NPs-induced liver toxicity. It implied that the signaling pathway of liver injury in the TiO(2) NPs-stimulated mouse liver sequentially might occur via activation of TLRs→NIK→IκB kinase→NF-κB→TNF-α→inflammation→apoptosis→liver injury.

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Highlights d We introduce SOUL, a new step-function opsin with ultrahigh light sensitivity d SOUL activates deep mouse brain and change behaviors via transcranial illumination d SOUL activates macaque cortical neurons via illumination through the dura d Transdural activation of SOUL in macaques induces oscillatory activity reversibly

The oxygen reduction reaction (ORR) at the cathode of fuel cells and metal–air batteries requires efficient electrocatalysts to accelerate its reaction rate due to its sluggish kinetics. Nitrogen- and phosphorus-doped biocarbon has been fabricated via a simple and low-cost biosynthesis method using yeast cells as a precursor. The as-prepared biocarbon exhibits excellent electrocatalytic activity for the ORR. An onset potential of −0.076 V (vs Ag/AgCl) and a negative shift of only about 29 mV in the half-wave potential of the biocarbon as compared to commercial Pt/C (20 wt % Pt on Vulcan XC-72, Johnson Matthey) is achieved. The biocarbon possesses enhanced electron poverty in carbon atoms and a decreasing amount of less electroactive nitrogen and phosphorus dopants due to the biomineralization during the synthesis. The surface gap layer along with the mesopores in the biocarbon increases accessible active sites and facilitates the mass transfer during the ORR. These factors correlate with the high ORR activity of the biocarbon. The results demonstrate that biomineralization plays a critical role in tailoring the structure and the electrocatalytic activity of the biocarbon for ORR.

Soil salinity results in nutrient imbalances and potassium deficiency.

The organ toxicity of lanthanides (Ln) on organisms had been recognized, but very little is known about the oxidative injury of brain caused by Ln. In order to study the mechanisms underlying the effects of Ln on the brain, ICR mice were injected with a single 20 mg/kg body weight dose of LaCl 3 , CeCl 3 , and NdCl 3 into the abdominal cavity daily for 14 days. We then examined the coefficient of the brain, the brain pathological changes and oxidative stress-mediated responses, and the accumulation of Ln and levels of neurochemicals in the brain. The results showed that CeCl 3 and NdCl 3 could induce some neurons to turn inflammatory cells and slight edema but did not observe the brain pathological changes from LaCl 3 -treated group. The concentrations of La, Ce, and Nd in the brain were significantly different and ranked in the order of Ce, Nd, and La. The injury of the brain and oxidative stress occurred as Ln appeared to trigger a cascade of reactions such as lipid peroxidation, the decreases of the total antioxidation capacity and activities of antioxidative enzymes, the excessive release of nitric oxide, the increase of glutamic acid, and the downregulated level of acetylcholinesterase activities. Furthermore, both Ce 3+ and Nd 3+ exhibited higher oxidative stress and toxicity on brain than La 3+ , and Ce 3+ caused more severe brain injuries and oxidative stress than Nd 3+ , implying that the differences in the brain injuries caused by Ln might be related to the number of 4f electrons of Ln.