A supramolecular radical cation: folding-enhanced electrostatic effect for promoting radical-mediated oxidation.

We report a supramolecular strategy to promote radical-mediated Fenton oxidation by the rational design of a folded host-guest complex based on cucurbit[8]uril (CB[8]). In the supramolecular complex between CB[8] and a derivative of 1,4-diketopyrrolo[3,4-c]pyrrole (DPP), the carbonyl groups of CB[8] and the DPP moiety are brought together through the formation of a folded conformation. In this way, the electrostatic effect of the carbonyl groups of CB[8] is fully applied to highly improve the reactivity of the DPP radical cation, which is the key intermediate of Fenton oxidation. As a result, the Fenton oxidation is extraordinarily accelerated by over 100 times. It is anticipated that this strategy could be applied to other radical reactions and enrich the field of supramolecular radical chemistry in radical polymerization, photocatalysis, and organic radical battery and holds potential in supramolecular catalysis and biocatalysis

Initiation and regulation of prophenoloxidase activation in tobacco hornworm, Manduca sexta

Melanization is insect acute-phase defense response to invading bacteria, fungi, protozoa, and endoparasitoids. Phenoloxidase (PO) participates in multiple steps of the melenization reaction. Produced as an inactive zymogen, prophenoloxidase (proPO), it is activated by a serine proteinase cascade upon recognition of the invaders. In Manduca sexta, the final step involves a proPO activating protease and a serine proteinase homolog (SPH) complex. After the proPO is activated, its activity is tightly regulated. I purified a ? -1,3-glucan Recognition Protein 2 (?GRP2) from Manduca cuticle extract. ?GRP2 specifically binds to laminarin, a soluble form of ? -1,3-glucan. This binding is linked with proPO activation. Based on this and other evidence, we conclude that ?GRP2 functions as a pattern recognition receptor for proPO activation in Manduca. Using recombinant proSPH1 and proSPH2 as substrates, I attempted to purify their activating enzymes. I observed cleavage of proSPH1 and proSPH2 by plasma fractions, and detected PO cofactor activity from the processed SPHs. More importantly, I found that the copresence of SPH1 and SPH2 is necessary for manifesting the cofactor activity. I expressed a Manduca PO inhibitor in E. coli and insect cells. The recombinant peptides moderately inhibit PO. My effort to isolate the natural inhibitor from the hemolymph was unsuccessful. Instead, I found a low molecular weight chemical with strong inhibitory activity to Manduca PO and mushroom tyrosinase. A clip-domain SPH, Vn50, from the endoparasitoid wasp Cotesia rubecula, venom, was found to inhibit PO from its host insect Pieris rapae. I used Manduca proPO system to study its inhibitory mechanism. I found that Vn50 down-regulated proPO activation by disrupting the protein-protein interactions among proPO, PAP, and SPH1/SPH2

Effect of Na Doping on the Nanostructures and Electrical Properties of ZnO Nanorod Arrays

The p-type ZnO nanorod arrays were prepared by doping Na with hydrothermal method. The structural, electrical, and optical properties were explored by XRD, Hall-effect, PL, and Raman spectra. The carrier concentrations and the mobility of Na-doped ZnO nanorod arrays are arranged from 1.4×1016 cm−3 to 1.7×1017 cm−3 and 0.45 cm2 v−1 s−1 to 106 cm2 v−1 s−1, respectively

Sevoflurane induces ho-1-mrna expression by regulating P13K/Akt/P70S6K signaling pathway and affects neuronal apoptosis

Purpose: To determine the effect of sevoflurane (SE) on neuronal apoptosis, and the mechanism involved.Methods: Sixty healthy male Sprague-Dawley rats were assigned to control, model and SE groups. Sham surgery was performed in control group, while middle cerebral artery infarction (MCAO) was established in model group. The expression of HO-1 mRNA was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Apoptosis, autophagy and protein content of P13K/Akt/P70S6K signaling pathway were assessed by Western blot assay.Results: Apoptosis was significantly lower in SE rats, relative to model rats. There were markedly higher protein levels of LC3 II / I, beclin-1, bad, Bcl-2 and caspase-3 in model and SE groups than in control rats (p < 0.05). The HO-1 mRNA was significantly up-regulated in model and SE groups, relative to controls, but it was significantly up-regulated in SE group, relative to model rats (p < 0.05). The expression levels of phosphorylated proteins of the P13K/Akt /P70S6K signal-related proteins in model and SE groups were significantly up-regulated, relative to control, but elevated in SE mice, when compared to model mice (p < 0.05).Conclusion: SE improves the behavior of MCAO rats, reduces cerebral infarction, and inhibits apoptosis and autophagy of nerve cells by regulating autophagy and apoptosis-related proteins through a mechanism that may be related to the induction of HO-1-mRNA expression by regulating P13K/Akt /P70S6K signal pathway. This provides new insights for the development of anti-neuronal apoptosis drugs