The mechanism for the decreasing critical temperature (T(C)) of the metal-insulator transition (MIT) in vanadium dioxide (VO2) by tungsten (W) doping is a matter of debate. Here, to clarify the correlation between W doping and T(C), the electronic and geometrical structures around W and V atoms in W(x)V(1-x)O2 samples are systematically investigated by X-ray absorption fine structure (XAFS) spectroscopy. The evidence of electron doping of W(6+) ions in VO2 is obtained from the reduction of V(4+) to V(3+) ions. This kind of electron doping has been considered to favor the MIT process. Moreover, from the XAFS results, the local rutile structure around W dopants is identified even at low doping, and acts as the structure-guided domain to facilitate the MIT in VO2. Considering the electronic band structures of W(x)V(1-x)O2 samples, the internal stresses induced by W(6+) doping yield the detwisting of the nearby monoclinic VO2 lattice. This lattice detwisting will drive the downward shift of the ?* electron band and a smaller separation between antibonding and bonding d? orbitals in the band structure of VO2, which induces the decreased band gaps of W(x)V(1-x)O2 samples. As a consequence, the potential energy barrier for phase transition is lowered and the reduced T(C) is observed.
A hydrothermal route has been developed to synthesize lead telluride (PbTe) nanostructures through the reaction between Pb(CH3COO)2 and Na2TeO3. When the surfactant poly(vinyl pyrrolidone) (PVP) was introduced into the solution, uniform PbTe nanorods with a diameter of about 30 nm could be prepared, while absent of PVP, PbTe nanotubes could be synthesized. Furthermore, some interesting Y-, V-, crisscross-shaped PbTe nanotubes were reported for the first time. The resulting materials were characterized by X-ray diffraction (XRD), transmission electron microscopy (TEM) and high-resolution TEM (HRTEM). Two different mechanisms are identified to explain the formation of the nanorods and nanotubes herein. A surfactant-assisted oriental attachment mechanism is explained to describe the formation of PbTe nanorods, whereas, we deduce PbTe nanotubes follow a self-generated template route.
The S component (LukS-PV) is one of the two components of Panton-Valentine leukocidin (PVL), which is a pore-forming cytotoxin secreted by Staphylococcus aureus, with the ability to lyse leukocytes. In this study, LukS-PV had the ability to induce apoptosis in the human acute myeloid leukemia (AML) cell line THP-1. Therefore, we investigated the mechanisms of LukS-PV-induced apoptosis in THP-1 cells. THP-1 cells treated with LukS-PV, resulted in a significant inhibition of proliferation in a dose- and time-dependent manner, and induced G0/G1 arrest associated with an inhibition of cell cycle arrest regulatory protein (cyclin D1) in a dose- and time-dependent manner, as measured by flow cytometry (FCM). After 12h exposure to LukS-PV (1.00 ?M), annexin V-EGFP/propidium iodide (PI) FCM revealed that 19.5±3.6% of THP-1 cells were apoptotic, and terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) staining also revealed THP-1 cells were apoptotic. Chip analysis of 84 apoptosis-related genes demonstrated that 9 genes were up-regulated at least 2-fold and that 5 genes were down-regulated at least 2-fold in the treatment group when compared with levels in the control group. Western blotting reveled that the expression of caspase-8 increased significantly (approximately 4-fold). The levels of caspase-9, -3 and Bax increased significantly, and levels of Bcl-2 decreased rapidly with LukS-PV treatment. These data suggest that LukS-PV acts as an anti-leukemia agent and activates AML cell apoptosis via the mitochondrial pathway. Therefore, LukS-PV may be a multi-targeting drug candidate for the prevention and therapy of AML.
Poly(amino acid)s are well-known as biodegradable and environmentally acceptable materials. In this study, a series of poly(L-aspartic acid)-b-poly(L-phenylalanine) (PAA-PPA) compounds with different degrees of polymerization were used to prepare copolymer micelles for a poorly water-soluble drug 4-amino-2-trifluoromethyl-phenyl retinate (ATPR, a novel all-trans retinoic acid derivative) and in vivo pharmacokinetics, biodistribution and antitumor efficacy of ATPR delivered by PAA-PPA micelles were evaluated. The area under the plasma concentration time curve AUC0?? of ATPR-loaded PAA20PPA20 micelles was 2.23 and 1.97 times higher than that of ATPR solution and ATPR CrmEL solution, respectively; In addition, the mean residence time (MRT) was increased 1.67 and 1.97-fold, respectively and the total body clearance (CL) was reduced 2.25 and 1.98-fold, respectively. The biodistribution study indicated that most of the ATPR in the ATPR-M group was distributed in the liver and there was delayed liver aggregation compared with the ATPR solution and ATPR CrmEL solution groups. Furthermore, the antitumor efficacy of ATPR-loaded PAA20PPA20 micelles was demonstrated in in vivo antitumor models involving mice inoculated with the human gastric cancer cell line SGC-7901. At the same dose of 7mg/kg, the ATPR-loaded micelles group demonstrated a better tumor growth inhibition and induced differentiation than the groups given ATPR solution and ATPR CrmEL solution. Therefore, the ATPR-loaded PAA-PPA micelles appear to be a potentially useful drug delivery system for ATPR and suitable for the chemotherapy of gastric cancer.
A novel block copolymer containing two polymeric components, poly(L-aspartic acid)-b-poly (L-phenylalanine) (PAA-PPA), was synthesized and its potential for the preparation of copolymer micelles with a poorly water-soluble drug was investigated in this study. The chemical structure and physical properties of PAA-PPA were characterized by FTIR, 1H NMR and TG. The degree of polymerization of PAA-PPA was calculated by analyzing the relative area of N-CH signal and C-CH3 of 1H NMR spectra. The critical micelle concentration (CMC) of the PAA-PPA achieved a minimum of 11.1 mg/L. Studies on the drug-free PAA-PPA solutions showed PAA-PPA aggregation into micellar type in the sub-150 nm size range. Furthermore, the size of the PAA-PPA micelles was found to be pH-independent between the pH range of 4.0 and 8.0, which could be favorable to avoid the limitation of the size change at the specified pH value seeking drug stability. 4-amino-2-trifluoromethyl-phenyl retinate (ATPR) was studied as a poorly water-soluble model drug. The drug-loading and entrapment efficiency of the ATPR-loaded PAA-PPA micelles were 30.9 wt% and 87.9 %, respectively. The high drug-loading and entrapment efficiency were due to the synergistic effect of the micellar encapsulation and the binding interaction between drug and PAA-PPA. The ATPR-loaded PAA-PPA micelles showed a narrow size distribution, low zeta potential, high drug-loading capacity and good stable. The PAA-PPA was safer than Tween-80 and Cremophor EL (CrmEL) as an injectable pharmaceutical adjuvant for ATPR as indicated by the hemolysis and cytotoxicity studies. The novel amphiphilic amino acid copolymer can be considered as a prospective injectable delivery system for ATPR in terms of the pH-independent, greater drug-loading capacity and safety.
Gastric cancer is one of the most common and lethal cancers worldwide. However, despite its clinical importance, the regulatory mechanisms involved in the aggressiveness of this cancer are still poorly understood. A better understanding of the biology, genetics and molecular mechanisms of gastric cancer would be useful in developing novel targeted approaches for treating this disease. In this study we used protein-protein interaction networks and cluster analysis to comprehensively investigate the cellular pathways involved in gastric cancer. A primary immunodeficiency pathway, focal adhesion, ECM-receptor interactions and the metabolism of xenobiotics by cytochrome P450 were identified as four important pathways associated with the progression of gastric cancer. The genes in these pathways, e.g., ZAP70, IGLL1, CD79A, COL6A3, COL3A1, COL1A1, CYP2C18 and CYP2C9, may be considered as potential therapeutic targets for gastric cancer.
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