NH4+ directed assembly of zinc oxide micro-tubes from nanoflakes

A simple precipitation process followed with the heat treatment was developed to synthesize ZnO micro-tubes by self-assembly of nanoflakes composed of nanoparticles. The resulting ZnO micro-tubes demonstrated excellent photocatalytic performance in degrading methylene blue (MB) under UV illumination. It was found that NH4+ ion played a critical role in directing the assembly of the nanoflakes to form the micro-tube structure. A critical reaction ratio existed at or above which the ZnO micro-tubes could be obtained. For the mixtures of solutions of (NH4)2CO3 and zinc salt, the ratio () was 2:1

Experimental observation of the crystallization of a paired holon state

A new excitation is observed at 201 meV in the doped-hole ladder cuprate Sr$_{14}$Cu$_{24}$O$_{41}$, using ultraviolet resonance Raman scattering with incident light at 3.7 eV polarized along the direction of the rungs. The excitation is found to be of charge nature, with a temperature independent excitation energy, and can be understood via an intra-ladder pair-breaking process. The intensity tracks closely the order parameter of the charge density wave in the ladder (CDW$_L$), but persists above the CDW$_L$ transition temperature ($T_{CDW_L}$), indicating a strong local pairing above $T_{CDW_L}$. The 201 meV excitation vanishes in La$_{6}$Ca$_{8}$Cu$_{24}$O$_{41+\delta}$, and La$_{5}$Ca$_{9}$Cu$_{24}$O$_{41}$ which are samples with no holes in the ladders. Our results suggest that the doped holes in the ladder are composite bosons consisting of paired holons that order below $T_{CDW}$.Comment: Accepted for publication in Physical Review Letters (4 figures

Histamine induced high mobility group box-1 release from vascular endothelial cells through H-1 receptor

BackgroundSystemic allergic reaction is characterized by vasodilation and vascular leakage, which causes a rapid, precipitous and sustained decrease in arterial blood pressure with a concomitant decrease of cardiac output. Histamine is a major mediator released by mast cells in allergic inflammation and response. It causes a cascade of inflammation and strongly increases vascular permeability within minutes through its four G-protein-coupled receptors (GPCRs) on endothelial cells. High mobility group box-1 (HMGB1), a nonhistone chromatin-binding nuclear protein, can be actively secreted into the extracellular space by endothelial cells. HMGB1 has been reported to exert pro-inflammatory effects on endothelial cells and to increase vascular endothelial permeability. However, the relationship between histamine and HMGB1-mediated signaling in vascular endothelial cells and the role of HMGB1 in anaphylactic-induced hypotension have never been studied. Methods and resultsEA.hy 926 cells were treated with different concentrations of histamine for the indicated periods. The results showed that histamine induced HMGB1 translocation and release from the endothelial cells in a concentration- and time-dependent manner. These effects of histamine were concentration-dependently inhibited by d-chlorpheniramine, a specific H-1 receptor antagonist, but not by H-2 or H-3/4 receptor antagonists. Moreover, an H-1-specific agonist, 2-pyridylethylamine, mimicked the effects of histamine, whereas an H-2-receptor agonist, 4-methylhistamine, did not. Adrenaline and noradrenaline, which are commonly used in the clinical treatment of anaphylactic shock, also inhibited the histamine-induced HMGB1 translocation in endothelial cells. We therefore established a rat model of allergic shock by i.v. injection of compound 48/80, a potent histamine-releasing agent. The plasma HMGB1 levels in compound 48/80-injected rats were higher than those in controls. Moreover, the treatment with anti-HMGB1 antibody successfully facilitated the recovery from compound 48/80-induced hypotension. ConclusionHistamine induces HMGB1 release from vascular endothelial cells solely through H-1 receptor stimulation. Anti-HMGB1 therapy may provide a novel treatment for life-threatening systemic anaphylaxis

Analysis of terahertz generation via nanostructure enhanced plasmonic excitations

This is the published version. Copyright © 2009 American Institute of PhysicsIn this paper, we conduct a quantitative study on the physical mechanism of electrons dynamics near the nanostructured metalfilmsurfaces, as well as the efficiency of generated terahertz radiation associated with different types of nanostructures. The simulation results show that although the oscillating motion of emitted electrons outside the metal surface may affect the terahertz generation efficiency to some extent, this efficiency is predominantly determined by the electric field magnitude inside the metalfilm associated with nanostructure enhanced plasmonic excitations. Due to the field enhancement effect of the nanostructure, an appropriately designed nanostructured surface could greatly enhance the strength of generated terahertz signal via the increased nonlinear interactions between the light and the nanostructures

Colony-Forming Progenitor Cells in the Postnatal Mouse Liver and Pancreas Give Rise to Morphologically Distinct Insulin-Expressing Colonies in 3D Cultures

In our previous studies, colony-forming progenitor cells isolated from murine embryonic stem cell-derived cultures were differentiated into morphologically distinct insulin-expressing colonies. These colonies were small and not light-reflective when observed by phase-contrast microscopy (therefore termed “Dark” colonies). A single progenitor cell capable of giving rise to a Dark colony was termed a Dark colony-forming unit (CFU-Dark). The goal of the current study was to test whether endogenous pancreas, and its developmentally related liver, harbored CFU-Dark. Here we show that dissociated single cells from liver and pancreas of one-week-old mice give rise to Dark colonies in methylcellulose-based semisolid culture media containing either Matrigel or laminin hydrogel (an artificial extracellular matrix protein). CFU-Dark comprise approximately 0.1% and 0.03% of the postnatal hepatic and pancreatic cells, respectively. Adult liver also contains CFU-Dark, but at a much lower frequency (~0.003%). Microfluidic qRT-PCR, immunostaining, and electron microscopy analyses of individually handpicked colonies reveal the expression of insulin in many, but not all, Dark colonies. Most pancreatic insulin-positive Dark colonies also express glucagon, whereas liver colonies do not. Liver CFU-Dark require Matrigel, but not laminin hydrogel, to become insulin-positive. In contrast, laminin hydrogel is sufficient to support the development of pancreatic Dark colonies that express insulin. Postnatal liver CFU-Dark display a cell surface marker CD133^(+)CD49f^(low)CD107b^(low) phenotype, while pancreatic CFU-Dark are CD133^-. Together, these results demonstrate that specific progenitor cells in the postnatal liver and pancreas are capable of developing into insulin-expressing colonies, but they differ in frequency, marker expression, and matrix protein requirements for growth

Detection of concealed and buried chemicals by using multifrequency excitations

This is the published version. Copyright © 2010 American Institute of PhysicsIn this paper, we present a new type of concealed and buried chemical detection system by stimulating and enhancing spectroscopic signatures with multifrequency excitations, which includes a low frequency gradient dcelectric field, a high frequency microwave field, and higher frequency infrared (IR) radiations. Each excitation frequency plays a unique role. The microwave, which can penetrate into the underground and/or pass through the dielectric covers with low attenuation, could effectively transform its energy into the concealed and buried chemicals and increases its evaporation rate from the sample source. Subsequently, a gradient dcelectric field, generated by a Van De Graaff generator, not only serves as a vapor accelerator for efficiently expediting the transportation process of the vapor release from the concealed and buried chemicals but also acts as a vapor concentrator for increasing the chemical concentrations in the detection area, which enables the trace level chemical detection. Finally, the stimulated and enhanced vapors on the surface are detected by the IR spectroscopic fingerprints. Our theoretical and experimental results demonstrate that more than sixfold increase in detection signal can be achieved by using this proposed technology. The proposed technology can also be used for standoff detection of concealed and buried chemicals by adding the remote IR and/or thermal spectroscopic and imaging detection systems

Targeting BTK for the treatment of FLT3-ITD mutated acute myeloid leukemia

Approximately 20% of patients with acute myeloid leukaemia (AML) have a mutation in FMS-like-tyrosine-kinase-3 (FLT3). FLT3 is a trans-membrane receptor with a tyrosine kinase domain which, when activated, initiates a cascade of phosphorylated proteins including the SRC family of kinases. Recently our group and others have shown that pharmacologic inhibition and genetic knockdown of Bruton's tyrosine kinase (BTK) blocks AML blast proliferation, leukaemic cell adhesion to bone marrow stromal cells as well as migration of AML blasts. The anti-proliferative effects of BTK inhibition in human AML are mediated via inhibition of downstream NF-κB pro-survival signalling however the upstream drivers of BTK activation in human AML have yet to be fully characterised. Here we place the FLT3-ITD upstream of BTK in AML and show that the BTK inhibitor ibrutinib inhibits the survival and proliferation of FLT3-ITD primary AML blasts and AML cell lines. Furthermore ibrutinib inhibits the activation of downstream kinases including MAPK, AKT and STAT5. In addition we show that BTK RNAi inhibits proliferation of FLT3-ITD AML cells. Finally we report that ibrutinib reverses the cyto-protective role of BMSC on FLT3-ITD AML survival. These results argue for the evaluation of ibrutinib in patients with FLT3-ITD mutated AML