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Mesenchymal stromal cells (MSCs) are well known for their immunoregulatory roles on allergic inflammation particularly by acting on T cells, B cells, and dendritic cells (DCs). MSC-derived small extracellular vesicles (MSC-sEV) are increasingly considered as one of the main factors for the effects of MSCs on immune responses. However, the effects of MSC-sEV on DCs in allergic diseases remain unclear. MSC-sEV were prepared from the induced pluripotent stem cells (iPSC)-MSCs by anion-exchange chromatography, and were characterized with the size, morphology, and specific markers. Human monocyte-derived DCs were generated and cultured in the presence of MSC-sEV to differentiate the so-called sEV-immature DCs (sEV-iDCs) and sEV-mature DCs (sEV-mDCs), respectively. The phenotypes and the phagocytic ability of sEV-iDCs were analyzed by flow cytometry. sEV-mDCs were co-cultured with isolated CD4

Single-phase β-Yb2Si2O7 was synthesized by solid-state reaction using Yb2O3 and SiO2 gel. SiO2 gel significantly decreased the synthesis temperature and shortened the holding time. Bulk Yb2Si2O7 was obtained by pressureless sintering. Grain size, relative density (92.9%), and flexural strength [(182.3 ± 2.0) MPa] were enhanced as the sintering temperature increased and equiaxed grains were obtained with an average grain size of approximately 3 μm. Bulk Yb2Si2O7 possessed a suitable thermal expansion coefficient [(4.64 ± 0.01) × 10−6/K] between 473 and 1573 K, and the thermal conductivities at 300 and 1400 K were 4.31 and 2.27 W/m·K, respectively.

Background Persistence of stent polymer coating has been associated with incomplete endothelialization, expansive vessel remodeling, neoatherosclerosis, and delayed healing associated with inflammation that may contribute to late adverse events. Methods The BICARE (Lepu Medical, Beijing, China) stent is a novel polymer-free, nanotechnology-based stent eluting sirolimus and probucol. As a first in human feasibility study, patients with a single de novo native coronary stenosis

Objective To investigate the outcomes of overlapping drug-eluting stenting (DES) in small and diffuse lesions. Background Clinical outcomes of overlapping heterogeneous versus homogeneous DES of diffuse lesions (requiring ≥30 mm of length) in small coronary arteries (requiring ≤2.75 mm of diameter) are unknown. Methods From January 2005 to December 2009, there were 99 patients with diffuse lesions in small coronary arteries receiving overlapping heterogeneous DES, and 558 patients receiving overlapping homogeneous DES at our institution. The clinical end-point of the study included in-hospital and 12-month major adverse cardiac events (death, nonfatal myocardial infarction, and target vessel revascularization (TVR). Results There were no statistically significant differences between overlapping heterogeneous and homogeneous DES groups in-hospital (2.0% vs. 1.4%, respectively; P = 0.66) and 12-month (9.1% vs. 9.3%, respectively; P = 0.94) major adverse cardiac events. After adjustment, no significant differences for major adverse cardiac events were noted, but the rate of nonfatal myocardial infarction was lower in overlapping homogeneous DES group (odds ratio: 4.20, P = 0.03). Conclusion In this analysis, there were no significant differences in major adverse cardiac events between the 2 types of overlapping DES for diffuse lesions in small coronary arteries, except for higher nonfatal myocardial infarction in overlapping heterogeneous DES. (J Interven Cardiol 2013;26:264–270)

Dermal papilla cells (DPCs) show phenotypic plasticity during wound healing. The multipotency of DPCs is well recognized, but the signaling pathways that regulate the differentiation of these cells into fibroblasts are poorly understood. A preliminary experiment showed that transforming growth factor beta1 (TGF-β1) can induce DPCs to differentiate into fibroblast-like cells, which suggests that DPCs may be a source of wound-healing fibroblasts. Bone morphogenetic protein-7 (BMP-7), a member of the TGF-β superfamily, can prevent and reverse fibrosis by counteracting the TGF-β1-mediated profibrotic effect. To determine whether BMP-7 attenuates the TGF-β1-induced differentiation of DPCs into fibroblasts, we established an in vitro system for DPC differentiation and recorded the gene expression patterns that distinguished DPCs from fibroblasts. The proportion of fibroblast-like cells was significantly enhanced in DPCs treated with TGF-β1, as evidenced by immunocytochemistry, flow cytometry, quantitative real-time reverse transcriptase polymerase chain reaction, and Western blot analysis. BMP-7 and TGF-β1 administration substantially decreased fibroblast-like differentiation, indicating inhibition of TGF-β1-induced differentiation. The antagonistic BMP-7- and TGF-β1-activated signaling pathways can be used to promote wound healing or suppress hypertrophic scarring.

Highly dispersed α-Fe2O3/NaY, NiO/NaY, and CuO/NaY catalyst systems were prepared by impregnation method. Dispersion thresholds of the transition metal oxides on NaY zeolite were determined by XRD phase analysis. The dispersion capacities of the transition metal oxides on NaY zeolite are much lower than that estimated on the basis of a closed packed monolayer in the micro pores. The catalytic activity and selectivity of the highly dispersed oxide catalyst systems for ethylbenzene and cyclohexane dehydrogenation reactions were reported.

Background The introduction of drug-eluting stents (DES) dramatically changed the practice of percutaneous coronary intervention (PCI) in the 2000s. Little is known about trends in in-hospital outcome after PCI in the DES era. Hypothesis The in-hospital outcomes after PCI might be continuously improved over time. Methods We analyzed in-hospital outcomes of 21 667 patients who underwent PCI at Fu Wai Hospital in the past 5 years. The patients were divided into 5 groups according to the time of their intervention: group 1 (June 2004 to May 2005), group 2 (June 2005 to May 2006), group 3 (June 2006 to May 2007), group 4 (June 2007 to May 2008), and group 5 (June 2008 to May 2009). Results Procedural success rates for the 5 groups were 93.6%, 95%, 94.4%, 94.2%, and 94.3%, respectively (P = 0.39). Significant reduction in in-hospital major adverse cardiac events (3.1%, 3.4%, 2.8%, 1.6%, and 1.0%, P < 0.001) and need for target-vessel revascularization (2.0%, 2.2%, 1.5%, 0.4%, and 0.2%, P < 0.001) was noted over time, which was associated with a significant increase in use of DES (from 56.6% to 97.0%, P < 0.001). On multivariate analysis, use of DES, dissection during procedure, left main lesion, prior myocardial infarction, and age ≥ 65 years were independent predictors of major adverse cardiovascular events. Conclusions There were substantial reductions in in-hospital major adverse cardiac events and target-vessel revascularization over the past 5 years. This reduction was associated with the concurrent increased use of DES. Copyright © 2010 Wiley Periodicals, Inc. This work was performed at the Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. The authors have no funding, financial relationships, or conflicts of interest to disclose.

Objectives Visfatin is a new cytokine that act as an insulin analogue on the insulin receptor and may link obesity and insulin resistance. It was recently shown that visfatin plays a role in plaque destabilization. However, the role of visfatin in atherosclerosis remains to be elucidated. We sought to assess whether plasma visfatin level is independently associated with inflammation, atherosclerosis and acute coronary syndromes (ACS). Design and patients Two hundred and fifty-three patients undergoing coronary angiography were divided into three subgroups: chronic coronary artery disease (CAD) (n = 102), ACS (n = 100) and control patients (n = 51). The plasma samples were thawed and analysed for circulating visfatin, monocyte chemoattractant protein 1 (MCP-1), interleukin-6 (IL-6), high sensitivity C-reactive protein (hs-CRP). The association of visfatin with risk factors, inflammation, atherosclerosis, and ACS was determined. Results Plasma visfatin levels were significantly higher in chronic CAD and ACS compared with control patients. Multiple regression analysis demonstrated that plasma visfatin levels correlated with inflammatory factors and were associated with chronic CAD (odds ratio [OR][95% confidence interval], for second, third and fourth quartiles were 1.74 [0.96-2.69], 1.54 [0.85-2.28] and 1.84 [0.98-2.87], respectively) and ACS (ORs for second, third and fourth quartiles were 2.56 [1.57-3.34], 4.61 [1.94-10.96] and 6.52 [2.34-18.12], respectively) following adjustment for established risk factors and other inflammatory factors. Conclusions Plasma visfatin levels are significantly associated with CAD, particularly ACS, independent of well-known CAD risk factors.

Double the fun! Singlet–triplet dual emission at ambient temperature has been achieved in compounds containing a triarylboron acceptor and an N-(2′-pyridyl)-7-azaindolyl donor group bridged by a tetrahedral Si linker (see figure). PtII chelation and chelate-mode switching from N,N to N,C have been found to greatly enhance phosphorescent emission. Furthermore, both singlet and triplet emission bands are responsive to fluoride ions. A triarylboron compound Si-BNPA (1) containing a BMes2 acceptor and an N-(2′-pyridyl)-7-azaindolyl (NPA) donor linked by a tetrahedral silane group has been synthesised. This molecule displays unusual white singlet–triplet dual emission at 77 K, with an exceptionally long phosphorescent decay time (2.2 s). Fluoride titration experiments established that the singlet and triplet emission peaks are due to acceptor-based Mes→B charge transfer and donor-based 3π→π* transitions, respectively. This dual emission was found to be persistent and observable at ambient temperature in its PtII complex [Pt(N,N-Si-BNPA)Ph2] (2 a). Furthermore, 2 a was found to undergo intramolecular “roll-over” CH activation to produce the N,C-chelate complex [Pt(N,C-Si-BNPA)(SMe2)Ph] (2 b). This compound also displays ambient temperature singlet–triplet dual emission, but with a much greater phosphorescent efficiency than 2 a due to the formation of a more stable chelate ring. Addition of fluoride was found to have little impact on the phosphorescent emission of 2 a, but resulted in a large enhancement of the phosphorescent emission intensity of 2 b. To establish the impact of donor–acceptor geometry on this singlet–triplet dual emission, the properties of linearly conjugated donor–acceptor complexes [Pt(N,N-BNPA)Ph2] (3 a) and [Pt(N,C-BNPA)Ph2] (3 b) were also examined. Consistent with 2 a and 2 b, the N,C-chelate complex 3 b has a much higher phosphorescent efficiency than the N,N-chelate 3 a. Although 3 a and 3 b show bright and fluoride-switchable phosphorescence at ambient temperature, they are not dual emissive and show only metal-to-ligand chage-transfer-based phosphorescence. The non-conjugated donor–acceptor geometry and the overlap of the donor and acceptor singlet and triplet excitation bands in Si-BNPA and its PtII complexes may thus be the key for achieving singlet–triplet dual emission on two separated chromophores in a single molecule.

A variety of evolutionarily related defensin molecules is found in plants and animals. Plant gamma-thionins and scorpion neurotoxins, for instance, may be categorized in this functional group, although each class recognizes a distinct receptor binding site. Such molecules are also categorized into the superfamily of cysteine-rich proteins. Plant defensins were generally believed to be involved in antimicrobial or antifungal mechanisms and, unlike scorpion toxins, little is known about whether these molecules are also endowed with the function of insect resistance. We have previously reported the isolation of a cDNA encoding a small cysteine-rich protein designated VrD1 (VrCRP) from a bruchid-resistant mungbean, which is apparently the first discovered plant defensin exhibiting in vitro and in vivo both insecticidal and antifungal activities. Our previous data also successfully demonstrated that VrD1 is toxic to E. coli and able to completely arrest the growth of Sf-21 insect cells at low concentration. However, the molecular and structural basis of this unique insecticidal activity of VrD1 is not clear. Therefore, in the present study, we use structural approach and phylogenic analysis to investigate the evolutionary and functional relations for such unique insecticidal activity. From our results, it is suggested that VrD1, in addition to gamma-thionins and several amylase inhibitors, is highly homologous to scorpion toxins, especially the short toxins. Moreover, based on the observation from our homology structures, VrD1 may utilize a newly found cluster of basic residues to achieve its insecticidal function, whereas all the other plant gamma-thionins were known to use a previously identified basic cluster conserved for gamma-thionins. Considering the general feature of short scorpion toxins to act on insect cell membranes with K(+)- or Cl(-)-channels as molecular targets, our analysis of interaction and recognition modes provides reasonable correlations between this newly found basic cluster and the insecticidal activity of VrD1, which is also comprehended as a possible link for "homoplasy evolution" between plant and animal defensin molecules.

MnCl2, NiCl2, FeCl3, and several Cu(I) and Cu(II) salts are disclosed as efficient oxidation catalysts for 1,4-dihydropyridines.