Orange-emissive carbon quantum dots for ligand-directed Golgi apparatus-targeting and in vivo imaging.

The Golgi apparatus is one of the most important organelles in cells. Targeting and monitoring the morphology and structure of the Golgi apparatus are crucial and challenging. Aimed at the cysteine (Cys) receptor on the surface of the Golgi apparatus, ligand-directed carbon quantum dots (CQDs) were synthesized for Golgi apparatus-targeting imaging. In order to reduce the interference of tissue self-fluorescence and enhance the tissue penetration depth, orange-emissive levorotatory CQDs (L-CQDs) with Golgi apparatus-targeting ability were synthesized using the strategy of inheriting Cys residues and the inherent conjugated electronic structure of neutral red. They exhibit excitation-dependent, fluorescence stability, rich surface Cys residues, excellent biocompatibility, and low toxicity. As a Golgi apparatus-targeting agent, L-CQDs can quickly enter cells for Golgi apparatus-targeting imaging, and can also penetrate through biological tissue for imaging in vivo. The surface Cys residues of CQDs actively target the Cys receptors on the surface of the Golgi apparatus to achieve Golgi apparatus-targeting imaging.

Effect of Surfactant Polyvinyl Pyrrolidone on the Properties of Microporous Carbon Nanospheres Reinforced Magnesium Matrix Composites.

Microporous carbon nanospheres (PCNS)-reinforced magnesium (Mg) composites were prepared using polyvinyl pyrrolidone (PVP) as surfactant and PCNS as reinforcement. The influence of PVP treatment and the effectiveness of PCNS on the mechanical properties of Mg-based composites were investigated. The results show that the PCNS can enhance the properties of the Mg matrix. Moreover, the PVP can effectively improve the dispersion of PCNS in the Mg matrix but had a negative influence on the tensile properties of composites. The MgO films with high tensile strength were produced between matrix and reinforcement after removing PVP, which effectively promotes the interface compatibility and improves the properties of the composite. The tensile yield strength and specific strength of PCNS-reinforced Mg matrix composite exhibited 177 MPa and 102.4 × 103 N∙m/kg, respectively, which were 77% and 78% higher than those of the Mg matrix.

Cigarette smoke extract induces the epithelial-to-mesenchymal transition via the PLTP/TGF-ß1/Smad2 pathway in RLE-6TN cells.

Aim: The role of phospholipid transfer protein (PLTP) in the pathogenesis of the cigarette smoke extract (CSE)-induced epithelial-to-mesenchymal transition (EMT) has not been well described. In this study we investigated the effect of PLTP on the CSE-induced EMT of rat alveolar epithelial cells (RLE-6TN). Methods: The rats were exposed to air and cigarette smoke (CS) for 3 d and then the lungs were sectioned and examined using immunohistochemistry techniques. RLE-6TN cells were treated with different concentrations of CSE. PLTP siRNA was transfected into cells or SB431542 - an inhibitor of the transforming growth factor-ß1 (TGF-ß1) type I receptor - was administered prior to CSE exposure. The expression of EMT markers and PLTP was detected by qRT-PCR. The levels of PLTP, TGF-ß1, p-Smad2, Smad2, and EMT proteins were analyzed by western blotting. Results: Lung injury and EMT were accompanied by up-regulation of PLTP and TGF-ß1 in the CS-exposed rat model. EMT was induced by CSE in vitro, and the expression of PLTP, TGF-ß1, and p-Smad2 was significantly increased after exposure to CSE (P < 0.05). Moreover, knockdown of PLTP and blocking of the TGF-ß1/Smad2 pathway restrained the CSE-induced activation of the TGF-ß1/Smad2 pathway and partly inhibited EMT by reversing E-cadherin expression and retarding the induction of N-cadherin and vimentin. In contrast, SB431542 had no effect on the expression of PLTP, while it ameliorated CSE-induced EMT. Conclusion: PLTP promotes the CSE-induced EMT process, in which the TGF-ß1/Smad2 pathway is activated.

Type 1 Metallothionein (ZjMT) Is Responsible for Heavy Metal Tolerance in Ziziphus jujuba.

Metallothioneins (MTs) are a family of low molecular weight, cysteine-rich, metal-binding proteins that are able to make cells to uptake heavy metals from the environment. Molecular and functional characterization of this gene family improves understanding of the mechanisms underlying heavy metal tolerance in higher organisms. In this study, a cDNA clone, encoding 74-a.a. metallothionein type 1 protein (ZjMT), was isolated from the cDNA library of Ziziphus jujuba. At the N- and C-terminals of the deduced amino acid sequence of ZjMT, six cysteine residues were arranged in a CXCXXXCXCXXXCXC and CXCXXXCXCXXCXC structure, respectively, indicating that ZjMT is a type 1 MT. Quantitative PCR analysis of plants subjected to cadmium stress showed enhanced expression of ZjMT gene in Z. jujuba within 24 h upon Cd exposure. Escherichia coli cells expressing ZjMT exhibited enhanced metal tolerance and higher accumulation of metal ions compared with control cells. The results indicate that ZjMT contributes to the detoxification of metal ions and provides marked tolerance against metal stresses. Therefore, ZjMT may be a potential candidate for tolerance enhancement in vulnerable plants to heavy metal stress and E. coli cells containing the ZjMT gene may be applied to adsorb heavy metals in polluted wastewater.

Global Harmonization of Maximum Residue Limits for Pesticides.

International trade plays an important role in national economics. The Codex Alimentarius Commission develops harmonized international food standards, guidelines, and codes of practice to protect the health of consumers and to ensure fair practices in the food trade. The Codex maximum residue limits (MRLs) elaborated by the Codex Committee on Pesticide Residues are based on the recommendations of the FAO/WHO Joint Meeting on Pesticides (JMPR). The basic principles applied currently by the JMPR for the evaluation of experimental data and related information are described together with some of the areas in which further developments are needed.

MicroRNA-362 induces cell proliferation and apoptosis resistance in gastric cancer by activation of NF-κB signaling.

BACKGROUND: According to cancer-related microRNA (miRNA) expression microarray research available in public databases, miR-362 expression is elevated in gastric cancer. However, the expression and biological role of miR-362 in gastric progression remain unclear. METHODS: miR-362 expression levels in gastric cancer tissues and cell lines were determined using real-time PCR. The roles of miR-362, in promoting gastric cancer cell proliferation and apoptosis resistance, were assessed by different biological assays, such as colony assay, flow cytometry and TUNEL assay. The effect of miR-362 on NF-κB activation was investigated using the luciferase reporter assay, fluorescent immunostaining. RESULTS: MiR-362 overexpression induced cell proliferation, colony formation, and resistance to cisplatin-induced apoptosis in BGC-823 and SGC-7901 gastric cancer cells. MiR-362 increased NF-κB activity and relative mRNA expression of NF-κB-regulated genes, and induced nuclear translocation of p65. Expression of the tumor suppressor CYLD was inhibited by miR-362 in gastric cancer cells; miR-362 levels were inversely correlated with CYLD expression in gastric cancer tissue. MiR-362 downregulated CYLD expression by binding its 3' untranslated region. NF-κB activation was mechanistically associated with siRNA-mediated downregulation of CYLD. MiR-362 inhibitor reversed all the effects of miR-362. CONCLUSION: The results suggest that miR-362 plays an important role in repressing the tumor suppressor CYLD and present a novel mechanism of miRNA-mediated NF-κB activation in gastric cancer.