Four types of water-soluble quantum dots (QDs) grafted with different organic coating layers were fabricated, and their sensitivities for hypochlorite/hypochlorous acid (HClO) were examined. It was found that QDs with HClO reactive (methylamino and sulphide groups) coating layers exhibited a protective effect on HClO quenching of QD fluorescence, whereas QDs with hydrocarbon and carboxylate coating layers showed least protection to QD fluorescence quenching by HClO and, thus, has the highest sensitivity for the detection of HClO. The QDs with carboxylate coating layers (QDs-poly-CO(2)(-)) was successfully applied to the quantification of HClO in tap water. The excellent selectivity of the QDs-poly-CO(2)(-) toward hypochlorite against other reactive oxygen species allowed us to monitor myeloperoxidase activity. Finally, the QDs-poly-CO(2)(-) was also used for the detection of hypochlorite in HL60 cells by fluorescent imaging. Hence, QD-poly-CO(2)(-) exhibits great promise as a selective and sensitive HClO probe in chemical and biological systems.

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) gefitinib has demonstrated dramatic clinical efficacy in non-small cell lung cancer (NSCLC) patients. However, its therapeutic efficacy is ultimately limited by the development of acquired drug resistance. The aim of this study was to explore the potential utility of chromosome region maintenance 1 (CRM1) inhibitor leptomycin B (LMB) in combination with gefitinib to overcome primary and acquired gefitinib resistance in NSCLC cells. The combinative effects of gefitinib and LMB were evaluated by MTT and its underlining mechanism was assessed by flow cytometry and Western blot. LMB displayed a synergistic effect on gefitinib- induced cytotoxicity in A549 (IC50: 25.0±2.1 μM of gefitinib+LMB vs. 32.0±2.5 μM of gefitinib alone, p<0.05). Gefitinib+LMB caused a significantly different cell cycle distribution and signaling pathways involving in EGFR/survivin/p21 compared with gefitinib. A549 cells then were treated with progressively increasing concentrations of gefitinib (A549GR) or in combination with LMB (A549GLR) over 10 months to generate gefitinib resistance. IC50 of gefitinib in A549GLR (37.0±2.8 μM) was significantly lower than that in A549GR (53.0±3.0 μM, p<0.05), which indicates that LMB could reverse gefitinib-induced resistance in A549. Further mechanism investigation revealed that the expression patterns of EGFR pathway and epithelial- mesenchymal transition (EMT) markers in A549, A549GR, and A549GLR were significantly different. In conclusion, LMB at a very low concentration combined with gefitinib showed synergistic therapeutic effects and ameliorated the development of gefitinib- induced resistance in lung cancer cells.

One new stilbene derivative (3,5,3'-trihydroxy-4'-methoxy-5'-isopentenylstilbene, MIP) and two new stilbene dimers (arahypin-11 and arahypin-12) together with three known stilbenoids (arachidin-1, arachidin-3, and SB-1) were isolated from black skin peanut seeds challenged by the fungal strain Rhizopus oligoporus . The structures of the three new compounds were elucidated by analysis of HRESIMS, UV, 1D and 2D NMR spectra. The antiadipogenic and cytotoxic effects of the isolated compounds were investigated using 3T3-L1 cells at a concentration range of 1-10 μM. Among the compounds tested, arachidin-1 inhibited the 3T3-L1 adipocyte differentiation dose-dependently, whereas arahypin-11 and arahypin-12 exhibited significant cytotoxicity in 3T3-L1 preadipocytes.

No abstract

No abstract