Gold nanorods-mediated efficient synergistic immunotherapy for detection and inhibition of postoperative tumor recurrence

Tumor recurrence after surgery is the main cause of treatment failure. However, the initial stage of recurrence is not easy to detect, and it is difficult to cure in the late stage. In order to improve the life quality of postoperative patients, an efficient synergistic immunotherapy was developed to achieve early diagnosis and treatment of post-surgical tumor recurrence, simultaneously. In this paper, two kinds of theranostic agents based on gold nanorods (AuNRs) platform were prepared. AuNRs and quantum dots (QDs) in one agent was used for the detection of carcinoembryonic antigen (CEA), using fluorescence resonance energy transfer (FRET) technology to indicate the occurrence of

Quantification of human plasma 7α-hydroxy-4-cholesten-3-one and bile acids by UPLC-MS/MS / 上海交通大学学报（医学版）

Objective : To develop a quantitative method of 7α-hydroxy-4-cholesten-3-one (C4), cholic acid (CA) and chenodeoxycholic acid (CDCA) in human plasma. Methods ¡¤ After extraction of C4, CA and CDCA with acetonitrile from plasma, they were quantified with stand-ard curve corrected by the internal standards based on Ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Results ¡¤ The limits of detection (LOD) of C4, CA and CDCA were 0.16, 0.02 and 0.04 nmol/L respectively; All three metabolites had good linear relationships (correlation coefficients R2 were over than 0.998). The relative standard deviations (RSDs) of repeatabilities were below 3.0%. The RSDs of inter-day and intra-day precision were less than 6%, and the RSDs of stabilities at 4 °C were below 10% within 7 days. The average added recoveries of C4, CA and CDCA were 97.7%, 113.3% and 105.0%, respectively. Conclusion ¡¤ This method is of high detective sensi-tivity, good precision and stability, which meets the quantitative requirements of plasma biological samples.

New compound NL-608 (a nutlin analog) induces apoptosis in human breast cancer MCF-7 cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To observe the effect of NL-608 (a nutlin analog) on apoptosis induction in human breast cancer MCF-7 cells in vitro, and investigate the relevant molecular mechanism.</p><p><b>METHODS</b>The effect of NL-608 on proliferation of MCF-7 cells was determined by MTT assay. The apoptosis in MCF-7 cells was determined by flow cytometry with annexin V-FITC and PI. The activity of caspase 3, caspase 8 and caspase 9 was determined with caspase activity assay kit and Western blot, and the proteins of Fas and FasL were determined by Western blot.</p><p><b>RESULTS</b>NL-608 showed a dose-dependent inhibitory effect on the proliferation of MCF-7 cells. It induced apoptosis in MCF-7 cells in a dose-dependent manner. The activity of caspase 3 and caspase 8 in MCF-7 cells was increased with the increasing concentration of NL-608, but caspase 9 had no changes. The proteins of Fas and FasL were increased in a dose-dependent manner.</p><p><b>CONCLUSION</b>NL-608 induces apoptosis in MCF-7 cells in vitro through inducing caspase 3 activity and death receptor-mediated signal pathway.</p>

Inhibitory effects of saponins from Anemarrhena asphodeloides Bunge on the growth of vascular smooth muscle cells / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the effects of saponins from Anemarrhena asphodeloides Bunge (SAaB) (Botanical Name: Anemarrhena Asphodeloidis Rhizoma) on the growth of vascular smooth muscle cells (VSMCs).</p><p><b>METHODS</b>Cell proliferation was measured by a newly developed cell proliferation reagent, WST-1. Cell apoptosis was assayed by flow cytometry through detecting annexin V. Nitric oxide production was evaluated using confocal laser scanning microscopy with diaminofluorescein diacetate (DAF-2, DA). Cell aldose reductase (AR) activity, as well as the effect of Epalrestat and interleukin-1beta were also explored.</p><p><b>RESULTS</b>WST assay showed that cell proliferation induced by serum was significantly inhibited by SAaB (P<0.01). Flow cytometry analysis revealed that SAaB could enhance apoptotic rate of VSMCs (P<0.01). Nitric oxide production was significantly enhanced after administration of SAaB and interleukin-1beta. Moreover, AR activity of VSMCs was also remarkably inhibited by both SAaB and Epalrestat (P<0.01).</p><p><b>CONCLUSION</b>SAaB can inhibit proliferation and enhance apoptosis of VSMCs. It may protect vascular cells by inhibiting VSMC proliferation and augmenting apoptotic rate of VSMCs via NO-dependent pathway.</p>