[The Comparison Between Extraction Methods of Exosomes From Ascites of Colorectal Cancer].

OBJECTIVE: To compare the two different methods to isolate the exosome from the ascites of colorectal cancer (CRC) patient and find the efficient one. METHODS: Exosome from the ascites of CRC patient were isolated by two different methods: density gradient exosome isolation (DG-Exo) and Exo-Quick isolation, and followed by identification with transmission electron microscopy observation and Western blot analysis. And then, Nanodrop was used for protein quantification. RESULTS: Exosome were isolated by both of the two methods. The protein concentration of the exosome isolated by the Exo-Quick isolation were higher than that of DG-Exo. CONCLUSION: Exo-Quick isolation can obtain higher purity and more complete exosome from the ascites.

Regulatory effect of Act1 on the BAFF pathway in B-cell malignancy.

The aim of the present study was to ascertain whether nuclear factor (NF)-κB Activator 1 (Act1) was involved in B cell-activating factor (BAFF) regulation in B-cell malignancy. The human B-cell malignancy cell lines Raji, Daudi and BALL-1 were cultured and the expression of BAFF receptor (BAFF-R) mRNA and protein was analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting, respectively. NF-κB signaling was also assessed using western blotting. Act1 silencing was performed using Act1 small interfering RNA. BAFF-R levels were assessed using flow cytometry. It was demonstrated that BAFF-R was upregulated in all three cell lines and RT-qPCR, and western blotting confirmed these results. Act1 overexpression was demonstrated to induce BAFF-R upregulation, whereas Act1 knockdown resulted in BAFF-R downregulation. Furthermore, the NF-κB pathway was activated by Act1 overexpression and inhibited following Act1 knockdown. The results of the present study demonstrated that Act1 can regulate BAFF via targeting NF-κB signaling, which suggests that Act1 may be a promising therapeutic target for the treatment of B-cell malignancy.

Building an evaluation instrument for China's hospital emergency preparedness: a systematic review of preparedness instruments.

OBJECTIVES: The aim of this report is to identify from the literature common themes relating to the concept of hospital preparedness for emergencies to develop an agreed framework for evaluation. METHOD: A systematic literature search identified appropriate articles for critical appraisal. A meta-ethnography approach was used to synthesize the findings, using both reciprocal translation and line-of-argument synthesis. RESULTS: From an initial 2162 articles, we identified 13 articles that specifically addressed the aims of this review and formed the basis of the intended analysis. CONCLUSION: Hospital emergency preparedness is essential for effective disaster relief. Developing a systematic and structured methodology is necessary to assess hospital preparedness.

Induced IGF-1R activation contributes to gefitinib resistance following combined treatment with paclitaxel, cisplatin and gefitinib in A549 lung cancer cells.

Gefitinib demonstrates excellent performance in the treatment of lung adenocarcinoma patients; yet, there was no added benefit in combination with chemotherapy as reported in a phase III clinical trial. For exploring the mechanism of the failed combination therapy in lung cancer, in the present study, four therapy assessment groups, including a control group, a chemotherapy group [paclitaxel+cisplatin (TP)], a gefitinib monotherapy group (G) and a combination group[paclitaxel+cisplatin+gefitinib (TP+G)], were established in an A549 cell line and mouse xenotransplanted tumor models.By HPLC, we found that the gefitinib concentration was significantly higher in the combination group when compared to that in the G group in the non-small cell lung cancer cell line, A549 (p<0.05). Following the treatment time extension,an increased cell growth rate was observed in the combination group, while the cellular concentration of gefitinib was not decreased. The expression levels of P-IGF-1R, P-SRC and P-ERK in the fourth combination treatment group were significantly higher than levels in the fourth G treatment and control groups (p<0.05). Following downregulating of IGF-1R in the fourth combination treatment group, drug sensitivity was recovered in vitro. In the mouse model, compared with the gefitinib monotherapy group, the combination group exhibited a smaller tumor volume, lower body weight and reduced survival rate (p<0.05). Gefitinib concentrations in the serum and tumor tissues in the combination therapy group were also decreased when compared with these concentrations in the gefitinib alone group. The present study is the first to demonstrate that the decreased gefitinib concentration in serum and tumor tissues is one of the reasons resulting in the failed combination treatment (chemotherapy+gefitinib) in vivo study. Frequent use of the combination treatment in A549 lung cancer cells induced IGF-1R activation which contributed to gefitinib resistance and gave rise to the failure of the combination therapy.