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Objective@#To obtain chimeric antigen receptor macrophages ( CAR-M) targeting HER2 stably transfected．@*Methods @#CAR lentivirus vector targeting HER2 was constructed and infected with human monocytic leukemia cell line (THP-1) ．CAR THP-1 cells with green fluorescent labeling were selected by sorting flow cytometry and continued to be cultured in vitro．The CAR THP-1 cells targeting HER2 were co-cultured with the endometrial cancer cell line Ishikawa with negative and positive HER2 expression，and their targeted phagocytosis of CAR-M to HER2 positive tumor cells was detected by imaging flow cytometry ，and the targeted phagocytosis efficiency of CAR-M to HER2 positive tumor cells was detected by flow cytometry. @*Results @#CAR lentivirus infection with THP- 1 cells was less efficient ; After co-culture with cancer cells，flow cytometry and imaging flow cytometry showed that CAR THP-1 cells had enhanced phagocytosis of HER2 positive Ishikawa cells compared with the empty body group (P＜0. 01) ．@*Conclusion @#In this experiment，CAR THP-1 cell line targeting HER2 was established by constructing CAR lentivirus vector and transfecting THP-1 cells ，and it was proved that CAR THP-1 could phagocytize HER2 positive Ishikawa cells through specific targeting.
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Objective To explore the value ofintraoperative CT (iCT) in endoscopic endonasal surgery for pituitary adenomas.Methods A retrospective analysis was conducted in the clinical data of 37 patients with pituitary adenomas performed endoscopic endonasal surgery with assistance of iCT in our hospital from November 2012 to June 2013.The influences of iCT on surgical process and results were analyzed.Results Intraoperative scanning was performed 1 to 3 times in each patient,averaging 1.43 times.The scanning time was only 50-60 s.Among the 37 patients,iCT revealed residual tumor in 11,9 of which underwent further resection with total removal in 6 and subtotal in 3,and the tumors in the other two patients were unable to be resected because the adenomas were tenacious and adhered closely to the internal carotid artery.Finally,the rate of gross total removal increased from 70.3％ to 86.5％,rising by 16.2％.No iCT related complications and severe surgical complication occurred.Conclusion The application of iCT in endoscopic endonasal surgery for pituitary adenomas provides objective evidence for the guidance of surgical procedure and real-time judgment of surgical results,which not only leads to higher percentage of tumor removal but also eliminates the unnecessary blind surgical manipulation to increase the safety of the operation.
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Objective To discuss the effect of hyperthermia on tight junctions of the endothelial cells in the blood-brain barrier and explore the molecular mechanism. Methods An in vitro blood-brain barrier model was established by coculture of ECV304 and astrocytes. Transendothelial resistance (TER) of in vitro blood-brain barrier was determined by Millicell-ERS system. The morphological change of tight junctions of the endothelial cells in the in vitro blood-brain barrier was determined by the method of silver staining. The expression levels of zonula occluden 1 (ZO-1) and occludin were analyzed by means of semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western bloting. Results After two hours at 43℃, the mean value of TER was decreased from (321.30? 58.59) ??cm2 to (65.67?6.02) ??cm2. The integrity of tight junctions was destroyed and the expressions of ZO-1 and occludin decreased significantly. Conclusions Hyperthermia can destroy the tight junctions of the endothelial cells in the in vitro blood-brain barrier. The expression decrease of ZO-1 and occludin induced by hyperthermia is one of the most important molecular mechanisms.
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AIM: To investigate the effects of glioma cells on aquaporin expression in blood-brain barrier and their importance in pathophysiology. METHODS: A blood-brain barrier model was established by coculture of ECV304 and astrocytes in vitro . HPLC was used to determine the change of water transport of in vitro blood-brain barrier model after the influence of glioma cells. The expression levels of AQP1 and AQP4 were analyzed by semiquatitative RT-PCR. RESULTS: Glioma cells decreased expression level of AQP4 of astrocytes and induced abnormal expression of aquaporin-1 in endothelial cell line. The water transport of in vitro blood-brain barrier model from luminal side to abluminal side was increased after coculture with glioma cells. CONCLUSION: The vasogenic brain edema induced by glioma cells may not be the result of hyperpermeability of blood-brain barrier to macromolecules in plasma. The changes of aquaporin expression may be the molecular basis of brain edema induced by glioma cells.