ObjectiveTo compare the effects of dexmedetomidine and propofol for stereotactic brain surgery in patients with intractable psychosis.MethodsThirty male patients with intractable psychosis,aged 22-33 yr,weighing 60-90 kg,scheduled for stereotactic surgery,were randomized to receive either propofol (group P,n =15) or dexmedetomidine (group D,n =15).Anesthesia was induced with iv injection of midazolam 0.05-0.10 mg/kg and fentany 1-2 μg/kg in the two groups,and in addition,dexmedetomidine was infused at 0.3-0.7μg· kg- 1 · h- 1 after a loading dose of 1 μg/kg (duration of infusion ＞ 10 min) and propofol 1-2 mg/kg was injected intravenously before endotracheal intubation in group D and propofol 2-3 mg/kg was injected intravenously and then propofol was infused at a rate of 3-4 mg· kg- 1 · h- 1 in group P.Orotracheal intubation was performed under the guidance of direct laryngoscope.The patients kept spontaneous breathing.The adverse events such as body movement,bucking,apnea,adverse cardiac events and hypoxemia were recorded during location.ResultsThe incidence of body movement,bucking,apnea,tachycardia,hypotension and hypoxemia was significandy lower,while the incidence of bradycardia was significantly higher in group D than in group P ( P ＜ 0.01 ).There was no significant difference in the incidence of hypertension between the two groups (P ＞ 0.05).ConclusionDexmedetomidine provides better anesthesia,exerts less effect on the respiratory and circulatory functions and is safer than propofol for stereotactic surgery in patients with intractable psychosis.

Aim To study the mechanism of cucurb-itacin E ( CuE )-induced autophagy in HeLa cells. Methods Improved MTT assay was adopted to meas-ure the effect of CuE on cell proliferation. Western blot was used to determine the phosphorylation levels of downstream signaling proteins of mTORC1 and the ex-pression of autophagy associated proteins. ResultsCuE inhibited the proliferation of HeLa cells in a dose-dependent manner, and the 24-h IC50 of CuE was 4. 01μmol· L-1 . CuE significantly inhibited the phospho-rylation of p70 S6 K in a time-and dose-dependent man-ner as evidenced by decreased phosphorylation levels of
the mTORC1 substrate. Meanwhile, the expression of LC3-II, a marker for autophagosome formation, was elevated by CuE treatment, and was further increased in the presence of chloroquine. Furthermore, CuE re-duced the levels of p62/SQSTM1 . These results indi-cated that CuE induced autophagy in HeLa cells. The decreased levels of phosphorylated ULK1 S757 were posi-tively correlated with autophagy induction in HeLa cells. Conclusion CuE is likely to induce autophagy through inhibiting mTORC1 activity.

Adult ; Antineoplastic Agents ; adverse effects ; therapeutic use ; Benzamides ; Gynecomastia ; chemically induced ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; Male ; Piperazines ; adverse effects ; therapeutic use ; Pyrimidines ; adverse effects ; therapeutic use

Objective:To summarize the experience of surgical methods without repairing the fistula for 92 cases with gastrointestinal intrathoracic fistula.Methods:The surgical methods without repairing the fistula were performed through VATS, small incision assisted with VATS or thoracotomy. The focus of the surgery was to promote lung expansion, eliminate the residual cavity of chest cavity and keep effective drainage. After entering the chest cavity from the affected side, wash chest cavity with a large amount of warm normal saline and sterilize intermittently with iodophor to ensure the sterile environment in the pus cavity. Then completely remove the pleural cellulose or fiberboard on visceral pleura to promote lung expansion, eliminate the residual cavity of the chest cavity. The fistula was covered tightly and supported firmly by the visceral pleura on the lung. Multiple T-tubes were placed in thoracic cavity and fistula to keep effective postoperative drainage.Results:Among 92 cases, 85 cases were cured and the cure rate was 92.4% (85/92).7 cases died and the mortality rate was 7.61% (7/92). The 7 dead cases include 5 cases with esophagogastric anastomotic fistula (the death of 3 cases was cause by aortic esophagogastric fistula, the death of 1 case was cause by thoracic gastric tracheal fistula and 1 case was dead because of pulmonary infection and respiratory failure), 1 case with esophageal rupture (the cause of death was septic shock ), and 1 case with esophageal perforation(the cause of death was pulmonary infection and respiratory failure).Conclusion:Most of the surgeries without repairing gastrointestinal intrathoracic fistula are conducted simply through VATS or small incision assisted with VATS., which is safe and effective.

Phosphoprotein Phosphatases ; Kinetics ; Protein Phosphatase 2/metabolism*

Objective: To investigate the reversal effect of cinobufagin ( CINO) combined with 5-fluorouracil (5- FU) on human colorectal cancer ( CRC) drug-resistant cell line HCT15 /5-FU，and to clarify the regulatory role of hypoxia-inducible factor-1α (HIF-1 α) / vascular endothelial growth factor (VEGF) pathway in reversing chemoresistance of colorectal cancer． Methods : MTT assay was used to detect the changes of drug resistance and drug resistance index，flow cytometry was used to evaluate the apoptosis of cells ，scratch test and Transwell assay were used to detect the changes of cell migration and invasion ability．Western blot was used to detect the expressions of epithelial-mesenchymal transition (EMT) related proteins and HIF-1 α/ VEGF pathway-related proteins. Results: Compared with HCT15 cells，the resistance index of HCT15 /5-FU was about 8. 720． CINO combined with 5-FU could significantly enhance the drug sensitivity of HCT15 /5-FU cells，reduce drug resistance index，up-regulate the level of apoptosis，and inhibit cell migration and invasion in a dose-dependent manner．Western blot results showed that CINO combined with 5-FU could inhibit the activity of EMT and HIF-1 α/ VEGF pathway． Conclusion CINO can reverse 5-FU resistance of colorectal cancer in vitro，and its mechanism may be related to the regulation of the HIF-1 α/ VEGF pathway and the inhibition of EMT and angiogenesis.