ABSTRACT
@#Objective To summarize the clinical experience of Da Vinci robotic-assisted left upper lobectomy for treating lung cancer. Methods We retrospectively analyzed the perioperative data of 33 patients with primary lung cancer who underwent Da Vinci robotic-assisted left upper lobectomy between December 2016 and December 2018 in our hospital. Meanwhile, the perioperative data of 41 patients with lung cancer who underwent video-assisted thoracoscopic left upper lobectomy during the same period by the same surgeon were studied as a control group. The resection was followed by the principle of "from back down to front up" way. Systemic lymph node dissection including No.4-9 was performed for all patients. Results All patients received successful surgery with no case of conversion to thoracotomy and perioperative death. Comparing to video-assisted thoracoscopic surgery, the Da Vinci robotic-assisted left upper lobectomy had longer operating time (191.21±61.77 min vs. 154.51±38.81 min, P=0.003), more cost (82 307.75±11 859.03 yuan vs. 58 966.57±5 640.07 yuan, P=0.000), shorter chest tube duration (4.58±1.77 d vs. 5.41±1.52 d, P=0.031) and postoperative hospital stay (6.48±1.82 d vs. 7.66±2.12 d, P=0.014). However, there was no significant difference between the two groups regarding to blood loss, lymph node dissection, postoperative pain score, total chest drainage volume, chest drainage volume per day and the rate of pulmonary complications. Conclusion The Da Vinci robotic-assisted left upper lobectomy for treating lung cancer is safe and more minimally invasive, but more expensive.
ABSTRACT
@#Objective To analyze the surgical outcome of patients with lung cancer using double micro-portal video-assisted thoracic surgery (VATS) technique. Methods We retrospectively analyzed the perioperative data of 200 patients with primary lung cancer who underwent successful two micro-portal VATS lobectomy between September 2016 and June 2018 at our unit. There were 125 males and 75 females, aged 61.01±8.71 years. The length of the main operating hole was about 2.0–2.5 cm, the size of the secondary operating hole and the observation hole was 0.5 cm individually. Thus, the total length of the three incisions was 3.0–3.5 cm. Results The mean operating time was 99.18±21.77 min, blood loss was 170.35±105.12 ml, and the mean number of dissected lymph node was 15.82±3.33. The mean volume and duration of chest tube were 446.90±195.32 ml and 3.67±1.85 days. The postoperative hospital stay was 5.54±2.41 days. Only one patient died of pulmonary embolism after surgery. There were 7 patients who were converted to thoracotomy. Postoperative pulmonary infection after lobectomy was found in 8 patients. Postoperative air leak over 5 days was developed in 7 patients. Conclusion The double micro-portal VATS procedure is a safe and effective strategy for patients with lung cancer, which is associated with decreased surgical trauma and less postoperative pain. This emerging technology may benefit patients by enhancing comfort during their postoperative hospitalization.
ABSTRACT
Objective:To investigate the pro-apoptotic effect of berberine (Ber) on human lung adenocarcinoma PC-9 cell line, and to detect the role of c-Jun N-terminal kinase (JNK)/forkhead box protein O3 (FOXO3) signaling in this process. Methods:The PC-9 cells were randomly divided into the control group and the Ber group, which was treated with 30 and 60μM Ber. The survival rate, apoptot-ic rate, ROS generation, caspase-3 activity, and mitochondrial membrane potential of cells were detected. Western blot was per-formed to detect the expression of JNK/FOXO3 signaling and apoptosis-related proteins. A JNK-specific activation inhibitor, SP600125, was used to block the phosphorylation of FOXO3 in PC-9 cells, and then treated with Ber (30 and 60μM) for further detection after 24 h. Results:Ber treatment resulted in an obvious reduction in cell viability, promotion of cell apoptosis, downregulation of mitochondri-al membrane potential, and an increase of ROS and caspase-3 in a dose-dependent manner. Western blot analysis demonstrated that Ber treatment resulted in a significant upregulation of p-JNK, FOXO3, and Bax expression, and a downregulation of p-FOXO3 and Bcl2 levels. Moreover, the inhibition of JNK activation by SP600125 antagonized the anti-FOXO3 phosphorylation role and the pro-apoptotic role of Ber on PC-9 cells. Conclusion:Ber treatment effectively inhibits the viability of PC-9 cells and enhances apoptosis and oxidative stress injury, which may be related to the upregulation of p-JNK and FOXO3 and the downregulation of p-FOXO3.
ABSTRACT
Objective:To investigate the pro-apoptotic effect of berberine (Ber) on human lung adenocarcinoma PC-9 cell line, and to detect the role of c-Jun N-terminal kinase (JNK)/forkhead box protein O3 (FOXO3) signaling in this process. Methods:The PC-9 cells were randomly divided into the control group and the Ber group, which was treated with 30 and 60μM Ber. The survival rate, apoptot-ic rate, ROS generation, caspase-3 activity, and mitochondrial membrane potential of cells were detected. Western blot was per-formed to detect the expression of JNK/FOXO3 signaling and apoptosis-related proteins. A JNK-specific activation inhibitor, SP600125, was used to block the phosphorylation of FOXO3 in PC-9 cells, and then treated with Ber (30 and 60μM) for further detection after 24 h. Results:Ber treatment resulted in an obvious reduction in cell viability, promotion of cell apoptosis, downregulation of mitochondri-al membrane potential, and an increase of ROS and caspase-3 in a dose-dependent manner. Western blot analysis demonstrated that Ber treatment resulted in a significant upregulation of p-JNK, FOXO3, and Bax expression, and a downregulation of p-FOXO3 and Bcl2 levels. Moreover, the inhibition of JNK activation by SP600125 antagonized the anti-FOXO3 phosphorylation role and the pro-apoptotic role of Ber on PC-9 cells. Conclusion:Ber treatment effectively inhibits the viability of PC-9 cells and enhances apoptosis and oxidative stress injury, which may be related to the upregulation of p-JNK and FOXO3 and the downregulation of p-FOXO3.