Laparoscopic surgery for upper-third gastric cancer has gradually been accepted by experienced surgeons as the mature of this technique.Different from the standardized and programmed D2 lymph node dissection in Laparoscopy-assisted Billroth Ⅰ gastrectomy,the indications and methods for laparoscopic splenic hilar lymphadectomy in the upper-third gastric cancer remains controversial.Unsolved problems include joint organs resection,appropriate surgical approach selection and variable vascular anatomy of the splenic hilum.Meanwhile,the long-term efficacy and safety of laparoscopic splenic hilar lymphadectomy for the upper-third gastric surgery need to be confirmed by evidence-based medical trials.With the advance of the theory and clinical practice,laparoscopic splenic hilar lymph node dissection will continue to progress.

Objective To observe the expression changes of matrix metalloproteinase 9(MMP-9),vascular endothelial growth factor(VEGF)in the esophageal squamous cell carcinomas,and to study the chinical significance. Methods The expression of MMP-9 and VEGF in 60 patients with esophageal carcinoma and 20 cases with adjacent normal mucosa were tested with immunohistochemical SP method. Results The positive rate of MMP-9,VEGF in the esophageal squamous cell carcinomas were 70%(42/60)and 80%(48/60),the positive rate of adjacent normal mucosa were 10%(2/20)and 20%(4/20).The positive rates of the two groups were compared,all the differences had statistical significance(P＜0.05); expressions of MMP-9,VEGF in the esophageal squamous cell carcinomas related to invasive depth of carcinoma and lymph node metastasis(P＜0.05).There were positive correlation(r=2.330,P＜0.05). Conclusion The higher expression of MMP-9 and VEGF in the esophageal squamous cell carcinomas played an important role in invasion and metastasis of esophagus squamous cancer.

Objective: To explore the effect of ginsenoside Rgl on the ubiquitin-modified protein aggregation in the cortex after cerebral ischemia reperfusion (I / R) injury in the rats, and to further clarify the therapeutic mechanism of ginsenoside Rgl in the cerebral I/R injury. Methods: The middle cerebral artery occlusion (MCAO) model was set up with suture method for 1. 5 h of embolization. A total of 72 rats were divided into sham operation group, I/R model group, positive drug control (nimodipine) group, low, middle, and high doses 10, 20, and 40 mg ' k g - 1) of ginsenoside Rgl groups. All 12 rats in each group were given intraperitoneal injection. TTC staining and Longa' s score method were used to detect the infarction areas and the neurological deficit scores of the rats in various groups 24 h after modeling. The death of neurons in the cortex and hippocampus after cerebral ischemia of the rats in various groups were observed with HE staining. Immunohistochemistry and Western blotting method were used to detect the expression of ubiquitin-modified protein aggregation in the cortex of the rats in various groups. Results: Compared with I/R group, the percentages of infarction areas of the rats in nimodipine group and ginsenoside Rgl groups were significantly decreased (P < 0 . 05). and the neurological deficit scores were decreased (P < 0 . 05). The HE staining results showed that compared with sham operation group, the neurons in I/R model group were sparse, showing fragmentation and dissolution; compared with I/R model group, the phenomena of cell nucleus fragmentation, dissolution and powder staining in nimodipine group and different doses of ginsenoside Rgl groups were all improved to different degrees. The immunohistochemical results showed that compared with sham operation group, the positive expression level of ubiquitin-modified protein in I/R model group was increased significantly (P < 0 . 05); compared with I/R model group, the positive expression levels of ubiquitin-modified protein in nimodipine group and different doses of ginsenoside Rgl groups were decreased (P < 0 . 05), especially in high dose of ginsenoside Rgl group (P < 0 . 05). The Western blotting results showed that compared with sham operation group, the level of ubiquitin-modified protein aggregates in I/R model group was significantly increased (P < 0 . 0 5); compared with I/R model group, the levels of ubiquitin-modified protein aggregates in nimodipine group and different doses of ginsenoside Rgl were decreased (P < 0 . 05), especially in high dose of ginsenoside Rgl group. Conclusion: Ginsenoside Rgl can inhibit the formation of ubiquitin-modified protein aggregates induced by I/R injury in the cortex, thereby alleviating the I/R injury in the rats.

Objective: To evaluate the consistency in detection of T790M mutation of epidermal growth factor receptor gene (EGFR) in plasma and tumor samples of patients with lung adenocarcinoma. Methods: The tumor tissues or cytological specimens of 12 patients with operable lung adenocarcinoma(stage Ⅰ-ⅢA) and 100 patients with advanced stage ⅢB-Ⅳ lung adenocarcinoma were collected, among which 11 patients showed acquired resistance for gefitinib (11/100). In the same period, peripheral blood samples were collected from all patients and 50 healthy volunteers. Amplification refractory mutation system (ARMS) was used to detect EGFR mutations in tumor specimens. Next Generation Sequencing(NGS) based circulating single-molecule amplification and resequencing technology (cSMART)was performed to quantitatively detect the EGFR mutations in circulating tumor DNA (ctDNA) from plasma specimens. Results: The sensitivity, specificity and concordance rate of EGFR T790M mutation between plasma and tissue specimens from 100 advanced stage patients were 50.0%, 72.9% and 72.0%, respectively. For L858R mutation and exon 19 deletion mutations, the above mentioned sensitivity, specificity and concordance rate were 91.7%, 100.0%, and 98.0%, as well as 79.2%, 100.0% and 95.0%, respectively. The L858R mutation and exon 19 deletion mutations were not detected in plasma of 50 healthy volunteers, whereasT790M mutation(1.0±0.0 copies) was found in 7 individuals(7/50, 14.0%). Similarly, in 12 resectable patients, 4 (4/12, 33.3%) T790M mutations were found in plasma (1.2±0.2 copies), but no L858R mutation and 19 exon deletion mutations. In comparison, 28.0% of patients with advanced lung adenocarcinoma (28/100)had detectable T790M mutation in plasma with copy numbers (34.0±22.7 copies). Furthermore, the copy numbers of T790M were 268.2±119.9 in plasma of 5 cases with acquired gefitinib-resistance. Conclusions In patients with advanced stages of lung adenocarcinoma, the detection of T790M mutation in plasma and tumor specimens is low. The T790M mutation also exists in the plasma of some healthy controls, suggesting that T790M mutation participates in EGFR signaling pathway and it might function in healthy population.