Surgical resection is the most effective treatment for benign and low-grade malignant pancreatic tumors. However, classical pancreatectomy constantly requires simultaneous resection of organs surrounding pancreatic tissues, which has the disadvantages of severe trauma, high-risk complications and poor long-term quality of life. In order to preserve organ function as much as possible, multiple organ-preserving pancreatectomy have been widely applied in clinical practice, which mainly include tumor enucleation, central pancreatectomy, spleen-preserving distal pancreatectomy and duodenum-preserving pancreatic head resection, etc. In recent years, with the advancement of minimally invasive technologies, robotic organ-preserving pancreatectomy has also been carried out in clinical setting. In this article, clinical application status of robotic organ function-preserving pancreatectomy was mainly illustrated.

Objective To evaluate the application of flexible thoracoscopy in the diagnosis of pleural effusion.Methods Thoracoscopy was performed in 20 pleural effusion patients in our hospital from May to December 2007.Biopsies were performed in 16 patients,not in the other 4 patients since difinite diagnosis had been reached before thoracoscopy.Results Rate of accurate diagnosis via thoracoscopy was 93.75%(15/16).Results Of biopsy were as follows:adenocarcinoma 8 cases,squamous carcinoma 1 case,adenosquamous carcinoma 1 case,malignant pleural effusion 1 case,tuberculous pleuritis 4 cases,malignant mesothelioma 3 cases,chronic suppurative pleuritis 1 case,failed diagnosis 1 case.Presentations of lesions under thoracoscope were as follows:diffused miliary nodules 10 cases(10/20),multiple mass 7 cases(7/20),fibrous compartmentation or conglutination 9 cases(9/20).There were no severe complications.Conclusion Flexible medical thoracoscopy is a safe and efficient method of etiologic diagnosis of pleural effusion.

Objective To investigate the role of lipopolysaccharide(LPS)in regulating the inflammatory response of neutrophil through the leucine-rich α-2 glycoprotein 1(LRG1)/Rho-associated protein kinase(ROCK1)signaling.Methods HL-60 cells were treated with 1 μmol/L all-trans retinoic acid(ATRA)and 12.5 μL/mL dimethyl sulfoxide(DMSO)for 72 h and 96 h,and the morphological changes were observed by Wright-Giemsa staining.The expression of CD11b was detected by flow cytometry.LPS induced the activation of dHL-60 and human peripheral blood neutrophils.The transcription and secretion levels of LRG1,ROCK1 and inflammatory cytokines were detected by qPCR and ELISA,respectively.The expression levels of LRG1 and ROCK1 after the activation of dHL-60 were detected by Western blotting.Furthermore,dHL-60 was treated with the recombinant protein LRG1 and ROCK1 inhibitor Y-27632;the transcription levels of inflammatory cytokines were detected by qPCR.Results Neutrophils were activated by LPS.The expression levels of LRG1 and ROCK1 were significantly increased,and the transcription levels of inflammatory cytokines were significantly increased.The recombinant protein LRG1 activated dHL-60 in vitro,and the transcription levels of ROCK1 and inflammatory cytokines were significantly increased.Using the ROCK1 inhibitor Y-27632,the production levels of inflammatory cytokines were significantly reduced.Conclusion LPS can regulate the production levels of neutrophil inflammatory cytokines through activating the LRG1/ROCK1 signaling,thus exacerbating the inflammatory response.

Objective: To screen the differential expression profile of circular RNA (circRNA) in pancreatic cancer and analyze its potential function. Methods: Four pairs of pancreatic cancer tissues and corresponding adjacent pancreatic tissues were selected for high⁃throughput sequencing , and the differentially expressed circRNA was screened according to fold change > 2 and P < 0. 05. qRT⁃PCR was used to detect the expression of 5 randomly selected differentially expressed circRNA in 20 pairs of pancreatic cancer tissue samples. GO and KEGG enrichment analysis of differentially expressed circRNA was performed , and the top 50 circRNA⁃microRNA interaction network was constructed. The relationship between hsa_circ_0046523 and the clinicopathological features of pancreatic cancer was further analyzed , and the effects of hsa_circ_0046523 on the proliferation , migration and invasion of pancreatic cancer cells were observed by functional experiments. Results: A total of 17 182 circRNA were predicted by high⁃throughput sequencing , of which 302 circRNA were differentially expressed including 137 circRNA were upregulated and 165 circRNA were downregulated in pancreatic cancer tissues. The qRT⁃PCR results showed that the expression levels of hsa_circ_0046523 , hsa_circ_0004220 and hsa_circ_0000690 in pancreatic cancer tis⁃sues were significantly upregulated (P<0.05)，while the expression levels of hsa_ ir_0008676 and hisa _ circ_0004416 were significantly downregulated (P<0.05）.which was consistent with the sequencing results.GO analysis indicated that differentially expressed circRNA were mainly involved in substrate-dependent cell migration, protein kinase complex and cytoskeletal protein bindinig.KEGG pathway enrichment analysis showed that differentially expressed circRNA were mainly involved in protein digestion and absorption , ABC transporters , central carbon metabolism in cancer,and glycineserine and threonine metabolism pathways.The expression level of hsa_ circ_0046523 was closely correlated with tumor differentiation (P=0.002),T stage (P=0.006),lymph node metastasis (P=0.011) and TNM stage (P=0.001).Compared with HPDE6-C7 cells the expression of hsa_circ_0046523 significantly inc increased in pancreatic cancer SW1990, Mia PaCa-2BxPC-3 and Capan-2 ceIls (P<0.05). hsa_circ_ 0046523 knockdown significantly inhibited the proliferation, migration and invasion of pancreatic cancer Mia PaCa⁃2 BxPC⁃3 cells (P < 0. 05) . Conclusion There are characteristic differentially expressed circRNAs in pancreatic cancer tissues , and these differentially expressed circRNAs may be involved in the occurrence and development of pancreatic cancer.