Objective To explore the clinical safety and validity of Da Vinci surgical system in distal pancreatic tumor resection.Methods The clinical data of 14 patients with distal pancreatic tumor underwent robotic surgeries by using Da Vinci surgical system from January 2009 to June 2012 were retrospectively analyzed.Results The average operation time was 343.93 (170-575) min,average blood loss was 192.5 (10-700) ml,without blood trahsfusion.Pathologic examination showed:pancreatic ductal adenocarcinoma in 7 patients,pancreatic cystadenoma in 1 patient,mucous cystadenoma in 1 patient,cystadenocarcinoma in 1 patient,high levels of pancreatic ductal intraepithelial neoplasia in 1 patient,insulinoma in 1 patient,solid pseudo-papillary tumor in 2 patients.Two patients with pancreatic leaks after operation and then relieved after conservative medical therapy.Others were discharged from hospital without complications.The average hospital stay was 10.64 d.Conclusions Da Vinci surgical system is safe and effective in treatment for patients with distal pancreatic rumor with minimally invasive advantage.Because lack of surgical experience and small sample,a large sample with long term follow-up of high-quality clinical research is required and then update the system to evaluate the efficacy and safety.

OBJECTIVE: To analyze carbapenemases genotype of imipenem-resistant Gram-negative bacilli in intensive care unit (ICU) of 3 third grade class A hospitals from Qingdao area, so as to provide reference for drug-resistant bacteria infection prevention and treatment in clinic. METHODS: From Jan. 2013 to Jun. 2016, each 60 strains of imipenem-resistant Klebsiella pneumoniae (IRKP), imipenem-resistant Pseudomonas aeruginosa (IRPA) and imipenem-resistant Acinetobacter baumanii (IRAB) were collected from 3 third grade class A hospitals from Qingdao area. Drug sensitivity test was performed by using Kirby-Bauer method. Phenotypes of carbapenemases were determined by Carba NP trial. PCR was applied to amplify carbapenemase gene; Sanger seqnencing method was adopted for bi-directional sequencing; Blast comparison with GenBank database was conducted. RESULTS: Three kinds of imipenem-resistant Gram-negative bacilli showed high drug resistance to majority commonly used antibiotics as piperacillin, cefazolin, imipenem and cilastatin sodium, gentamicin, etc., but were sensitive to polymyxin B (resistance rate of 0). Among 180 drug-resistant strains, there were 52 strains of class A carbapenems, 13 strains of class B carbapenems and 39 strains of class D carbapenems; the detection rates of them were 28. 89％, 7. 22％ and 21. 67％, respectively. There were 52 strains of KPC-2 gene (IRKP), 4 strains of IMP-1 gene (IRPA), 8 strains of VIM-2 gene (7 strains of IRPA, 1 strain of IRAB), 39 strains of OXA-23 gene (IRAB); the detection rates of them were 28. 89％, 2. 22％, 4. 44％, 21. 67％; all strains were not detected 1MP-2, VIM-1, NDM-1, OXA-24, OXA-58 genes. Results of Blast comparison showed that above detected genes were absolutely homology with the corresponding genes in GenBank database. CONCLUSIONS: Drug resistance of imipenem-resistant Gram-negative bacilli in ICU of 3 third grade class A hospitals is serious in this region, which are nearly no-sensitive to most of commonly used antibiotics in clinic. Main genotypes included KPC-2 (K. pneumoniae), OXA-23 (A. baumanii) and IMP-1 and VIM-2 (P. aeruginosa).

The morbidity of inflammatory bowel diseases (IBD) is rising rapidly but no curative therapies to prevent its recurrence. Cell death is crucial to maintaining homeostasis. Necroptosis is a newly identified programmed cell death and its roles played in IBD need to be explored. Necroptosis is mediated by receptor interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like protein (MLKL), which resulted in cell swelling, plasma membrane rupture, intracellular content leaking, and eventually cell death as well as the promotion of inflammation. Studies have found that inhibiting necroptosis alleviated IBD in animal models and IBD patients with an increased level of necroptosis in inflammatory tissues, indicating that necroptosis is related to the pathogenesis of IBD. However, due to the complexity in regulation of necroptosis and the involvement of multiple functions of relevant signaling molecules, the specific mechanism remains elusive. Necroptosis may play a vital regulatory role in the pathogenesis of IBD, which provides a new idea and method for further exploring the therapeutic target of IBD.