Isolated tuberculosis of pancreas is very rare clinical entity. Since 1970, we have treated 9 patients, 3 men and 6 women (average 48.3 years), with isolated tuberculosis of pancreas. 2 patients were diagnosed as pancreatic tuberculosis, 1 patient pancreatic cyst and 6 patients pancreatic carcinoma before operation. They all underwent exploratory laparotomy, and were confirmed to be pancreatic tuberculosis by histopathology. Their common characteristics were that tuberculosis was only localized in pancreas without tuberculosis at extrapancreatic sites and that the treatment of anti-TB drugs had much effect on them. By analysis, it was considered that isolated tuberculosis of pancreas was usually mistaken for pancreatic carcinoma because it localized in pancreas, the contents of masses in pancreas should be noted carefully in order to avoid misdiagnosis and treatment of anti-TB drugs should be taken in time.

Objective:To clarify the effect of miR-200c on the proliferation of retroperitoneal fibroblast, and analyze its molecular mechanism, which provide theoretical basis for the inhibition of retroperitoneal fibrosis. Methods: 36 cases of retroperitoneal tissues were collected, and the primary fibroblasts were cultured. The cells stimulated by 5 ng/ml transforming growth factor-β1 (TGF-β1) were used as TGF-β1 group;the cells were transfected with pcDNA3.1-miR-200c first, and then stimulated by 5 ng/ml TGF-β1 were used as miR-200c group;the cells transfected only by pcDNA 3.1 were used as pcDNA 3.1 group;the normal cultured cells were used as control group. The MTT assay, cell scratch and Transwell chamber were used to detect the proliferation and migration of fibroblast, respectively. The ELISA experiment was used to detect the content of Akt protein in the lysis liquid of each group. Results: The OD value of fibroblast proliferation in miR-200c group was obviously lower than that of TGF-β1 group (P<0.01);compared with TGF-β1 group, the cell migration rate was decreased significantly in miR-200c group (P<0.01);the content of Akt protein in miR-200c was obviously lower than that of TGF-β1 group (P<0.01). Conclusion: miR-200c inhibits the effect of TGF-β1 on the proliferation and migration of fibroblast by down-regulating Akt signaling pathway, which has important significance in inhibiting peritoneal fibrosis.

Objective To investigate the treatment strategy for the re-operation patients with gallbladder cancer revealed by pathological results after laparoscopic cholecystectomy .Methods The clinical data in 15 cases of gallbladder cancer found by pa-thology after laparoscopic cholecystectomy in the general surgery department of this hospital during 2009-2013 were retrospective-ly analyzed .Results The pathological results on 3-5 d after laparoscopic cholecystectomy in 15 cases showed gallbladder cancer , tumor located at the gallbladder fundus in 2 cases ,the gallbladder body in 2 cases and gallbladder neck in 9 cases;there were 1 case of severe atypical hyperplasia ,2 cases of high differentiation adenocarcinoma ,9 cases of middle differentiation adenocarcinoma and 3 cases of low differentiation adenocarcinoma ;there were 1 case of Tis ,8 cases of pT Ⅰa ,6 cases of pTⅠb ,and 15 cases of bile tube incisal edge were negative .All 15 cases received re-laparotomy and hepatic duodenal ligament lymph nodes resection on 6-11 d af-ter cholecystectomy ,There were 1 case in the stage 0 ,8 cases in the stage Ⅰa ,5 cases in the stage Ⅰb ,1 case in the stage Ⅲb by TNM classification .The postoperative follow up lasted for 28 -79 months ,the accumulative survival rate was 100% in 1 year , 100% in 2 year ,93% in 3 year ,93% in 5 year .One case of stage Ⅲb was found repeated metastasis obstructive jaundice ,received transcutaneous puncture bile tract drainage and died after 3 months;no postoperative incision implantation metastasis was found . Conclusion Gallbladder cancer found by pathological examination after laparoscopic cholecystectomy is generally in early stage . Therefore ,early conducting the additional hepatic duodenal ligament lymphadenectomy has relatively good prognosis .

Objective To investigate the serological and molecular characteristics of twenty blood samples carrying ABO?AW.37 allele and to analyze ABO allelic enhancement.Methods The ABO phenotype of the twenty samples was de-termined by serological methods and the genotype of 1-7 ABO exons was analyzed by Sanger sequencing.Results Sequen-cing analysis showed that all twenty samples contained a c.940A>G(p.Lys314Glu)mutation of A allele,which was defined as ABO?AW.37.When ABO?AW.37 and B alleles were inherited simultaneously in 9 cases,in forward typing anti-A anti-bodies all agglutinated and the serological phenotype was Aw B.Among the 11 cases with ABO?AW.37 and O alleles inherited simultaneously,there was no agglutination of anti-A in forward typing.For absorption and elution tests,5 cases were weakly positive and the serological phenotype was Ael,while 6 cases were negative for absorption and elution tests and the serologi-cal phenotype was O type.Conclusion Allelic enhancement occured when both ABO?AW.37 allele and B allele were in-herited simultaneously.When ABO? AW.37 was inherited simultaneously with O allele,the serological phenotype was Aelor O type and attention should be paid to blood type identification.

Objective·To identify the functional motifs of mucin 1(MUC1)involved in regulating tumor cell proliferation,migration,and stemness maintenance.Methods·Mutational characteristics of the MUC1 gene across different cancers were identified from The Cancer Genome Atlas(TCGA)database.Various MUC1 mutation sites were analyzed and localized,followed by ranking based on mutation frequency.Western blotting was used to screen high-frequency MUC1 mutants with stable protein expression.BT549 cell line with MUC1 knocked out and MCF-10A cell line were used to stably overexpress MUC1 wild-type(MUC1-WT)and mutants by using lentiviral technology.Immunofluorescence was used to detect the cellular localization of MUC1 mutants.Using MUC1-WT as a positive control and MUC1-AQA,a loss-of-function mutant,as a negative control,the biological functions of different MUC1 mutant cells were analyzed:cell proliferation ability was assessed by cell counting kit-8(CCK-8)assay and colony formation assay;cell migration ability was evaluated by wound-healing and Transwell assays;cell stemness was examined by sphere formation assay.Structural localization of MUC1 mutants was analyzed by using PyMOL software,and molecular docking analysis was performed by using a protein docking software(ZDOCK Server).Results·A total of 102 mutations located in the MUC1 coding region were identified in the TCGA database,among which five missense mutations(P418S,S251R,V359I,N271S,and N465H)exhibited higher frequencies and were located in the non-variable number of tandem repeats(non-VNTR)region.Further examination revealed that the MUC1-S251R,N271S,and V359I mutants could be stably expressed.The cellular localization assay indicated that these three mutants predominantly localized in the cytoplasm,but were also presented in the nucleus.The nuclear-to-cytoplasmic ratio showed minimal differences between MUC1-WT and the mutants.Analysis of the tumorigenic biological functions of the cells expressing different MUC1 mutants revealed that:① High expression of MUC1-WT significantly enhanced the proliferation ability of both BT549 and MCF-10A cells;the proliferation of MUC1-AQA,S251R,and N271S mutant cells was decreased compared to MUC1-WT cells,while MUC1-V359I mutant cells exhibited a similar proliferative profile to MUC1-WT cells.② The migration ability of MUC1-WT high-expressing cells was significantly enhanced,whereas MUC1-AQA cells demonstrated attenuated migration.In the BT549 cells,the migration ability of MUC1-S251R and V359I cells was similar to that of MUC1-WT cells,whereas MUC1-N271S cells showed reduced migration.In the MCF-10A cells,the migration ability of MUC1-N271S and MUC1-V359I cells was similar to that of MUC1-WT cells,whereas MUC1-S251R cells exhibited significantly decreased migration.③ Stemness was enhanced in both cell types with high MUC1-WT expression,while MUC1-AQA cells lost stemness;the cells with MUC1-N271S,V359I and MUC1-WT showed comparable maintenance of stemness,whereas MUC1-S251R cells demonstrated compromised stemness.PyMOL software analysis unveiled that MUC1-N271S and V359I were located in or around the sperm protein-enterokinase-agarin(SEA)region,specifically in the loop region and the β-sheet,respectively.The molecular docking analysis revealed that the stability of the complex formed by MUC1-WT or V359I with the extracellular domain of epidermal growth factor receptor(EGFR)surpassed that of MUC1-N271S or S251R,indicating a stability hierarchy of V359I>WT>N271S>S251R.Conclusion·MUC1 mutants exhibit diverse impacts on the biological functions of tumor cells,with their effects on proliferation correlating with the EGFR signaling pathway.MUC1-V359I is similar to MUC1-WT,indicating a negligible effect on tumor cell proliferation,migration,and stemness maintenance.Conversely,MUC1-S251 and N271 sites may be involved in the regulation of signaling pathways governing cell proliferation and migration and the MUC1-S251 site plays a critical role in maintaining cell stemness.