Familial pancreatic cancer is a known hereditary cancer syndrome with autosomal dominant inheritance and accounts for about 3% of all pancreatic cancers. With the development of molecular genetics,several genes have been identified related with the familial pancreatic cancer, including breast cancer susceptibility gene 2, Palladin, cyclin-dependent kinase inhibitor 2A, et al. In particular, mutations in some of these genes have been defined as the hereditary basis of particular cancer syndromes. Molecular genetics surveillance for high risk populace can lead to the diagnosis of asymptomatic, early-stage pancreatic cancer or precancerous lesions.

The proto-oncogene, c-kit gene, widely expresses on the mast cell, melanoeyte, haemopoietic stem cell, intestinal cell of cajal and germoeyte. Recent researches have revealed the relationship between the e-kit gene and the carcinogenesis, proliferation, infiltration and metastasis of some malignant tumor. This article aimed to make a review of its biological function, lab and clinical research advancement in the digestive tract tumor.

Objective To investigate the role of P21 protein and survivin on the cell apoptosis of non-small cell lung cancer (NSCLC) induced by mevastatin. Methods The inhibitory effect of mevastatin on A549 and NCI-H520 cell line was evaluated by MTT assay. The cell cycle distribution and apoptosis induction were determined with flow cytometer and transmission electron microscope. The expression of p21 protein was assessed with flow cytometer. The mRNA expression of p21 and survivin was assessed with RT-PCR. Results Flow cytometry showed that mevastatin induced G_0/G_1 cell arrest in NSCLC cell lines. The results indicated that mevastatin caused apoptosis in concentration-dependent manner. Mevastatin produced no change in expression of P21 mRNA and total P21 protein. Concomitantly, P21 protein localized on cellular membrane was decreased. It was also found that mevastatin suppressed the expression of survivin mRNA in NSCLC cell lines. All these effects were reversed by mevalonate. Conclusions Mevastatin inhibited the proliferation of NSCLC cell lines. Mevastatin exerts growth inhibitory effect and induces apoptosis effect by inhibiting mevalonate synthesis. Its mechanisms might involve blockade of the isoprenylation of p21 protein and down-regulation of the expression of survivin mRNA.

6 hours). The APACHE Ⅱ and POSSUM scoring system during perioperative period was in positive correlation with postoperative morbidity and mortality. Conclusions Pancreatoduodenectomy for the treatment of periampullary carcinomas is with high risks. Postoperative mortality and morbidity were in close correlation with the risk factors.

Objective To investigate the changes in the expression of phosphatidylinositol 3?kinase(PI3?K),mammalian target of rapamycin (mTOR)and Beclin?1 in the hippocampus of normal rats and intermittent hypoxia rats with cerebral ischemia/reperfusion ,so as to explore the role of PI3K/mTOR/autophagy pathway in global cerebral ischemia/reperfusion injury aggravated by intermittent hypoxia. Methods A total of 80 healthy male Wistar rats were randomly divided into sham operation group(SO group,n=20),merely ischemia/reperfusion group(I/R group,n=20),intermittent hypoxia for 7?day ischemia/reperfusion group(IH7+I/R group,n=20),and intermittent hypoxia for 21?day ischemia/reperfusion group(IH21+I/R group,n=20). IH7+I/R group and IH21+I/R group were respectively given intermittent hypoxia for 7 days and 21 days before ischemia/reperfusion. The cerebral ischemia/reperfusion model was established by modified Pulsinelli four?vessel occlusion method. The morpholog?ical changes of nerve cells in hippocampal CA1 region were observed by HE staining and electron microscope. The protein expressions of PI3?K, mTOR and Beclin?1 of nerve cells in hippocampal CA1 region were detected by immunohistochemical staining and RT?PCR. The learning memory capacity of rats were assessed by the Morris water maze test. Results Compared with SO group,I/R group increased the never cells morphology damages,reduced the number of survival neurons,and declined the ability of learning and memory(P<0.05). Immunohistochemistry showed that the number of PI3?K immunoreactive cell,mTOR immunoreactive cell and Beclin?1 immunoreactive cell increased in I/R group compared with S0 group(P<0.05). RT?PCR showed that the expressions of PI3?K,mTOR and Beclin?1 increased in I/R group compared with S0 group(P<0.05). Compared with I/R group,intermittent hypoxia groups increased the never cells morphology damages,decreased the number of survival neu?rons,and declined the ability of learning and memory(P<0.05). Immunohistochemistry showed that the number of PI3?K immunoreactive cell, mTOR immunoreactive cell and Beclin?1 immunoreactive cell increased in IH7+I/R and IH21+I/R groups compared with I/R group(P<0.05). RT?PCR showed that the expressions of PI3?K,mTOR and Beclin?1 increased in IH7+I/R and IH21+I/R groups compared with I/R group(P<0.05),and the changes were more significant in IH21+I/R group(P<0.05). Conclusion Intermittent hypoxia can aggravate neurological injury after ischemia,which is related to PI3K/mTOR/autophagy pathway activation.

The process of exercise regulating bone metabolism is complicated, which involves a number of signaling pathways. A large number of studies in vitro have indicated that mechanical stress regulates bone metabolism by Wnt, bone morphogenetic protein (BMP), and osteoprotegerin (OPG)/receptor activator of NF-κB ligand (RANKL)/receptor activator of NF-κB (RANK) signaling pathways. Both the in-tensity and frequency of mechanical stress have varing impact on bone tissue and cells. Plenty of studies in vivo also have shown that exer-cise regulates bone metabolism by key factors in bone metabolism signaling pathways. This paper reviewed the effects of exercise on bone metabolism pathways and their mechanisms.

Objective:To investigate the volatile constituents in Folium isatidis. Methods:The volatile constituents from Folium isatidis were analyzed by head-space solid micro-extraction coupled with GC-MS for the first time. Results: Thirty-five compounds (89. 95%) were identified from the volatile constituents in Folium isatidis. The main volatile constituents of Folium isatidis were 6, 10, 14-trimethyl-2-pentadecanone (6. 32%), nonanal (5. 99%), phenethyl isothiocyanate (5. 79%) and palmitic acid (5. 62%). Conclusion:Palmitic acid and benzyl alcohol may be the main effective constituents in Folium isatidis.

OBJECTIVE To investigate the effect of furanodiene(FDE),a diterpene derived from the medicinal plant Zedoary,on apoptosis of human gastric cancer MGC-803 cells induced in vitro. METHODS MGC-803 cells were treated with FDE 46.29~740.74μmol·L-1 for 24,48 and 72 h,and the cell viability was detected with MTT assay. Cell morphology was observed by light microscopy and Hoechst33342 staining. Flow cytometry was used to detect cell apoptotic rate and cell cycle. Rh123 staining and fluorescence probe DCFH-DA were employed to detect the changes in mitochondrial membrane potential (MMP) and reactive oxygen species(ROS). RESULTS MTT Results showed that FDE 46.29-740.74μmol · L-1 exhibited significantly higher cytotoxicity to gastric cancer MGC-803 cells. IC50 for MGC-803 of 24,48 and 72 h treatment was 347.91,257.41 and 101.01μmol·L-1,respectively. Treatment with FDE 92.58-370.32μmol·L-1 for 24 h also caused significant morphological changes in MGC-803 cells. AnnexinⅤ-FITC/PI double staining showed that the apoptotic rate increased after FDE 92.58-370.32μmol·L-1 treatment for 24 h(P<0.05). FDE enabled MGC-803 cell cycle arrest in S phase. DCFH-DA staining showed that FDE resulted in an increase in intracellular ROS levels(P<0.05) when PDE concentration was 370.37μmol·L-1(P<0.05). MMP decreased after FDE treatment when PDE concen?tration was 370.37μmol·L-1(P<0.05). CONCLUSION FDE Possesses potent tumor selected toxicity and can induce apoptosis of MGC-803 cells through cell cycle arresting,which is related to inhibition of DNA biosynthesis.

ObjectiveTo investigate the action mechanism of CD20 lymphocyte infiltration in the renal allograft biopsy with chronic allograft nephropathy (CAN).MethodsCAN cases confirmed by renal biopsy within 2 years after renal transplantation served as study subjects. By using immunohistochemistry,the deposition of C4d and the CD20-positive lymphocytes infiltration in the renal grafts were examined.The clinical follow-up data were analyzed.ResultsForty-four cases of CAN were enrolled in the study, including 13 cases (29.5％ ) of CD20-positive lymphocytes infiltration,and 31cases (70.5％ )of CD20-negative lymphocytes infiltration. CD20-positive lymphocytes in biopsy showed nodular and scattered lymphocytes infiltration.There were 5 (26.3％)cases of CAN Ⅰ,4 cases (25.0％) of CAN Ⅱ,and 4 (44.4％) of CAN Ⅲ in CD20-positive group.There was no statistically significant difference between the only CAN group and CAN with AR group in CD20-positive rate.Immunohistochemical staining showed there were 12 cases (27.3％) with C4d linear deposition in peritubular capillary endothelial cells (PTC).C4d positive rate had no significant difference among the CAN classifications. There was no significant relationship between C4d deposition and CD20-positive lymphocytic infiltration.The average serum creatinine in CD20-negtive group and CD20-posigtive group was 140.8 ± 22.0 and 183.5 ± 25.5μmol/L before biopsy,and 165.6 ± 37.6 and 242.2 ± 59.1 μmol/L one year after biopsy.The average serum creatinine level in CD20-positive group was higher than in CD20-negtive group before and after biopsy.ConclusionProgressive chronic humoral immunity is high risk in the process of CAN. The CD20-positive lymphocyte infiltration has no relevance with CAN grade and C4d deposition in PTC,but is associated with circulating antibody PRA and allograft long-term outcome. Pathogenetic mechanism may not contribute to chronic humoral immune,but B cells presenting donor antigens,are recognized and activated by T cells as antigen-presenting cells.

Objective To investigate the major chemical composition in rhizome of Pterocypsela elata and explore the activity of lactuside B against brain ischemia.Methods The compounds were isolated and purified by silica gel column chromatography and elucidated by spectroscopic experiments;The model of partial brain ischemia was used to detect water content,MDA and SOD levels in brain tissue in order to observe the activity of lactuside B against brain ischemia.Results Ten compounds were obtained and established as lactuside B(1),11?,13-dihydrolactucin acetate(2),?-sitosterol(3),daucosterol(4),(24R)-5?-stigrnast-7,22(E)-dien-3?-ol(5),3,3',4-trimethoxylellagic acid(6),?-amyrin(7),oleanolic acid(8),n-hexacosanic acid(9),and stearic acid(10).Lactuside B was a key component,and it's yield was 0.15%.Contents of water and MDA level in the brain tissue were significantly decreased,and the SOD content notably increased in all groups of lactuside B.Conclusion Ten compounds are all isolated from this plant for the first time.Compound 1 is a key component which possesses obvious activity against brain ischemia.