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.

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.

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 mechanism of cyclooxygenase-2 ( COX-2) in bone loss in a postmenopausal osteoporosis (PMOP) rat mode with ovarietomy (OVX).Methods Forty female Sprague Dawley adult rats at age of 3 months were randomly divided into 4 groups,10 in each group,including shamoperated (sham) group,OVX group,OVX treated with nilesteriol (OVX + E) group and OVX treated with aspirin ( OVX + P) group.All rats in OVX,OVX + E and OVX + P groups underwent ovarietomy under abdominal anesthesia with 10％ chloral hydrate.Rats in sham group were only taken with fat tissue with same weight under bilateral ovary.After surgery,penicillin was administered to prevent infection.At day 7 after surgery,agents were given by intragastric administration for 12 weeks.Nilestriol at 1.0 mg/kg was used in OVX + E group once a week,aspirin at 45 mg · kg - 1 · d- 1 was used in OVX + P group once a day.Saline with same volume was used in rats in sham and OVX groups.All agents were administered one time per day.Dose of agents were adjusted by weight per week.At end of study,bone mineral density (BMD) of right femurs and lumbar vertebrae 3 -5 (L3-5) were measured.Morphology of bone was detected by hematoxylineosin,and expression of COX-2 was determined by immunohistochemistry staining.Results ( 1 ) BMD:BMD of right femur and L3-5 was (0.209 ±0.010) g/cm2 and (0.230 ±0.012) g/cm2 in sham group and (0.181 ±0.008) g/cm2 and (0.201 ± 0.016) g/cm2 in OVX group,which reached statistical difference (P＜0.01).BMD of right femur and L3-5 was (0.203 ±0.009) g/cm2 and (0.224 ±0.028) g/cm2 in OVX + E group and (0.200 ± 0.011 ) g/cm2 and (0.204 ± 0.003 ) g/cm2 in OVX + P group,which were all higher than those in OVX group (P ＜0.01,P ＜0.05).However,there was no statistical difference in BMD between OVX + E and OVX + P group ( P ＞ 0.05).(2) Morphology of bone:bone trabeculae became fewer and degenerated in OVX group.However,bone trabeculae were regular and dense in OVX + P group and OVX + E group,which were similar to those in sham group.(3) Expression of COX-2:cells with COX-2 positive and expression of COX-2 around bone trabeculae in OVX group were more than those in sham,OVX + E and OVX + P group.Conclusion COX-2 plays an important role in PMOP.Aspirin could prevent bone loss by decreasing COX-2 expression in OVX rats.

BACKGROUND: Therapist-assisted treadmill training is good gait training, but it consumes great physical strength of therapists, and requires many persons. Clinical application was limited. Robot-assisted treadmill training has been paid great attention. OBJECTIVE: To summarize the role of robot in recovery of walking after spinal cord injury (SCI) and its influence on muscle activation patterns and kinematic patterns.RESULTS AND CONCLUSION: Although there is currently no evidence that robot-assisted gait training improves walking function more than other locomotor training strategies. Several advantages of robotic devices are obvious for applications targeting gait rehabilitation. Robotic devices are passive in nature and focus primarily on repeated movements of the limbs via fixed kinematic trajectories. These types of training abolish the cycle-to-cycle variation in the kinematics and the sensorimotor pathways. They also cannot sensitively monitor important characteristics of the training as therapists do. Therapists need to know the robot devices, understand how to change parameters to continuously challenge the subjects, and are able to assess when the workload is inappropriate for the subject's abilities so that they can maximize voluntary locomotor performance during assisted stepping to augment the recovery of functional walking.

Objective:To study the effect of endothelin receptor antagonist BQ-123 on the nerve function damage after subarachnoid hemorrhage (SAH)in the rats,and to explore the mechanisms.Methods:Total 120 male SD rats were divided into sham group,SAH group,low dose of BQ-123 group (50 μg· kg-1 )and high dose of BQ-123 group (75 μg·kg-1 ).The SAH rat models were established by injecting the autologous blood into cisterna magna twice.The morphological changes of hippocampus nerve cells of rat brain tissue were detected with HE staining, and the expressions of mTOR, Beclin-1 and LC3-Ⅱ in the hippocampus of rats were detected with immunohistochemistry and RT-PCR;the shuttle-box experiment was used to evaluate the abilities of learning and memory,and the holding power evaluation was used to evaluate the forelimb pulling force of the rats in various groups at each time point.Results:Compared with sham group,the morphological damages of neurons of the rats in SAH group were increased,the survival rate of neurons of the rats in SAH group was decreased (P <0.05),the expression levels of mTOR mRNA,Beclin-1 mRNA and LC3-Ⅱ mRNA in hippocampus tissue of the rats were increased (P < 0.05),and the abtilities of learning and memory and the values of holding power were decreased (P <0.05).Compared with SAH group,the morphological damages of neurons of the rats in BQ-123 groups were decreased,the survival rates of neurons of the rats in BQ-123 groups were increased (P < 0.05),the expression levels of mTOR mRNA of rats were decreased (P <0.05),the expression levels of Beclin-1 mRNA and LC3-ⅡmRNA in hippocampus tissue were increased (P <0.05),and the abilities of learning and memory and the values of holding power were increased (P < 0.05 ). The changes were more significant in high dose of BQ-123 group compared with low dose of BQ-123 group (P <0.05).Conclusion:BQ-123 can improve the nerve function damage after SAH in the rats,its mechanism may be related to regulating the mTOR/autophagy signaling pathway.

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.