Pancreatic cancer is a highly malignant tumor and its treatment is still a challenge.Recent studies have shown that medication plays an important role in preoperative and postoperative adjuvant therapy for locally advanced pancreatic cancer and is also a major thera-peutic method for advanced pancreatic cancer.It can improve the survival time and quality of life in patients with pancreatic cancer.Tradi-tional chemotherapy regimens based on gemcitabine and fluorouracil have limited effects in the treatment of advanced pancreatic cancer,and studies on molecular targeted therapies have achieved some progress in recent years.With reference to related guidelines or consensus on the diagnosis and treatment of pancreatic cancer and important clinical trials of the treatment of pancreatic cancer,this article elaborates on the selection and therapeutic effect evaluation of chemotherapy regimens for pancreatic cancer.We believe that with the research and develop-ment of new drugs and the application of new techniques,the treatment of pancreatic cancer will achieve new breakthroughs in future.

AIM: The purpose of the study was to examine colon cancer cell lines to determine whether Stat5b/Survivin plays an important role in the process of apoptosis in colon cancer cells. METHODS: Protein lysates were extracted from colon cancer cells. Human colon cancer cell line HT29 was transfected with Stat5b antisense oligonucleotide mediated by liposome. MTT assay was used to measure the proliferation. Flow cytometry was applied to analyze the cell cycle and apoptosis. EMSA was used to detect the activity of Stat5. Western blotting was applied to measure the expression of Stat5, p-Stat5, cyclin D1, Survivin, Bcl-2 and Bcl-xL. RESULTS: Targeting of Stat5 using antisense oligonucleotide against the translation site resulted in apoptosis and downregulaed the expressions of Stat5, p-Stat5, cyclin D1 and Survivin, but not Bcl-2 and Bcl-xL. CONCLUSION: Constitutive activation of Stat5 is associated with the carcinogenesis of colon cancer cells. Blocking of Stat5 signaling inhibits the expression of Survivin and induces apoptosis in colon cancer cells.

Objective To scan significant clinicopathologic parameters in brainstem gliomas (BG) for outcome. Methods 54 cases with BG were reviewed and followed up. Results and Conclusion 41 cases were followed up. The main complaint included hoarseness and bucking, dizziness. The higher tumor grade, higher mitotic-index, necrosis of tumor, hyperplasy of blood vessel endothelium, Ki-67 index > 5% were associated with shorter survival. In opposite, Rosenthal fibers always presented in lower grade gliomas and associated with long survival.

Objective:To explore the influence of fermented red ginseng extract (FRGE) in the proliferation of rat glomerular mesangial cells (GMCs) and the degradation of extracellular matrix(ECM)under high sugar stimulation, and to clarify the prevention and treatment effects of FRGE on diabetic nephropathy (DN) and the possible mechanism.Methods:The rat GMCs were cultured and divided into normal concentration of D-glucose (NG) group, high concentration of D-glucose (HG) group and high concentration of D-glucose plus different concentrations (3.75, 7.50, 15.00 mg·L-1) of FRGE groups. The proliferation rates of rat GMCs were detected with MTT,and the type Ⅳcollagen(Col Ⅳ) levels in supernatants of the GMCs were detected by ELISA. The protein expressions levels of matrix metalloproteinase-2(MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) were detected with Western blotting m ethod.Results:Compared with NG group, the proliferation rate of GMCs in HG group was increased(P<0.01), the Col Ⅳ level was increased(P<0.01),the MMP-2 expression level was decreased, and the TIMP-2 expression level was up-regulated(P<0.01).Compared with HG group, the proliferation rates of GMCs in various FRGE groups were decreased(P<0.01), the Col Ⅳ levels were decreased(P<0.01),the expression levels of TIMP-2 were reduced(P<0.01),and the expression levels of MMP-2 were increased(P<0.01).Conclusion:FRGE can inhibit the proliferation of rat GMCs induced by high sugar and promote the ECM degradation to delay the occurrence and development of DN.

Objective To investigate the relationship between lipid fluctuations of daily diet and insulin resistance in patients with type 2 diabetes mellitus(T2DM) with normal fasting lipid profile. Methods One hundred and ninety?eight cases patients with T2DM who were treated in the Endocrinology Department of the General Hospital of Benxi Iron and Steel Group Corporation from October 2012 to September 2014 were selected. Patients were divided into three groups according to fasting and postprandial 4 h triglyceride( TG4 h)
level,the group with normal fasting TG and normal TG4 h with 38 cases,the group with normal fasting TG and rising TG4 h with 78 cases,the group with rising fasting TG and rising TG4 h with 82 cases. The control group was composed of healthy volunteers with 20 cases. The patients followed daily diet habits to eat,blood glucose, insulin and lipid level of fasting and 2 h,4 h after lunch were monitored. Homeostasis model insulin resistance index( HOMA?IR) was used as an index to evaluate insulin resistance,and the correlation analysis was carried out with fasting and dietary intake of postprandial lipid metabolism. Results (1)HbA1c,FPG,HOMA?IR,TG and insulin level in the patients of the group with normal fasting TG and normal TG4 h,the group with normal fasting TG and rising TG4 h,the group with rising fasting TG and rising TG4 h were higher than the control group (HbA1c:(8. 4±1. 9)%,(8. 2±2. 4)%,(7. 8±1. 8)% vs. (4. 3±0. 6)%);FPG:(8. 98±1. 93) mmol/L, (8. 62±1. 33) mmol/L,(8. 28±1. 26) mmol/L vs. (4. 82±0. 63) mmol/L;,HOMA?IR:11. 07±0. 11,6. 98 ±0. 08,3. 83±0. 09 vs. 1. 24±0. 16;TG:0 h TG:(2. 35±1. 85) mmol/L,(1. 60±0. 41) mmol/L,(1. 58±0. 46) mmol/L vs. (0. 82±0. 25) mmol/L;2 h TG:(3. 97±2. 96) mmol/L,(2. 98±1. 49) mmol/L,(1. 83±0. 62) mmol/L vs. (1. 22±0. 31) mmol/L;4 h TG:(4. 24±1. 57) mmol/L,(3. 15±1. 63) mmol/L,(1. 92±0. 53) mmol/L vs. (1. 16±0. 24) mmol/L;insulin(0 h insulin:(26. 51±3. 65) mU/L,(18. 18±6. 24) mU/L,(10. 31 ±2. 38) mU/L vs. (5. 87±1. 62) mU/L;2 h insulin:(59. 15±8. 34) mU/L,(43. 75±9. 83) mU/L,(34. 27 ±1. 61) mU/L vs. (25. 24±1. 98) mU/L;4 h insulin:(51. 22±6. 79) mU/L,(40. 06±7. 51) mU/L,(31. 06 ±1.77) mU/L vs. (13.36±1.37) mU/L;P<0.05). (2)WHR(0.90±0.08 vs.0.72±0.06),HOMA?IR, insulin level of fasting and 2 h,4 h after lunch,TG of 2 h,4 h after lunch in the group with normal fasting TG and rising TG4 h were higher than the group with normal fasting TG and normal TG4 h ( P<0. 05 ) . ( 3 ) BMI ((27. 3±3. 3) kg/m2 vs. (23. 1±1. 5) kg/m2),WHR(0. 96±0. 10 vs. 0. 72±0. 06),HOMA?IR,TG and insulin level of fasting and 2 h,4 h after lunch in the group with rising fasting TG and rising TG4 h were higher than the group with normal fasting TG and normal TG4 h( P<0. 05) . HOMA?IR,TG and insulin level of fasting and 2 h, 4 h after lunch in the group with rising fasting TG and rising TG4 h were higher than the group with normal fasting TG and rising TG4 h( P<0. 05) . ( 4) HOMA?IR was positively correlated with BMI,WHR,and fasting TG levels in the groups with diabetes(r=0. 297,0. 376,0. 326,P<0. 05). HOMA?IR was significantly positively correlated with TG of 2 h,4 h after lunch in the groups with diabetes( r=0. 529,0. 693,P<0. 05) . HOMA?IR was significantly positively correlated with BMI and WHR in the control group(r=0. 617,0. 728,P <0. 05). HOMA?IR was not significantly correlated with fasting and postprandial TG in the control group. Conclusion Postprandial lipid metabolism disorder after daily diet is in some of patients with T2DM with normal fasting lipid profile. Postprandial lipid metabolism disorder after daily diet is significantly positively correlated with insulin resistance in patients with T2DM. Insulin resistance may be one of the pathogenesis of postprandial dyslipidemia in patients with type 2 diabetes.

Objective To explore the repair method for wounds after excision of facial benign tumors.Methods Unilateral or bilateral deltopectoral skin flaps were expanded depending on the area of the facial benign tumor.Expander was implanted underneath deltopectoral flap region through an incision inferior to the clavicle.When expansion was completed,all or part of the benign tumor was excised before designing the flap according to the area of the skin defect.The area of the skin flap should be more than that of skin defect with 10％ to 15％.The pedicle wound could be sealed by rolling it around to form a tube or a hinge using the benign tumor and pedicle.The flap was delayed three weeks later and the pedicle was divided one week after flap delaying.Results All 20 cases got the satisfactory results with treatment of pedicled expanded deltopectoral skin flaps for repair of wounds after excision of facial benign tumor.Conclusions It is a better option to repair a large area wound after excision of facial benign tumor with an expanded deltopectoral skin flap.

Objective To investigate cyclic mechanical stimulation on expression of connective tissue growth factor (CTGF) in osteoblast-like cells (MG63) and to explore the rote of MAPK involved in the process.Methods Expressions of CTGF protein and mRNA in MG63 cells were detected by Western blot and RT-PCR,respectively. Phosphorylation levels of p38, ERK, JNK were examined by Western blot. Results Cyclic mechanical stimulation upregulated expressions of CTGF protein and mRNA. The levels reached a maximal response of 2-3 fold after 3-6 h. ERK and JNK signal pathways were activated by cyclic mechanical stimulation, the phosphorylated proteins increased within 10 min of stretch, phosphorylated ERK reached maximal levels by 60 min of stretch, phosphorylated JNK reached maximal levels by 15-30 min of stretch, but not for p38 signal pathway.Only the inhibitior of JNK signal pathway (SP600125) markedly suppressed stretch-induced CTGF expression,meanwhile the inhibitors of ERK (PD98059) and p38 (SB203580) did not show such effect. Conclusion Cyclic mechanical stimulation upregulates CTGF expression via JNK-dependent pathway in MG63 cells.

Objective To construct lentiviral vectors containing peptide P1-GFP fusion genes.Umbilical cord derived mesenchymal stem cells were infected with lentivirus carrying peptide P1 and GFP fusion genes.To inject the targeted umbilical cord derived mesenchymal stem cells into mice and to detect GFP expression in the spleen.Methods Umbilical cord derived mesenchymal stem cells were cultured with adhered tissues of umbilical cord smaller than 1 mm3 . Lentiviral vector containing P1-GFP fusion genes with engineering technology was constructed and infected the umbilical cord derive mesenchymal stem cells.Targeted umbilical cord derived mesenchymal stem cells were intravenously injected in the mouse tail vein and after 18 hours GFP expression was detected with immunohistochamical staining of the spleen tissues.Results Harvested umbilical cord derived mesenchymal stem cells grew well in culture medium. Green fluorescence on umbilical cord derived mesenchymal stem cells were observed under fluorescence microscope at 18 hours after infected with lentivirus.Green fluorescence intensity of umbilical cord derived mesenchymal stem cells was increasing over time and reached a peak at 72 hours.Umbilical cord derived mesenchymal stem cells highly expressed CD105 (90.0%)/CD44 (98%) and CD73 (85.0%)/CD90 (98.5%) molecules.GFP expression was detected in the spleen after intravenous injection of targeted umbilical cord derived mesenchymal stem cells in the mice 18 hours later.GFP expressing cells intimately contacted with lymphocytes.Conclusions Targeted umbilical cord derived mesenchymal stem cells contain P1-GFP fusion genes are constructed.Targeted umbilical cord derived mesenchymal stem cells can be targeted to mouse spleen and intimately contact with lymphocytes after intravenous injection.Our results lay the groundwork for further studies.

s To compare the clinical effects of intravenously and orally administered aspirin in the treatment for acute coronary syndrome (ACS),and to evaluate the adverse effects of intravenous administration of aspirin.Methods One hundred and twenty-five patients with unstable angina pectoris or acute myocardial infarction were randomized into three groups:group 1 received intravenous aspirin (300mg/d,n =40),while groups 2 (n =42) and 3 (n =43) received orally administered aspirin (100mg/d and 300mg/ d,respectively).The control group included 30 patients with no heart disease or blood disease,and they had never taken aspirin and clopidogrel.Blood samples were taken at 2nd and 7th day of hospitalization.Platelet aggregation and the level ofplatelet activation marker CD62p were measured and compared among the groups.Patients were followed up for 6 months for the occurrence of major adverse cardiovascular events.Results There were no statistically significant differences in the decrease in adenosine diphosphate (ADP)-induced platelet aggregation rate (12.01±10.45%,6.76±14.62% and 9.73±16.72% for group 1,group2 and group 3,respectively),the decrease in arachidonic acid (AA)-induced platelet aggregation rate (6.73±11.34%,6.95±12.45% and 7.57±13.11%,respectively),and the decrease in CD62p level (10.89±18.62%,8.92±11.57% and 7.05±15.67%,respectively).At six months,there were 4 deaths (10%) in group 1,4 deaths (9.5%) in group 2 and 5 deaths (11.6%) in group 3 (P＞0.05).Conclusions Intravenous administration of aspirin provides a new approach as an anti-platelet treatment for ACS patients,especially those who can not tolerate oral administration of aspirin.(J Geriatr Cardiol 2008;5:212-216)

Objective To observe the recurrence rate of colorectal adenoma and to explore its correlations to obesity and body weight changes.Methods A total of 1 236 cases of patients with colorectal adenoma admitted to our hospital from 2010 to 2012 were selected.Among them,913 cases of patients who had completed the 2-years follow-up were recruited in this study.According to body mass index (BMI),patients were divided into three gorups:normal weight group (BMI＜24 kg/m2),overweight group (BMI:24-＜28 kg/m2) and obesity group (BMI≥28 kg/m2).Colonoscopy was defined as the end-point performed after 2-years follow-up,and the body weights were remeasured.The correlations of recurrence rate of colorectal adenoma to patients' basal body mass and body weight change were analysed.Results A total of 361 patients (39.5％) suffered from recurrent colorectal adenoma.The recurrence rates of colorectal adenoma in the normal weight group,overweight group and obesity group were 34.5 ％,41.0％ and 41.9 ％,respectively;the recurrence rates in the overweight group and obesity group were higher than that in the normal weight group,there were statistically significant differences (P＜0.05).However,There was no significant difference in the recurrence rate of colorectal adenoma between patients with body weight changes of 2.5 kg or more and those with body weight changes less than 2.5 kg(P＞0.05).Conclusion The recurrence of colorectal adenoma is associated with obesity,but changes in body weight in the short term (two years) have no significant effect on the recurrence rate.