RESUMEN
Between May 2009 and February 2012,60 patients scheduled for laparoscopic appendectomy were randomly assigned to receive either transumbilical single-port laparoscopic appendectomy (TUSPLA) or three-port laparoscopic appendectomy (TPLA).The operative duration was significantly longer in TUSPLA than TPLA cases.No statistically significant differences existed in hospital stay,visual analog scale (VAS) score,analgesia requirement or complication rate.The abdominal scar was inconspicuous for TUSPLA.It suggested that TUSPLA with conventional instrumentation is technically feasible and safe with scarless healing.
RESUMEN
Objective To analyze the intratumoral and peritumoral microvessel density (MVD) and microlymphatic vessel density (MLVD) in pancreatic cancer and record the expression of vascular endothelial growth factor(VEGF)-C and VEGF-D. And to explore the significance of VEGF-C and VEGF-D during the lymphatic metastasis and development of pancreatic cancer. Methods The expression of VEGF-C and VEGF-D, VEGF-R3, CD34 were assayed by immunohistochemical staining in 30 cases of pancreatic cancer tissues. Results The positive rates of VEGF-C and VEGF-D protein in the central portion of tumors (30% and 16.7%) were significantly lower than those in the marginal portion (73.3% and 56.7%), P <0.01. The group with high expression of VEGF-C and VEGF-D in the marginal portion had significantly higher incidences of lymph node metastasis, lymphatic invasion and venous invasion( P <0. 01 ). MLVD in both of the VEGF-C and VEGF-D positive groups was higher than that in the negative groups( P <0. 01 ), and the lymph node me-tastasis increased. MVD in VEGF-C positive group was significantly higher than that in the negative group. MVD had no significant difference between VEGF-D positive and negative group ( P =0. 07). Conclusions The expression of VEGF-C and VEGF-D in the marginal portion of tumor is significantly correlated with lym-phatic metastasis in pancreatic cancer patients, and may induce lymphangiogenesis. VEGF-C may play an im-portant role in the regulation of angiogenesis and lymphangiogenesis in pancreatic cancer, and VEGF- D maybe only participate in the regulation of lymphangiogenesis.
RESUMEN
Objective:To investigate the expression of CXCL12-CXCR4 and VEGF-C in pancreatic cancer and relation to clinical pathology.Methods:The tissue samples including PAC,the cancerous peripheral tissues,the normal pancreatic tissues and peripheral lympho nodes were obtained from 30 patients with PAC.The expressions of CXCL12,CXCR4and VEGF-C proteins in these tissues were assayed by immunohistochemical staining.The expressions of CXCL12,CXCR4 and VEGF-C mRNA in PAC were also investigated by fluorescence quantitative real-time PCR.Results:In all the samples,the positive rates of CXCL12 protein in PAC,the cancerous peripheral tissues,the normal pancreatic tissues and peripheral lympho nodes were respectively 13.3%(4/30),46.7%(14/30),56.7%(17/30) and 50.0%(15/30).The positive rates of CXCR4 protein in PAC,the cancerous peripheral tissues,the normal pancreatic tissues and peripheral lympho nodes were respectively 80.0%(24/30),70.0%(21/30),26.7%(8/30) and 73.3%(22/30).The expression levels of CXCR4 mRNA in PAC tissues,the cancerous peripheral tissues and peripheral lympho nodes were higher than that in the normal pancreatic tissues(P
RESUMEN
Objective:To study the reversal effect of tamoxifen(TAM)on the expression of mdr1 in human pancreatic cancer cell lines.Methods:The inhibtion effect of TAM on pancreatic cancer cell line SW1999、Capan-Ⅱ and mammary cancer cell line T47D were studied;The influence of TAM on mdr1 protein/mRNA expression in SW1999、Capan-Ⅱ and T47D were studied using the method of flow cytometer and RT-PCR.Results:The high dose TAM could inhibit Capan-Ⅱ cell line.TAM could reverse the expression of mdr1 protein and mRNA in Capan-Ⅱ cell line and T47D cell line. Conclusion:The high dose TAM could inhibit Capan-Ⅱ cell line,maybe related with reduction of the expression of mdr1 protein and mRNA.
RESUMEN
ObjectiveTo study the operative procedure and effect of anastomostic pseudoaneurysm(APA). Methods Eleven patients with APA were treated surgically. The diagnosis of APA in all the patients was comfirmed by angiography and ultras onic examination. A small rupture leading to APA was repaired by lateral arteri orrhaphy using autologous vein patch in 4 cases; the APA caused by a big rupture of anastomosis,resection of the pseudoaneurysm and interposition o f a PTFE or antologous vein were used in 7 cases.Results10cas es were followed -up for 5-38 months (mean19.6 months),and 1case loss of follow-up.9 cases recovered to be normal in activities and works, only 1 ca se had nerve paralysis of the affect extremity caused by popliteal artery APA compression . All the cases have good blood perfusion of the extremities wit hout recurrence. Conclusions APA should be treated by surgery. During operation control blood vessels effectively and remove the pathological changetissues completely are important,and reasonable application of antibi otics and antithrombotic agents are the guarantee of getting successful results .
RESUMEN
AIM To evaluate the antagonizing activity of iQWcF, a modified tripeptide, to endothelin receptors. METHORDS ①Vasoconstriction experiments with aorta strips of rats. ② In vivo experiments:male normotensive Wistar rats were anesthetized with pentobarbital Na (50 mg?kg -1 ),and catheterized into the carotic artery for measurement of blood pressure, and into the femoral vein for administration of iQWcF (30 mg?kg -1 ) and ET 1(0 9 nmol?kg -1 ). The test compound was given intravenously 5 min before the bolus injection of ET 1. Control animals received saline on the same time schedule.The blood pressure was recorded at different time interval after injecting ET 1. RESULTS ①iQWcF prohibited the vascontriction of aorta induced by ET 1 in a concentration dependent fashion.②The compound(30 mg?kg -1 .iv) markedly antagonized ET 1 induced the long lasting pressor phase mediated by ET A without affecting early transient depressor phase by ET B. CONCLUSION iQWcF is one of ET A selective antagonists.