Objective To explore the relationship between expression of MDR1 gene in human esophageal and cardiac cancer and clinicopathological changes. Methods From Jan 2 000 to Dec 2001, a total of 161 patients with esophageal or cardiac carcinoma were recruited, and MDR1 were assayed by RT-PCR. Fresh tumor tissues were surgically resected without chemotherapy before operation. Results The positive rate of MDR1 was 34.78 % (56/161). Among them 5 cm 38.54 %, invasion to muscular layer 30.77 %, invasion to tunica serosa 35.14 %, squamous cell carcinoma 27.27 %, adenocarcinoma 41.67 %, lymphonode metastasis positive 35.19 %, negative 33.96 %, stage Ⅰ,Ⅱ 33.33 %, stage Ⅲ, Ⅳ 35.58 %. The correlation between MDR1 expression and the age and sex of patients, Tumor size depth of invasion histologic types lymph node involvement and TNM, was not significant. Conclusion Because of highly expressive level of MDR1 gene in untreated esophageal and cardiac carcinoma, we should choose appropriate chemotherapeutic regimen for esophageal and cardiac cancer. The expression of MDR1 gene in untreated cancer was independented of morphologic prognostic indexes without correlation between MDR1 gene expression and morphological indexes.

Aim To evaluate the mechanism of HG251-induced apoptosis in K562/DOX cells.Methods Cell viability was assessed by MTT assay;cell cycle distribution,apoptosis and mitochondrial membrane potential were measured by flow cytometry;the protein expressions of P-gp,caspase-3,caspase-8,caspase-9,p53,Bcl-xL and cytochrome c in the K562/DOX cells were evaluated by Western blot.Results HG251 was able to inhibit cells proliferation,induce apoptosis,lose mitochondrial membrane potential,activate caspase-3,caspase-8,caspase-9,up-regulate p53 protein and down-regulate Bcl-xL protein in a dose-dependent manner but it had no effect on P-gp protein expression.Conclusion HG251 could overcome apoptotic resistance via up-regulating p53 protein and down-regulating Bcl-xL protein.In addition,HG251 also induced K562/DOX cells apoptosis via mitochondrial pathway and membrane death receptor pathway.

AIM: To study the protective effects of Imipramine (Imi) on ischemic injury in cultured rat cerebral cortical neurons. METHODS: Cortical neurons of fetal rat were cultured in vitro. The protective effects of Imi on ischemic injury in cultured rat cerebral neurons were observed. RESULTS: Imi ( 10 -5, 10 -6, and 10 -7 mol?L -1) reduced the number of cell death, lowered LDH,NO,and MDA content, and increased of activity of SOD. CONCLUSION: Imi can protect rat cerebral cortical neurons from ischemic injury and toxicity of Glu. And it maybe attribute its to antioxidation and calcium antagonism.