Intensity-modulated radiation therapy (IMRT)is a more advanced radiotherapy technique than routine radiotherapy,and has been effectively utilized in the treatment of nasopharyngeal carcinoma (NPC).Rradiotherapy alone has disappointing effect to local advanced cases.Nevertheless,chemoradiotherapy provides long term survival.Chemoradiotherapy is becoming the standard therapeutic regimen for local advanced NPC.But different ways of chemomdiotherapy such as induction,concurrent,adjuvant chemotherapy still need to be defined.

Objective To explore the protection mechanism of glucocorticoids (GC) against the inflammatory injury of vascular endothelial cells (VEC). Methods An inflammatory injury model of VEC was reproduced by treating the human umbilical vein endothelial cells (HUVEC) with lipopolysaccharides (LPS) in vitro. The effect of dexamethasone (Dex) on apoptosis of HUVEC and the release of IL-6 and sICAM-1 of HUVEC was observed, and then the effect of RU486 (an antagonist for glucocorticoid receptor) on reversing the effect of Dex was also observed. Results LPS could induce apoptosis of HUVEC, and the apoptosis rate reached 36.7%?3.9%. On the other hand, glucocorticoid (Dex) could obviously inhibit the apoptosis of HUVEC in LPS, and the apoptosis rate was reduced to 13.2%?0.9%. The difference between the apoptosis rate between these two groups was very significant (P

Objective To investigate the effect of dexamethasone (Dex) on the transcription of 11 ?-hydroxysteroid dehydrogenase type 1 (11?-HSD1) gene in vascular endothelial cells. The roles of p38 mitogen-activated protein kinase (p38MAPK) signaling pathway and glucocorticoid receptor (GR) were also observed. Methods Vascular endothelial cells were co-cultured with different concentrations of Dex (10-9-10-3mol/L) for 24h. Reverse transcription polymerase chain reaction (RT-PCR) was employed to detect 11?-HSD1 mRNA in each group. Normally cultured cells, without contact with Dex, served as normal control group. The cells were co-cultured with p38MAPK specific inhibitor SB20358 (10-2mol/L) and GR specific inhibitor RU486 (10-6mol/L) for 24h, then RT-PCR was employed to detect 11?-HSD1 mRNA in each group. Among the groups, Dex-treated cells and non-intervened cells were grouped as negative control and normal control, respectively. Results 11?-HSD1 mRNA/?-actin mRNA of Dex-treated groups (respectively as 0.120?0.040, 0.140?0.020, 0.280?0.030, 0.360?0.060, 0.460?0.040) were significantly higher than that of the normal control (0.030?0.004, P

Background and purpose:It has been shown that chemotherapy could improve the quality of life and prolongation of survival time of the patients with advanced gastric cancer. There is still no standard chemotherapy regimen for advanced and metastatic gastric cancer, and regimens with high efficacy and safety are scare. Toxicities are considered to be limiting factors and in? uence the quality of life in the patients with advanced gastric cancer. The purpose of this study was to investigate the effi cacy and toxicity of docetaxel(DOC) in combination with oxaliplatin(OXA) as fi rst-line treatment in advanced gastric cancer and try to fi nd a regimen that would be more tolerable without deterioration of treatment response. Methods:48 patients with advanced gastric cancer were treated with docetaxel 35 mg/m2, ivgtt, d1,d8 combined with oxaliplatin 130 mg/ m2,ivgtt,d1 ;repeated every 3 weeks (one cycle) ,The effect was evaluated after two cycles. The effi cacy and toxicity were evaluated according to WHO standard. Results:48 patients could be evaluated for clinical response. Complete response in 3 pts and partial response in 24 pts were observed with an overall response rate of 56.25%, median time to progression (MTTP) was 5.6 months and median overall survival (MST) was 11.8 months. The most common toxicities were bone marrow suppression, peripheral neuritis, nausea and vomiting. All of them are reversible. Conclusion:Combining weekly docetaxel and oxaliplatin is an effective and well tolerated alternative treatment in advanced gastric cancer and has yielded promising results.

0.05)。The median time to progression (mTTP)was 5.8 months in XELOX group and 5.7 months in FOLFOX4 group. The median survival time (MST) was 10.0 months in XELOX group and 9.8 months in FOLFOX4 group, The toxicities were well tolerated,The incidence of grade Ⅲ+Ⅳ nausea and vomiting was significantly lower in XELOX group than in FOLFOX4 group (P0.05).Conclusions:Both of the two regimens were feasible, well tolerated and effective in treatment of advanced gastric cancer。XELOX regimen may be safer than FOLFOX4 regimen,especially in elderly patients or patients with ECOG PS of 1 to 2.

Chemotherapy for lung cancer is expected to prolong the survival of lung cancer patients. multidrug resistance is considered to be a major cause of failure of treatment. Many multidrug resistance mechanisms have contributed to lung cancer drug resistance, such as P glycoprotein (P gp), multidrug resistance associated protein (MRP), lung resistance related protein (LRP). The drug efflux pump mechanisms are the focus of recent researches.

AIM:To investigate the inhibitory effect of P12,a kind of lipopolysaccharide(LPS)-binding protein(LBP) inhibitory peptide,on the binding of LPS to macrophage in vitro.METHODS:Human monocyte-like cell line(U937 cells) was grown in RPMI-1640 and stimulated with PMA in order to induce their differentiation to macrophage stage.The relative affinity of P12 to LPS was determined by enzyme-linked immunosorbent assay(ELISA).The effects of P12 on the binding of LPS to U937 cells were determined by flow cytometry analysis.The production of tumor necrosis factor-alpha(TNF-?) was measured by ELISA.RESULTS:The relative binding activity of P12 to LPS was higher than that of LBP in the same mass concentration.P12 inhibited the binding of FITC-conjugated LPS(FITC-LPS) to U937 cells.The productions of TNF-? was also significantly suppressed by P12.CONCLUSION:The results suggest that blockage of LBP at the inflammatory sites might attenuate LPS-induced circulatory shock.

Objective To study the expressions of caudal type homeodomain transcription factors CDX1 and CDX2 in different subtype of intestinal metaplasia (IM) and gastric eareinoma,and investigate their roles in the development and progression of IM and gastric carcinogenesis, and determine the relationship between IM and gastric carcinoma. Methods Forty eases of chronic superficial gastritis, 40 cases of chronic atrophic gastritis (CAG), 46 eases of CAG with IM, 40 cases of gastric carcinoma, and 32 eases of IM foci in para-eancerous tissues were selected respectively to construct tissue microarrays. Immunohistechemistry and in situ hybridization were used to assess the expressions of CDX2 protein and CDX1, CDX2 mRNA in different gastric lesions respectively. Results The proportion of type Ⅲ IM in IM foci in para-caucerous tissues was significantly higher than that in CAG (56.25% vs 21.74% ,P< 0.01). There was no expression of CDX1, CDX2 mRNA and CDX2 protein in chronic superficial gastritis and CAG without IM. The expression of CDX2 protein and CDX2 mRNA in CAG with IM, para-cancerous tissues and gastric carcinoma was 69.57%, 53.12%,42.50% (CDX2 protein) and 63.04%,46.88%,35.00% (CDX2 mRNA), respectively. The exprossions of CDX1 mRNA in above throe gastric lesions were 67.39%, 50.00%, 40.00%, respectively. The expressions of CDX2 protein and CDX2, CDX1 mRNA in gastric carcinoma were significantly lower than those in CAG with IM (P< 0.01). But there was no significant difference between gastric carcinoma and IM foci in para-cancerous tissues (P> 0.05). Furthermoro,the expressions of CDX2 protein were significantly associated with histological type of gastric carcinoma, which in intestinal-type was significantly higher than those in diffuse-type(54.55% vs 27.78%, P< 0.05). The expression of CDX2 protein in type Ⅲ IM was also significantly lower than that in type Ⅰ IM(46.43% vs 79.31%,P< 0.05). Conclusions CDX1 and CDX2 may play important roles in the development and progression of IM and gastric carcinoma, and may be new gastric carcinoma associated genes. Type Ⅲ IM is a precancerous lesion of the intestinal-type gastric carcinoma.

A new and effective method to produce transgenic animals was established. Without a surgical incision, the recombinant plasmid containing green fluorescence protein (GFP) cDNA was repeatedly injected into male mouse testis at multi-sites. After few weeks of the final injection, the injected male was mated with normal oestrus female to produce transgenic mice. The presence of the GFP cDNA in F1 transgenic individuals were detected by polymerase chain reaction and Southern blot hybridization, which showed that the transgenic rate of mouse F1 offspring was 41%. The transferred gene was integrated into the host genome and could be transmitted to its offspring. When the positive F1 individuals were mated with the wild type ICR mice, the F2 individuals had a transgenic rate of 37%. The results indicate that the high efficiency of gene transfer and the limited number of manipulations make the method suitable for creating a large number of transgenic animals, especially, for producing domestic animals.

Objective　To establish a multidrug resistance cell line from human lung adenocarcinoma. Methods　The human lung adenocarcinoma cell line SPC-A-1 was exposed to cisplatin of a high and then increasing concentration for 192 d to establish multidrug resistance cell line (SPC-A-1/CDDP). The relative resistance was tested with MTT assay. The morphology of the cells was observed with transmission and scanning electron microscopy and the chromosome of them was analyzed with Giemsa stained specimens. Results　The resistance index of SPC-A-1/CDDP cells to cisplatin was 11.2 and the cells showed various cross-resistance to 5-Fu, doxorubicin, mitomycin, vincristine and etoposide, but not to hydroxycamptothecine. Electron microscopy showed the cells with irregular and enlarged nuclei and abundant microvilli. Conclusion　A multidrug resistance cell line (SPC-A-1/CDDP) from human lung adenocarcinoma is established. It can be used to downstream experiment.