AIM: To investigate the expression of midkine in bladder transitional cell carcinoma and to analyze its relationship with the features of clinical pathology and prognosis.METHODS: The expressions of midkine protein in 50 cases of bladder transitional cell carcinoma samples were detected by SP immunohistochemical method using polyclonal antibodies against human midkine.Survival time of 40 cases was recorded.RESULTS: The protein expression of midkine was found in cytoplasm of tumor cells.The overall positive rate of midkine in 50 cases of bladder carcinoma was 90%(45/50).The positive degree of midkine showed a trend of increasing in grade and stage.There was statistically significant difference among them(P0.05).Patients with high expression of MK predicted a poor clinical outcome.CONCLUSION: Midkine is overexpressed in bladder transitional cell carcinoma than that in normal bladder.MK expression in bladder cancer is higher in less differentiated and deeper invaded cases,but it has no correlation with age,sex,treatment,tumor number and size.Patients with higher MK expression have shorter survival time than those with lower MK expression.

In this paper, adriamycin-carboxymethyldextran magnetic nanoparticles (ADR-CMD MNPs) were prepared. After i.v. administration in mice, acute toxicity, cumulative toxicity and the distribution profiles of heart were studied both for free adriamycin(ADR) and ADR-CMD MNPs. The results showed conjugation with CMD MNPs, the acute toxicity of ADR was decreased significantly, the LD50 value of ADR-CMD MNPs was 5.06 times as high as that of the free ADR. Altogether, the cumulative toxicity of conjugate MNPs is significantly decreased as expressed by the mortality, the loss for both weight and leucocyte after repeated injection. Tissue distribution studies show the reduced cardiac uptake of ADR after i.v. which possibly contributes to minimizing the cardiotoxic effect of ADR.
Animals ; Dextrans ; Doxorubicin ; administration & dosage ; pharmacokinetics ; toxicity ; Drug Carriers ; Drug Delivery Systems ; Female ; Injections, Intravenous ; Magnetics ; Male ; Mice ; Myocardium ; metabolism ; Tissue Distribution

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.

Permeability is one of the determinants of intestinal absorption and oral bioavailability. The non-cell-based permeation model is a kind of in vitro permeability measurement tool, which has the advantages of high efficiency, low cost, stable property, easy to use and customizable. According to the barrier type, non-cell-based permeation model can be divided into biomimetic barriers containing (phosphate) lipids and non-biomimetic barriers without lipids. Biomimetic permeation models include parallel artificial membrane permeability assay, vesicle-based permeation assay and PermeaPad®. Non biomimetic permeation models include Hollow fiber membrane models based on polyether sulfone materials. In foreign countries, the application of these four barriers for different purposes is gradually becoming a hot spot in drug absorption research. However, in China, there are only more applied studies on PMAPM and few published applied studies on the other three barriers. In order to meet the development needs of insoluble drug formulations, the author summarized the permeability devices and permeability calculation methods, searched the application of non-cell-based permeation model in the permeability of BSCⅡ drugs in recent years, and summarized the characteristic applications of three Biomimetic permeation models and hollow fiber membranes.