BACKGROUND: To overcome the unfavorable issues associated with conventional anti-adhesive HA/CMC film, we developed an anti-adhesive thermally cross-linked gelatin film. OBJECTIVE: We tried to clarify the re-attachability of the film and the required properties concerning the film thickness, stiffness and anti-adhesion effect. METHODS: To determine the optimal thickness, 5 kinds of the thickness of gelatin film and the conventional film were analyzed by the tensile test, shearing test, buckling test and tissue injury test. Finally, using the optimal film thickness, we tried to clarify the anti-adhesion effect of the reattached film. RESULTS: The tensile and shearing test showed gelatin films ≥30 μm thick had greater tensile strength and a smaller number of film fractures, than the conventional film. The buckling and tissue injury test showed gelatin films ≥60 μm thick had higher buckling strength and worse injury scores than the conventional film. The anti-adhesive effect of re-attached gelatin film using optimal thickness (30–40 μm) found the anti-adhesion score was significantly better than that of the control. CONCLUSIONS: Provided it has an optimal thickness, gelatin film can be reattached with enough physical strength not to tear, safety stiffness not to induce tissue injury, and a sufficient anti-adhesion effect.
To understand genetic differences and similarities between tumorigenic and nontumorigenic HeLa x fibroblast hybrid cells, subtractive suppression hybridization (SSH), based on suppression PCR and a combination of normalization and subtraction in a single procedure, was used. Using the nontumorigenic CGL1 and tumorigenic CGL3, forward (CGL1-CGL3) and reverse (CGL3-CGL1) subtracted libraries were constructed. Among 192 clones, seven were identified as differentially expressed genes specific for either CGL1 or CGL3. All seven were not reported previously as differentially expressed genes in this hybrid system. In the forward subtraction, p16 was isolated, indicating the involvement of the loss of tumorigenic phenotype. Subsequent transfection of wild-type p16 to the tumorigenic CGL3 showed growth suppression in colony formation assay; however, no tumor suppression was observed when the transfectant was inoculated into nude mice. These results indicate that: (a) SSH is a suitable method to identify differentially expressed genes in two types of cells; and (b) although p16 plays some roles in growth suppression, the p16-transfected CGL3 is still capable to proliferate in vivo.
TNP-470, an analog of fumagillin, is one of the new angiogenesis inhibitors. Five days after an intraperitoneal inoculation of 10(7) cells of Walker 256 carcinosarcoma to SD rats, TNP-470 was injected intraperitoneally in the form of TNP aqueous solution or TNP-oil solution. Mean survival time of rats given TNP-oil solution or TNP aqueous solution was statistically prolonged, compared with that of the control rats. Our results showed that TNP-470 is an effective therapeutic drug for carcinomatous peritonitis.
Background: Recent studies suggest that a peroxisome proliferator activated receptor- γ (PPAR γ ) agonist pioglitazone reduces the incidence of ischemic cardiovascular events. However, it is unknown if pioglitazone induces therapeutic neovascularization after induction of ischemia. Moreover, novel drug delivery system may alleviate potential adverse effects of systemic administration of PPAR γ agonists. We recently reported that intramuscular injection of biodegradable polymeric NP resulted in cell-selective delivery of NP into vascular endothelial cells of ischemic muscles for 2 weeks post-injection in a murine model of hindlimb ischemia. Hence, we tested the hypothesis that nanoparticle (NP)-mediated endothelial cell selective delivery of pioglitazone is an effective therapy to induce ischemic neovascularization in vivo. Methods and Results: In a murine model of hindlimb ischemia, systemic oral administration of pioglitazone at a dose of 1000 μ g/kg per day, but not other lower doses, enhanced recovery of blood perfusion to the ischemic limb, increased angiogenesis and arteriogenesis 3 weeks after induction of ischemia (Figure A ). In contrast, single intramuscular injection of NP incorporated with pioglitazone at 1 or 10 μ g/kg into ischemic muscles immediately after induction of ischemia significantly enhanced ischemic neovascularization at 3 weeks post-ischemia (Figure B ). Intramuscular injection of PBS, FITC-NP, or pioglitazone only at 1–10 μ g/kg showed no effects on blood perfusion to the ischemic limb. Conclusion: NP-mediated endothelial cell-selective delivery of pioglitazone may effectively induce therapeutic neovascularization. A. Effects of Systemic Oral Administrate of Pioglitazone for 21 days B. Effects of Single Intramuscular Injection of Pioglitazone-NP
