Beauveria bassiana infection alters colony development and defensive secretions of the beetles Tribolium castaneum and Ulomoides dermestoides (Coleoptera: Tenebrionidae).

We studied the effect of the entomopathogenic fungus Beauveria bassiana strain GHA on a) colony development of the beetles Tribolium castaneum (Herbst) and Ulomoides dermestoides (Fairmaire) (Coleoptera: Tenebrionidae) under laboratory conditions; and 2) the volatile blend released by both beetles, containing defensive pheromones, by using the solid phase microextraction technique. Colony development of both species was strongly altered 3 mo after treatment with B. bassiana, showing a significant reduction in progeny of 37.5% for T. castaneum and 50.0% for U. dermestoides. We also showed that the volatiles released by T. castaneum diminished close to 20% compared with those of healthy beetles, whereas in U. dermestoides secretions dramatically dropped to 5%, 7 d after immersion in 1 x 10(9) conidia per ml. These results suggest that after infection events take place, fungus-induced diminished secretion of the defensive pheromones may be a physiologic clue for behavioral changes in infected beetles.

Applicability of anti-neovascular therapy to drug-resistant tumor: suppression of drug-resistant P388 tumor growth with neovessel-targeted liposomal adriamycin.

Anti-neovascular therapy, one of the effective anti-angiogenic chemotherapy, damages new blood vessels by cytotoxic agents delivered to angiogenic endothelial cells and results in indirect eradication of tumor cells. We previously reported that liposomes-modified with a pentapeptide, Ala-Pro-Arg-Pro-Gly (APRPG-Lip) homing to angiogenic site, highly accumulated in tumor tissue, and APRPG-Lip encapsulating adriamycin (APRPG-LipADM) effectively suppressed tumor growth in tumor-bearing mice. In the present study, we examined the topological distribution of fluorescence-labeled APRPG-LipADM as well as TUNEL-stained cells in an actual tumor specimen obtained from Colon 26 NL-17 carcinoma-bearing mice. The fluorescence-labeled APRPG-Lip dominantly localized to vessel-like structure: a part of which was also stained with anti-CD31 antibody. Furthermore, TUNEL-stained cells were co-localized to the same structure. These data indicated that APRPG-LipADM bound to angiogenic endothelial cells and induced apoptosis of them. We also investigated the applicability of anti-neovascular therapy using APRPG-LipADM to ADM-resistant P388 solid tumor. As a result, APRPG-LipADM significantly suppressed tumor growth in mice bearing the ADM-resistant tumor. These data suggest that APRPG-LipADM is applicable to various kinds of tumor including drug-resistant tumor since it targets angiogenic endothelial cells instead of tumor cells, and eradicates tumor cells through damaging the neovessels.