Prey species should avoid areas where predation risk is high. However, if this is impossible, prey should reduce activities that may make them conspicuous and attract predators, such as foraging or mating. Thus, predation risk should change behavioral pattern of prey species. Not all species have same anti-predator behavioral patterns because they have evolved in the presence of different types or number of predators in their habitat. In this study we measured microhabitat use and escape initiation distance to identify how sensitive each species is to approaching predators. We measured jumping performance and morphological characteristics to reveal the relationship between jumping and morphology and whether jumping is helpful for escaping from predators' attack. Finally, we compared the survival rate among three species to identify how survival rate is affected by anti-predator behavioral patterns. The survivorship was related to microhabitat use and to the escape initiation distance, rather than on the jumping ability. We predicted that a species with the best survival rate will have superior jumping ability in order to escape from predators at the moment when they were attacked by predators. The jumping ability, however, was probably limited by hydrodynamic and morphological constraints, so jumping appears to contribute little to successfully escaping from predators’ attacks.

Sulfur is commonly used in Asia as a n herba l medicine to treat infl ammation and cancel‘. and potent chemopreventive effects have been demonstrated in various in vivo and in vitromodels for sulfur-containing compounds found in naturally occun‘ ing products. Here, we report the growth inhibitory and apoptosis-related effects of a newly developedhigh- purity eclible sulfur (ES) on immortali zecl human oral keratinocytes (IHOKs) and on oral cancer cells representing two stages of oral can cer (HN4‘ HN12) basecl on an 3-(4. 5-Dimethylt hiazol-2-yl)-2.5-cliphenyl tetrazolium bromide (MTT) a ssay, Western blotting, cell cycle analysis, ancl nuclear staining. The puri ty of the ES used in th is s tucly was verified by high performance liquid chromat ography (HPLC) , amino acid analysis and energy di spersive spectroscopy (EDS). ES inhibitecl the proliferation of immor talized and malignant oral kerati nocytes in a dose- and time-dependent manner FITC-Annexin V staining. DNA fragmentation testing. and Hoechst 33258 staining revealed that ES inhibits cell growth via apoptosis . ES blocked cell-cycle progression at the sub- Gl phase, with decreased expression 0 1' cyclins Dl, D2, and E, and t heir activating partners cdk2, cdk4, and cdk6‘ and a concomitant induction of p53 and p21/WAF1. Furthermore, ES treatment increased the cytosolic level of cytochrome c a nd resulted in caspase-3 activation‘ and thi s effect was correlated wi th Bax up- regulation and Bcl-2 down- regulation Taken together, these clata suggest that ES is a potential chemopreventive and chemotherapeutic agent for oral cancel