The Earth's geomagnetic field (GMF) is known to act as a sensory cue for magnetoreceptive animals such as birds, sea turtles, and butterflies in long-distance migration, as well as in flies, cockroaches, and cattle in short-distance movement or body alignment. Despite a wealth of information, the way that GMF components are used and the functional modality of the magnetic sense are not clear. A GMF component, declination, has never been proven to be a sensory cue in a defined biological context. Here, we show that declination acts as a compass for horizontal food foraging in fruit flies. In an open-field test, adopting the food conditioning paradigm, food-trained flies significantly orientated toward the food direction under ambient GMF and under eastward-turned magnetic field in the absence of other sensory cues. Moreover, a declination change within the natural range, by alteration only of either the east-west or north-south component of the GMF, produced significant orientation of the trained flies, indicating that they can detect and use the difference in these horizontal GMF components. This study proves that declination difference can be used for horizontal foraging, and suggests that flies have been evolutionarily adapted to incorporate a declination compass into their multimodal sensorimotor system.
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), a member of the TNF superfamily, has garnered interest as it is relatively non-toxic to normal cells, but selectively induces apoptotic cell death in multiple types of transformed or malignant cells. Bufalin is the major digoxin-like immunoreactive component of Sum Su, which is obtained from the skin and parotid venom gland of the toad. Bufalin is known to inhibit cell proliferation and induce apoptosis in a variety of cancer cells. The present study investigated whether bufalin promoted TRAIL-induced apoptotic cell death. In the present study, a combined treatment using bufalin and TRAIL significantly increased TRAIL-mediated inhibition of cell viability and increased apoptosis in T24 human bladder cancer cells. The apoptotic effects were associated with the upregulation of death receptor proteins and the downregulation of cellular Fas-associated death domain-like interleukin-1β-converting enzyme inhibitory protein and X-linked inhibitor of apoptosis protein. Furthermore, the data revealed that bufalin and TRAIL activated caspase-3, −8 and −9 and subsequently increased the degradation of poly (ADP-ribose) polymerase. Taken altogether, the nontoxic doses of bufalin and TRAIL sensitized T24 cells to TRAIL-mediated apoptosis. Therefore, bufalin may provide an effective therapeutic strategy for the safe treatment of human bladder cancers that are resistant to TRAIL.
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