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Signaling at neuronal Y1- and Y5-receptors produces the orexigenic effects of NPY, and pharmacologic blockade or genetic deletion of the Y1- and Y5-receptors reduces food intake and weight in mice, with Y1-receptor signaling appearing to be the major mediator of the orexigenic effects of NPY
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CD38+ cell depletion with TAK-079 reduces arthritis in a cynomolgus collagen-induced arthritis (CIA) model
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