Therapies designed to reinforce the circadian axis (for example, administration of melatonin or light) have been reported to alleviate the disturbed circadian rhythms and disrupted sleep.
For example, administration of a peptide sequence unique to tissue remodeling/fibrotic (M2) macrophages identified by subtractive phage biopanning and fused to the KLA proapoptotic peptide [286] decreased mortality in CT-26 tumor-bearing mice by inducing a decreased number of tumor-associated macrophages [287].
For example, administration of cocaine or the presentation of drug-related cue can enhance evoked responses in the primary sensory cortex of experimental animals and humans [7], [8].
For example, administration of NT or NT analogue can stimulate DA-dependent behaviors, while NT antagonist can block the effect of NT analogue [19], [20].
In quail embryos, for example, administration of genistein after three days of incubation leads to a decrease of copulatory behavior at puberty [63], but the possible effects during embryogenesis have not been assessed.
For example, administration of the PPARγ ligand rosiglitazone reduces foam cell formation and atherosclerosis in LDL-R knockout mice [23], and transplantation of PPARγ-deficient bone marrow into recipient LDL-R knockout mice enhanced atherosclerosis [24].
For example, administration of the active CART55-102 peptintointhethe VTA results in a cocaine-like increase in locomotor activity and produces a conditioned place preference (CPP) similar to that induced by cocaine or amphetamine [11], indicating that CART signaling in this region is reinforcing.
In some tumor entities, for example, administration of glutamate antagonists inhibits cell proliferation, cell cycle arrest, and finally cell death.
For example, administration of anti-myostatin antibody improves exercise resistance in aged mice (LeBrasseur et al., 2009).
For example, administration of the TGR5-selective synthetic agonist (INT-777) to mice attenuated diet-induced obesity and improved glucose tolerance.
