The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The long term acute phase-like responses that follow acute stressor exposure are blocked by alpha-melanocyte stimulating hormone.

Both intracerebroventricular (i.c.v.) IL-1beta and exposure to inescapable tail shock (IS) activate acute phase responses (APRs) that include increases in core body temperature (CBT), increases in hypothalamic-pituitary-adrenal activity, decreases in carrier proteins such as corticosterone binding globulin ( CBG), aphagia and adipsia. A variety of data suggested that stressors produce APRs by inducing brain IL-1beta. The current series of studies further explored this possibility by determining whether the functional IL-1beta antagonist, alpha-melanocyte-stimulating hormone (alpha-MSH(1-13)), would block IS-induced APRs. Immediately following i.c.v. alpha-MSH(1-13) administration, rats were exposed to a single session of 100, 5 s, 1.6 mA ISs, or control treatment (home cage control). alpha-MSH(1-13) blocked IS-induced increased CBT, increased plasma corticosterone (CORT), decreased CBG, aphagia and adipsia 24 h after IS. The inhibitory effects of alpha-MSH(1-13) were shown not to be a consequence of alpha-MSH(1-13) producing its actions 24 h after its administration because alpha-MSH(1-13) given 24 h before IS did not block IS-induced increased CBT and CORT during IS. Additionally, alpha-MSH(1-13), given 24 h before IS, had no effect on increased CBT, increased CORT, decreased CBG, adipsia, or aphagia 24 h after IS. These data provide support for a specific mode of action for i.c.v. alpha-MSH(1-13), namely blockade of APRs with no impact on acute hyperthermia or increased levels of CORT produced during IS.[1]


  1. The long term acute phase-like responses that follow acute stressor exposure are blocked by alpha-melanocyte stimulating hormone. Milligan, E.D., Nguyen, K.T., Deak, T., Hinde, J.L., Fleshner, M., Watkins, L.R., Maier, S.F. Brain Res. (1998) [Pubmed]
WikiGenes - Universities