This may explain the ability of anti-prion agents to reduce the rate of PrPsc accumulation and extend animal survival, but not cure disease. Synthetic peptides derived from the primary sequence of PrPc have been shown to have anti-prion activity. Peptides generated against PrPc residues 106–126 or 109–141 prevented PrPsc conversion in cell-free systems. Additionally, the use of PrP119–136 peptide was effective in decreasing PrPsc in chronically infected cells. Soto et al generated a peptide corresponding to the amino acid residues of PrPc with the propensity to form beta-sheet structure and inserted incremental proline residues to disrupt the conformational requirements of an ordered beta-sheet. Pre-incubation of this peptide with mouse-adapted Scrapie prior to intracerebral inoculation increased survival time in mice. Moreover, iPrP13 was able to reduce PrPsc in cultured cells following exposure to Scrapie infected brain homogenate. This data demonstrates that a competitive peptide mimetic can impede PrPc to PrPsc conversion, result in reduced PrPsc accumulation and delay disease progression. Alternatively, transgenic mice expressing mutant PrP at low level persist as clinically normal but can be induced to develop neurodegeneration and amyloid deposits by inoculation of a synthetic beta-sheet peptide carrying the P101L substitution. These results suggest that a peptide mimetic can also induce PrPc conversion to PrPsc and promote disease. Here we report the anti-prion activity of a synthetic RADApeptide repeat that is unrelated to PrPc primary structure and selfassembles into a hydrated beta-sheet nanofiber matrix. Further hormonal key players antagonizing inflammation are glucocorticoids, which are rapidly released from the adrenal cortex following activation of the HPA axis and down-regulate inflammation. It was somewhat surprising that greatly increased levels of ALI occurred in ADX rats and that this was not related to engagement of mineralocorticoid or glucocorticoid receptors. Glucocorticoids ultimately inhibit SJN 2511 ALK inhibitor transcription, which takes up to several hours, whereas lung injury in the current model peaks 4 or 6 hr after initiation. Thus, it seems unlikely that various glucocorticoid effects could have been fully developed in this short period of time. Moreover, rats possess the ability to synthesize steroids in non-adrenal tissues. The rat CNS has been identified as a source of 11b-hydroxylase and aldosterone synthase. Other non-adrenal sources include the kidney and vascular tissues. Thus, it seems likely that, in the absence of the adrenal glands, these extra-adrenal sources of corticosterone and aldosterone compensate for the lack of the adrenal medulla in an attempt to maintain systemic levels of corticoids. This study suggests that catecholamines activate macrophage NFkB with subsequent cytokine production in a dose dependent manner. Upregulation of phagocyte-derived catecholamines results in intensification of the acute inflammatory response.