To substantiate this hypothesis, we studied protection by methylproamine at both clonogenic survival and radiation-induced DNA damage, assessed by gamma H2AX (histone 2AX phosphorylation at serine 139) focus formation endpoints.

Materials and methods: The human keratinocyte cell line FEP1811 was used to study clonogenic survival and yield of gamma H2AX foci following

irradiation ((137)Cs gamma-rays) JAK inhibitor of cells exposed to various concentrations of methylproamine. Uptake of methylproamine into cell nuclei was measured in parallel.

Results: The extent of radioprotection at the clonogenic survival endpoint increased with methylproamine concentration up to a maximum dose modification factor (DMF) of 2.0 at 10 mu M. At least 0.1 fmole/nucleus of methylproamine is required to achieve a substantial MI-503 concentration level of radioprotection (DMF of 1.3) with maximum protection (DMF of 2.0) achieved at 0.23 fmole/nucleus. The gamma H2AX focus yield per

cell nucleus 45 min after irradiation decreased with drug concentration with a DMF of 2.5 at 10 mu M.

Conclusions: These results are consistent with the hypothesis that radioprotection by methylproamine is mediated by attenuation of the extent of initial DNA damage.”
“Macrophages, a heterogeneous and ubiquitous cell population representing up to 15% of the cellular content of different types of tissue, are the principal cell mediators in response to pathogens, inflammation process, tissue homeostasis and repair and play a pivotal role in atherosclerosis

and insulin resistance because of their capacity to be the major source of inflammatory cytokines, which can function through paracrine and endocrine mechanisms. Recently, differently activated macrophage populations have been described, depending on a large variety of microenvironmental signals, and it is now recognized that their activation plays a crucial role in the development and progression of atherosclerosis. There is good evidence of the ability of conjugated linoleic acids BEZ235 manufacturer and polyphenolic compounds to modulate inflammation in experimental models involving macrophages. This observation leaves room to the intriguing hypothesis that macrophage polarization could represent one of the unifying mechanisms through which specific food components can exert anti-inflammatory effects in humans, contributing to the prevention of chronic diseases strongly linked to inflammation, such as atherosclerosis. Future studies should be addressed to substantiate this hypothesis, investigating whether or not physiological concentrations of food-derived metabolites can perturb macrophage activation in vitro.