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)
 
 
 
 
 

Aspects of the involvement of interleukin-1 and nitric oxide in the pathogenesis of insulin-dependent diabetes mellitus.

The possible involvement of the cytokine interleukin-1 ( IL-1) and nitric oxide (NO) in the pathogenesis of insulin-dependent diabetes mellitus (IDDM) is reviewed and current and potential therapies are discussed. IDDM is a common disorder in the Western world and it is rising in incidence. In IDDM, islet-infiltrating macrophages produce IL-1 which is cytotoxic specifically to beta-cells in vitro. IL-1 increases beta-cell formation of NO, ceramide, prostaglandins, heat-shock proteins, and activates a protease. Additionally, IL-1 depresses beta-cell energy production, insulin gene expression and cyclic AMP synthesis, and impacts negatively on different parts of the insulin stimulus-secretion coupling, actions mimicked by NO. Conversely, blocking NO formation prevented many of these effects in most reports published. Also, changes in cyclic AMP and prostaglandins seem unlikely events in mediating the cytotoxicity of IL-1, while the role of ceramide remains less clear. Peptides capable of blocking beta-cell IL-1 receptors, and agents blocking NO synthesis may prove valuable in preserving beta-cell function in IDDM. Although IDDM causes immense morbidity and expense, uniformly effective preventive or beta-cell protective therapy is not currently available. If IL-1 is causing beta-cell dysfunction in human IDDM through NO production, several processes in the IL-1-NO connection are appropriate targets for agents protecting beta-cells from destruction and functional inhibition in IDDM.[1]

References

 
WikiGenes - Universities