Following sacrifice, the isolation of fluorescent brain regions will enable postmortem analyses of distinct DA nuclei and axonal projections relevant to the PD brain. MJFF remains committed to providing the most optimal tools to PD researchers, and we believe this model, which is available from Taconic without restrictions on use to the entire academic and industrial research community, should be valuable for Parkinson’s disease research. Atherosclerosis is an inflammatory process that takes place in medium and large sized arteries. It is characterized by plaque formation on the endothelial wall, causing hardening and narrowing of arteries. The process is initiated by accumulation of fatty materials such as cholesterol and triglyceride. Lipid deposition in arteries triggers proliferation of vascular smooth muscle cells and results in recruitment of circulating inflammatory cells. Macrophages and smooth muscle cells then engulf lipids to form foam cells. With disease progression, VSMCs migrate to intima to form necrotic core which is surrounded by a fibrous cap consisting of VSMCs, collagen and other extracellular matrix. Plaque rupture occurs by induction of apoptosis of VSMCs and breakdown of collagen and ECM. This causes cerebral or cardiac events. Hydrogen sulfide is a gaso-transmitter along with nitric oxide and carbon monoxide. Similar to nitric oxide, H2S is a potent vasodilator and possesses vasoprotective effects, such as reduction of VSMC proliferations. Cystathionine gamma-lyase is one of the key enzymes producing endogenous H2S and is expressed abundantly in mammalian cardiovascular system. Recently, in vitro and in vivo studies were carried out to investigate the role of H2S in the pathogenesis of atherosclerosis. Deficiency of H2S appears to accelerate atherosclerosis. CSE-knockout mice were shown to have lower aortic H2S production and were found to develop early fatty streak lesions in the aortic root, elevated plasma levels of cholesterol and low-density lipoprotein cholesterol, hyperhomocysteinemia, increased lesional oxidative stress and adhesion molecule expression, as well as enhanced aortic intimal proliferation after being fed with atherogenic diet. On the contrary, supplementation with H2S inhibits atherosclerosis. It was found that H2S inhibited ICAM-1 expression in TNFa-induced HUVECs via the NF-kB pathway in ApoE knockout mice and induced superoxide dismutase expression, accompanied by a reduced level of reactive oxygen species. H2S also inhibited macrophage infiltration and reduced lesion size by down-regulation of CX3CR1 and CX3CL1 in macrophages. A recent report also showed that ApoE knockout mice with a H2S-releasing drug administration can decrease vascular TWS119 601514-19-6 inflammation and oxidative stress together with improved endothelial function and reduced atherosclerotic plaque formation. Thus far, the relationship between the metabolism of H2S and atherosclerosis has been evidenced using CSE knockout mice. CSE gene deletion led to decrease of H2S production with accelerated atherosclerosis and this can be ameliorated by treatment with NaHS or exogenous H2S donor.