This review looks particular at the role of COX-2 in the pathogenesis of Parkinson’s disease, involving the generation of PGs and the role of the two different parts of the cyclooxygenasecyclooxygenase and peroxidase activity. (C) 2012 International Union of Biochemistry www.selleckchem.com/products/rsl3.html and Molecular Biology, Inc.”
“Proline dehydrogenase (oxidase, PRODH/POX), the first enzyme in the proline degradative pathway, plays a special role in tumorigenesis

and tumor development. Proline metabolism catalyzed by PRODH/POX is closely linked with the tricarboxylic acid (TCA) cycle and urea cycle. The proline cycle formed by the interconversion of proline and ?1-pyrroline-5-carboxylate (P5C) between mitochondria and cytosol interlocks with pentose phosphate pathway. Importantly, by catalyzing proline to P5C, PRODH/POX donates electrons into the electron transport chain to generate ROS or ATP. In earlier studies, we found that PRODH/POX functions as a tumor suppressor to initiate apoptosis, inhibit tumor growth, and block the cell cycle, all by ROS signaling. It also check details suppresses hypoxia inducible factor signaling by increasing a-ketoglutarate. During tumor progression, PRODH/POX is under the control of various tumor-associated factors, such as tumor suppressor p53, inflammatory factor peroxisome proliferator-activated

receptor gamma (PPAR?), onco-miRNA miR-23b*, and oncogenic transcription factor c-MYC. Recent studies revealed the two-sided features of PRODH/POX-mediated regulation. Under metabolic stress such as oxygen and glucose deprivation, PRODH/POX can be induced to serve as a tumor survival factor through ATP production

or ROS-induced autophagy. The paradoxical roles of PRODH/POX can be understood considering the temporal and spatial context of the tumor. Further studies will provide additional insights into this protein and on its metabolic effects in tumors, which may lead to new therapeutic strategies.(C) 2012 International Union of Biochemistry and Molecular Biology, Inc.”
“BACKGROUND: The microbial biomass present in activated sludge contains lipidic compounds that can be used as biodiesel feedstock. In this study, the production of biodiesel from activated sludge from Tuscaloosa, AL was optimized Selleck LY2606368 based on the yield of fatty acid methyl esters (FAMEs). In situ transesterification was used with sulfuric acid as catalyst. A general factorial design of 4 x 6 x 5 for temperature, methanol to sludge ratio and catalyst concentration, respectively, was considered for optimization.

RESULTS: Biodiesel yield can be adequately described by the quadratic response surface model with R-2 of 0.843 and statistically insignificant lack of fit (p = 0.152). Numerical optimization showed that an optimum biodiesel yield of 4.88% can be obtained at 55 degrees C, 25 methanol to sludge ratio and 4% volume sulfuric acid. The optimum experimental biodiesel yield was indeed obtained at that condition but with a value of 4.79 +/- 0.02%.