Carbons produced from known organic compounds 2. Anthracene-biphenyl and phenanthrene- biphenyl systems

Carbonization of binary mixtures of anthracene biphenyl and penanthrene bipheny

Do enzyme activities during decomposition follow predicted patterns? A test of the conceptual model of litter decay.

Surprisingly, there remains a paucity of research examining specific interactions between the relationship between microbial community behavior and plant litter chemistry during decomposition. A more mechanistic understanding of the relationship between these drivers will ultimately help determine the trajectory of litter decomposition and the conditions in which soils serve as either a source or sink for atmospheric C. In order to examine these relationships, a laboratory incubation was established using _Acer saccharum_ litter and a sandy soil (< 1.5% organic matter). Extracellular enzyme activities ([BETA]-glucosidase, N-acetyl glucosaminidase, leucine-amino peptidase, acid phosphatase, phenol oxidase, and peroxidase) were monitored on a consistent basis along with instantaneous rates of carbon dioxide production, microbial biomass (carbon and nitrogen) and phospholipid fatty acid biomarkers (PLFA), and nitrogen and phosphorus availability. Microbial biomass and microbial respiration peaked within the first week of the experiment. This was likely due to the high availability of water soluble substrates early in decay that can be obtained without the production of extracellular enzymes. [BETA]-glucosidase (BG), N-acetyl glucosaminadase (NAG), and acid phosphatase activities increased quickly following the first week and peaked within the first month (at approximately 15% mass loss). Leucine amino peptidase was not detected during the incubation, which may be due to its strong positive correlation with soil pH, while other hydrolytic enzymes tend to track concentrations of soil organic matter. Phenol oxidase and peroxidase activities were not measurable until the second month of the experiment (> 25% mass loss), likely following the depletion of more labile substrates. A second increase in BG activity was observed between Days 83-111, which may be due to an increase in the availability of cellulose that was previously shielded by lignin, since oxidative enzyme activity was first detected on Day 68. We also observed some shifts in microbial PLFAs along with enzyme activities during decomposition. Prior to the increases in enzyme activity we observed a high proportion of PLFA 18:1[omega]7c, which is a bacterial biomarker. As enzyme activities increased, we observed a decrease in this biomarker and an increase in 18:2[omega]6,9c, a fungal biomarker that was correlated with BG and NAG activity. We did not observe any clear relationships between PLFAs and lignolytic enzyme activity, however. Overall, we observed a distinct functional shift in microbial substrate use that may be associated with either changes in composition of the microbial community or community shifts in enzyme production

RNAase III-Type Enzyme Dicer Regulates Mitochondrial Fatty Acid Oxidative Metabolism in Cardiac Mesenchymal Stem Cells

Cardiac mesenchymal stem cells (C-MSC) play a key role in maintaining normal cardiac function under physiological and pathological conditions. Glycolysis and mitochondrial oxidative phosphorylation predominately account for energy production in C-MSC. Dicer, a ribonuclease III endoribonuclease, plays a critical role in the control of microRNA maturation in C-MSC, but its role in regulating C-MSC energy metabolism is largely unknown. In this study, we found that Dicer knockout led to concurrent increase in both cell proliferation and apoptosis in C-MSC compared to Dicer floxed C-MSC. We analyzed mitochondrial oxidative phosphorylation by quantifying cellular oxygen consumption rate (OCR), and glycolysis by quantifying the extracellular acidification rate (ECAR), in C-MSC with/without Dicer gene deletion. Dicer gene deletion significantly reduced mitochondrial oxidative phosphorylation while increasing glycolysis in C-MSC. Additionally, Dicer gene deletion selectively reduced the expression of β-oxidation genes without affecting the expression of genes involved in the tricarboxylic acid (TCA) cycle or electron transport chain (ETC). Finally, Dicer gene deletion reduced the copy number of mitochondrially encoded 1,4-Dihydronicotinamide adenine dinucleotide (NADH): ubiquinone oxidoreductase core subunit 6 (MT-ND6), a mitochondrial-encoded gene, in C-MSC. In conclusion, Dicer gene deletion induced a metabolic shift from oxidative metabolism to aerobic glycolysis in C-MSC, suggesting that Dicer functions as a metabolic switch in C-MSC, which in turn may regulate proliferation and environmental adaptation

Role of arginase 2 in systemic metabolic activity and adipose tissue fatty acid metabolism in diet-induced obese mice

Visceral adipose tissue (VAT) inflammation and metabolic dysregulation are key components of obesity-induced metabolic disease. Upregulated arginase, a ureahydrolase enzyme with two isoforms (A1-cytosolic and A2-mitochondrial), is implicated in pathologies associated with obesity and diabetes. This study examined A2 involvement in obesity-associated metabolic and vascular disorders. WT and globally deleted A2(−/−) or A1(+/−) mice were fed either a high fat/high sucrose (HFHS) diet or normal diet (ND) for 16 weeks. Increases in body and VAT weight of HFHS-fed WT mice were abrogated in A2−/−, but not A1+/−, mice. Additionally, A2−/− HFHS-fed mice exhibited higher energy expenditure, lower blood glucose, and insulin levels compared to WT HFHS mice. VAT and adipocytes from WT HFHS fed mice showed greater A2 expression and adipocyte size and reduced expression of PGC-1α, PPAR-γ, and adiponectin. A2 deletion blunted these effects, increased levels of active AMPK-α, and upregulated genes involved in fatty acid metabolism. A2 deletion prevented HFHS-induced VAT collagen deposition and inflammation, which are involved in adipocyte metabolic dysfunction. Endothelium-dependent vasorelaxation, impaired by HFHS diet, was significantly preserved in A2−/− mice, but more prominently maintained in A1+/− mice. In summary, A2 is critically involved in HFHS-induced VAT inflammation and metabolic dysfunction