Browsing by Author "Li, Qin"

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    Controlling Light Oxidation Flavor in Omega-3 Fatty Acid Enriched 2% Milk by Packaging Films
    Li, Qin (Virginia Tech, 2011-06-01)
    Milk is often packaged in translucent containers providing little protection against flavor degradation from light. Addition of omega-3 fatty acid sources into milk increases the risk of light-initiated degradation of nutrients and sensory quality. The effectiveness of iridescent film materials in reducing light-induced oxidation of extended shelf-life omega-3 fatty acid enriched milk (2% total fat) was studied. Film selections were targeted to provide product visibility and control product exposure at targeted riboflavin excitation wavelength regions. Effectiveness was determined by sensory evaluation and measuring changes in volatile compounds on days 1, 7, 14, and 21 when stored under fluorescent light at 4°C. Five packaging treatments (films overwrapped on glass bottles) were evaluated: 446nm block, 570 nm block, broad spectrum block with 4% transmission (BS4T), light-protected (foil overwrap) control, and light-exposed (no overwrap) control. Experienced panelists (n=12) rated oxidized flavor intensity (0-9; 9=extreme) for milk samples. Light-protected milk was lower in oxidized flavor (mean score less than 3) throughout the storage period. Oxidized flavor in milk with BS4T film overwraps was not different compared to light-protected milk (p>.05) at the later stage (21 days), suggesting some level of protection to milk flavor. Milk without fish oil (milk fat only) shows relatively larger peak areas for 2-butanone on day 14, compared to other milk samples, suggesting antioxidants in the fish oil can prevent light oxidation. Overall, packaging that provides a complete light block is still the best way to prevent light-oxidized flavor in milk.
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    Myeloid cell-derived inducible nitric oxide synthase suppresses M1 macrophage polarization
    Lu, Geming; Zhang, Ruihua; Geng, Shuo; Peng, Liang; Jayaraman, Padmini; Chen, Chun; Xu, Feifong; Yang, Jianjun; Li, Qin; Zheng, Hao; Shen, Kimberly; Wang, Juan; Liu, Xiyu; Wang, Weidong; Zheng, Zihan; Qi, Chen-Feng; Si, Chuanping; He, John Cijiang; Liu, Kebin; Lira, Sergio A.; Sikora, Andrew G.; Li, Liwu; Xiong, Huabao (Nature, 2015-03-27)
    Here we show that iNOS-deficient mice display enhanced classically activated M1 macrophage polarization without major effects on alternatively activated M2 macrophages. eNOS and nNOS mutant mice show comparable M1 macrophage polarization compared with wild-type control mice. Addition of N6-(1-iminoethyl)-L-lysine dihydrochloride, an iNOS inhibitor, significantly enhances M1 macrophage polarization while S-nitroso-N-acetylpenicillamine, a NO donor, suppresses M1 macrophage polarization. NO derived from iNOS mediates nitration of tyrosine residues in IRF5 protein, leading to the suppression of IRF5-targeted M1 macrophage signature gene activation. Computational analyses corroborate a circuit that fine-tunes the expression of IL-12 by iNOS in macrophages, potentially enabling versatile responses based on changing microenvironments. Finally, studies of an experimental model of endotoxin shock show that iNOS deficiency results in more severe inflammation with an enhanced M1 macrophage activation phenotype. These results suggest that NO derived from iNOS in activated macrophages suppresses M1 macrophage polarization.