Monitoring of beta-Blockers Ozone Degradation via Electrospray Ionization Mass Spectrometry

Santos, LS (reprint author), Talca Univ, Lab Asymmetr Synth, POB 747, Talca, Chile.The structures of intermediate products of ozone degradation of different pharmaceutical compounds have been studied. Under the conditions employed, complete ozone degradation of nadolol was achieved after 100 min. The degradation products obtained in aqueous solution were characterized by electrospray ionization mass (and tandem mass) spectrometry (ESI-MS and ESI-MS/MS). The proposed mechanism for degradation, ozone attacks at the aniline amino group giving rise to nitro compounds and further degradation occurs via a series of oxidative processes. Continuous online monitoring by ESI-MS(/MS) with high accuracy mass measurements showed that ozone degradation of atenolol (ATE) and acebutolol (ACE) occurs via mechanisms similar to that of nadolo

Rituximab as maintenance treatment for systemic Lupus Erythematosus: a multicentre observational study of 147 patients

INTRODUCTION: The efficacy of rituximab (RTX) in Systemic Lupus Erythematosus (SLE) is debated. We describe the outcomes of a European SLE cohort treated with RTX, with emphasis on its role as a maintenance agent. METHODS: All patients with SLE receiving RTX as induction across four centres were included, follow-up post RTX was collected including the subgroup treated with RTX as maintenance treatment (RMT). Disease flares during the follow-up were defined as an increase in disease activity and immunosuppressive drugs. RESULTS: Of 147 patients, at 6 months 27% experienced treatment failure (TF), in a multivariate analysis, a low number of previous immunosuppressive therapies (p=0.034) and low C4 levels (p=0.008) reduced the risk of TF. Eighty patients received RMT over a median of 24.5 months during which 85 relapses, mainly musculoskeletal, were recorded (1.06 per patient), at the last RTX course, 84% of the patients were in remission. 28/80 (35%) patients never flared during the RMT with low damage accrual, active articular disease at the time of the first RTX course was associated with risk of flare during RMT (p=0.010). After RMT, relapse free survival was similar to patients receiving a single-RTX course (p=0.72). CONCLUSIONS: RMT is a potential treatment option in difficult to treat patients. Relapses occur during RMT and are more likely in those with active articular disease at the time of the first RTX. Relapse risk after RMT remains high and apparently comparable to the one seen after a single-RTX course

Age at symptom onset and death and disease duration in genetic frontotemporal dementia : an international retrospective cohort study

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49\ub75 years (SD 10\ub70; onset) and 58\ub75 years (11\ub73; death) in the MAPT group, 58\ub72 years (9\ub78; onset) and 65\ub73 years (10\ub79; death) in the C9orf72 group, and 61\ub73 years (8\ub78; onset) and 68\ub78 years (9\ub77; death) in the GRN group. Mean disease duration was 6\ub74 years (SD 4\ub79) in the C9orf72 group, 7\ub71 years (3\ub79) in the GRN group, and 9\ub73 years (6\ub74) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0\ub745 between individual and parental age at onset, r=0\ub763 between individual and mean family age at onset, r=0\ub758 between individual and parental age at death, and r=0\ub769 between individual and mean family age at death) than in either the C9orf72 group (r=0\ub732 individual and parental age at onset, r=0\ub736 individual and mean family age at onset, r=0\ub738 individual and parental age at death, and r=0\ub740 individual and mean family age at death) or the GRN group (r=0\ub722 individual and parental age at onset, r=0\ub718 individual and mean family age at onset, r=0\ub722 individual and parental age at death, and r=0\ub732 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35\u201362, for age at onset; 61%, 47\u201373, for age at death), and even more by family membership (66%, 56\u201375, for age at onset; 74%, 65\u201382, for age at death). In the GRN group, only 2% (0\u201310) of the variability of age at onset and 9% (3\u201321) of that of age of death was explained by the specific mutation, whereas 14% (9\u201322) of the variability of age at onset and 20% (12\u201330) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11\u201326) of the variability of age at onset and 19% (12\u201329) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society

Photocatalytic Degradation Of Phenol And Chlorinated Phenols Using Agtio2 In A Slurry Reactor

Photodegradation of phenol (PhOH), 2,4-dichlorophenol (2,4-DCP), 2,3,5-trichlorophenol (2,3,5-TCP) and pentachlorophenol (PCP) was investigated using an open upflow slurry reactor and TiO2 (Ag-loaded) as photocatalyst. Light was provided by three 125 W high-pressure mercury lamps. Best degradation rates were obtained using 250 mg l-1 of AgTiO2 in the presence of H2O2 and a constant supply of air (1.71 min-1). Under this optimized condition, destruction rate constants obtained for a 1 × 10-4M solution of PhOH, 2,4-DCP, 2,3,5-TCP and PCP were 0.0493, 0.0430, 0.0367 and 0.0356 min-1, respectively. Each gram of phenol required 1.70 kW for its photodestruction. © 1994.28818451849Al-Ekabi, Serpone, Pelizzetti, Minero, Fox, Draper, Kinetic studies in heterogenous photocatalysis. 2. TiO2 mediated degradation of 4-chlorophenol, 2,4-dichlorophenol and 2,4,5-trichlorophenol in air-equilibrated aqueous media (1989) Langmuir, 5, pp. 250-255Box, Investigation of the Folin-Ciocalteau phenol reagent for the determination of polyphenolic substance in natural waters (1983) Wat. Res., 17, pp. 511-525C&en, Chemical uses of solar energy found promising (1991) Chem. Engng News, 19, p. 8Davis, Huang, The removal of substituted phenols by a photocatalytic oxidation process with cadmium sulfide (1990) Wat. Res., 24, pp. 543-550D'Oliveira, Al-Sayyed, Pichat, Photodegradation of 2- and 3-chlorophenol in TiO2 aqueous suspensions (1990) Envir. Sci. Tehnol., 24, pp. 990-996Hisanaga, Harada, Tanaka, Photocatalytic degradation of organochlorine compounds in suspended TiO2 (1990) J. Photochem. Photobiol. A: Chem., 54, pp. 113-118Jardim, Pasquini, Guimaråes, Faria, Short-term toxicity using Escherichia coli: monitoring CO2 production by flow injection analysis (1990) Wat. Res., 24, pp. 351-354Kochany-Lipczynska, Bolton, Flash photolysis/HPLC applications 2 Direct photolysis vs hydrogen peroxide mediated photodegradation of 4-chlorophenol as studied by a flash photolysis/HPLC technique (1992) Environmental Science & Technology, 26, pp. 259-261Kondo, Jardim, Photodegradation of chloroform and urea using Ag-loaded titanium dioxide as catalyst (1991) Wat. Res., 25, pp. 823-827Kormann, Bahnemann, Hoffmann, Environmental photochemistry: is iron oxide (Hematite) an active photocatalyst? (1989) A comparative study: α-Fe2O3, ZnO, TiO2, 48, pp. 161-169. , J. Photochem. Photobiol. A: ChemMatthews, Photo-oxidation of organic material in aqueous suspensions of titanium dioxide (1986) Wat. Res., 20, pp. 569-578Matthews, Purification of water with near-UV illuminated suspensions of titanium dioxide (1990) Wat. Res., 24, pp. 653-660Okamoto, Yamamoto, Tanaka, Tanaka, Itaya, Heterogeneous photocatalytic decomposition of phenol over TiO2 powder (1985) Bulletin of the Chemical Society of Japan, 58, pp. 2015-2022Pruden, Ollis, Degradation of chloroform by photoassisted heterogeneous catalysis in dilute aqueous suspension of titanium dioxide (1983) Envir. Sci. Technol., 17, pp. 628-631Sclafani, Palmisano, Davi, Photocatalytic degradation of phenol in aqueous polycrystalline TiO2 dispersion: the influence of Fe+3, Fe+2 and Ag+ on the reaction rate (1990) J. Photochem. Photobiol. A: Chem., 58, pp. 113-123Sclafani, Palmisano, Davi, Photocatalytic degradation of phenol by TiO2 aqueous dispersions: rutile and anatase activity (1991) New J. Chem., 14, pp. 265-268Turchi, Ollis, Photocatalytic degradation of organic water contaminants: mechanisms involving hydroxyl radical attack (1990) J. Catal., 122, pp. 178-192Wei, Wang, Wan, Photocatalytic oxidation of phenol in the presence of hydrogen peroxide and titanium dioxide powers (1990) J. Photochem. Photobiol. A: Chem., 55, pp. 115-12

Heterogeneous Photocatalysis: An Emerging Technology For Remediation Of Voc Contaminated Environments

Heterogeneous photocatalysis has been studied in the last two decades for the treatment of contaminated water and wastewaters, and more recently, in the clean up process of contaminated atmosphere. Scientific principles of the method and a survey of the recent literature for aqueous and gas-phase photocatalytic oxidation of volatile organic compounds (VOCs) are presented. The influence of different parameters, types of photoreactors and kinetics of photodegradation are discussed.4901/02/15142

Selective Trace Level Analysis Of Phenolic Compounds In Water By Flow Injection Analysis-membrane Introduction Mass Spectrometry

Flow injection analysis coupled with membrane introduction mass spectrometry (FIA-MIMS) with on-line derivatization is shown to allow fast, accurate, nearly interference-free, and sensitive (low μg/L)quantitation of phenolic compounds in water. On-line FIA derivatization of the phenolic compounds is performed by acetic anhydride acetylation in a K2CO3buffered alkaline medium. The phenol acetates so formed efficiently permeate a silicone membrane and are directly transferred to the mass spectrometer, in which they are analyzed with selectivity and high sensitivity via selected ion monitoring. FIA-MIMS analysis was performed for aqueous solutions of phenol, 2-methylphenol, 4-chlorophenol, 4-chloro-3-methylphenol, 2,4-dichlorophenol, and 2,4,6-trichlorophenol, and detection limits in the 0.5-20 μg/L (ppb) range were observed for an analytical frequency of six samples/h. FIA-MIMS for phenolic compound analysis is considerably less time-consuming and labor intensive than most chromatographic methods based on liquid-liquid extraction and preconcentration procedures and is therefore applicable for on-line and in-situ monitoring of phenols in wastewaters and in the environment. FIA-MIMS employing acetic anhydride derivatization is also virtually free of interferences since it combines chemical, membrane, and enhanced MS selectivity; hence quantitation of phenolic compounds can be performed in the presence of congeners.351020842088Seiber, J.N., Crosby, D.G., Fouda, H., Soderquist, C.J.J., (1972) Chromatogr, 73, p. 89Realini, P.A.J., (1981) Chromatogr. Sci., 19, p. 124Davi, M.L., Gnudi, F., (1999) Water Res., 33, p. 3213(1995) CFR. Part 23 App. A. Effluents Guidelines and Standard, , Federal Register, U.S. GPO, Washington, DCMendes, M.A., Eberlin, M.N., Organoleptical properties of water (2000) The Handbook of Water Analysis, p. 75. , Nollet, L. M. L., Ed.Marcel Dekker: New York, Chapter 6Knutsson, M., Jönsson, J.A., Determination of phenolic compounds in water (2000) The Handbook of Water Analysis, p. 347. , Nollet, L. M. L., Ed.Marcel Dekker: New York, Chapter 18Emerson, E.J., (1938) Org. Chem., 3, p. 153Krijgsman, W., Van De Kamp, C.G., (1977) J. Chromatogr., 131, p. 412Realini, P.A.J., (1981) Chromatogr. Sci., 19, p. 124Neufeld, R.D., Poladino, S.B.J., (1985) Water Pollut. Control Fed., 57, p. 1040Tyagi, R., (1995) Fresenius Environ. Bull., 4, p. 751Bao, M.L., Pantani, F., Barbieri, K., Burrini, D., Griffini, O., (1996) Chromatographia, 42, p. 227Puig, D., Barceló, D., (1996) Trends Anal. Chem., 15, p. 362(1997) Standard Methods for the Examination of Water and Wastewater, 18th Ed., , American Public Health Association: New York, (5530 method)Farino, J., Norwitz, G., Boyko, W.J., Keliher, P.N., (1981) Talanta, 28, p. 70

Administration Of A Murine Diet Supplemented With Conjugated Linoleic Acid Increases The Expression And Activity Of Hepatic Uncoupling Proteins

Daily intake of conjugated linoleic acid (CLA) has been shown to reduce body fat accumulation and to increase body metabolism; this latter effect has been often associated with the up-regulation of uncoupling proteins (UCPs). Here we addressed the effects of a CLA-supplemented murine diet (∼2 % CLA mixture, cis-9, trans-10 and trans-10, cis-12 isomers; 45 % of each isomer on alternating days) on mitochondrial energetics, UCP2 expression/activity in the liver and other associated morphological and functional parameters, in C57BL/6 mice. Diet supplementation with CLA reduced both lipid accumulation in adipose tissues and triacylglycerol plasma levels, but did not augment hepatic lipid storage. Livers of mice fed a diet supplemented with CLA showed high UCP2 mRNA levels and the isolated hepatic mitochondria showed indications of UCP activity: in the presence of guanosine diphosphate, the higher stimulation of respiration promoted by linoleic acid in mitochondria from the CLA mice was almost completely reduced to the level of the stimulation from the control mice. Despite the increased generation of reactive oxygen species through oxi-reduction reactions involving NAD+/NADH in the Krebs cycle, no oxidative stress was observed in the liver. In addition, in the absence of free fatty acids, basal respiration rates and the phosphorylating efficiency of mitochondria were preserved. These results indicate a beneficial and secure dose of CLA for diet supplementation in mice, which induces UCP2 overexpression and UCP activity in mitochondria while preserving the lipid composition and redox state of the liver. © Springer Science+Business Media, LLC 2012.445587596Alberici, L.C., Oliveira, H.C., Patrício, P.R., Kowaltowski, A.J., Vercesi, A.E., Hyperlipidemic mice present enhanced catabolism and higher mitochondrial ATP-sensitive K+channel activity (2006) Gastroenterology, 131, pp. 1228-1234Alberici, R.M., Simas, R.C., Sanvido, G.B., Romão, W., Lalli, P.M., Benassi, M., Ambient mass spectrometry: Bringing MS into the real world (2010) Anal Bioanal Chem, 398, pp. 265-294Alberici, L.C., Oliveira, H.C., Catharino, R.R., Vercesi, A.E., Eberlin, M.N., Alberici, R.M., Distinct hepatic lipid profile of hypertriglyceridemic mice determined by easy ambient sonic-spray ionization mass spectrometry (2011) Anal Bioanal Chem, 401, pp. 1651-1659Azain, M.J., Hausman, D.B., Sisk, M.B., Flatt, W.P., Jewell, D.E., Dietary conjugated linoleic acid reduces rat adipose tissue cell size rather than cell number (2000) J Nutr, 130, pp. 1548-1554Banni, S., Carta, G., Angioni, E., Murru, E., Scanu, P., Melis, M.P., Distribution of conjugated linoleic acid and metabolites in different lipid fractions in the rat liver (2001) J Lipid Res, 42, pp. 1056-1061Bligh, E.G., Dyer, W.J., A rapid method of total lipid extraction and purification (1959) Can J Biochem Physiol, 37, pp. 911-917Buege, J.A., Aust, S.D., Microsomal lipid peroxidation (1978) Methods Enzymol, 52, pp. 302-310Cherian, G., Holsonbake, T.B., Goeger, M.P., Bildfell, R., Dietary CLA alters yolk and tissue FA composition and hepatic histopathology of laying hens (2002) Lipids, 37, pp. 751-757Choi, J.S., Koh, I.U., Jung, M.H., Song, J., Effects of three different conjugated linoleic acid preparations on insulin signalling, fat oxidation and mitochondrial function in rats fed a high-fat diet (2007) Br J Nutr, 98, pp. 264-275DeLany, J.P., West, D.B., Changes in body composition with conjugated linoleic acid (2000) J Am Coll Nutr, 19, pp. 487S-493SEaley, K.N., El-Sohemy, A., Archer, M.C., Effects of dietary conjugated linoleic acid on the expression of uncoupling proteins in mice and rats (2002) Lipids, 37, pp. 853-861Echtay, K.S., Murphy, M.P., Smith, R.A., Talbot, D.A., Brand, M.D., Superoxide activates mitochondrial uncoupling protein 2 from the matrix side. Studies using targeted antioxidants (2002) J Biol Chem, 277, pp. 47129-47135Echtay, K.S., Roussel, D., St-Pierre, J., Jekabsons, M.B., Cadenas, S., Stuart, J.A., Harper, J.A., Brand, M.D., Superoxide activates mitochondrial uncoupling proteins (2002) Nature, 415, pp. 96-99Fruchart, J.C., Duriez, P., Staels, B., Peroxisome proliferatoractivated receptor-alpha activators regulate genes governing lipoprotein metabolism, vascular inflammation and atherosclerosis (1999) Curr Opin Lipidol, 10, pp. 245-257Garcia-Ruiz, C., Colell, A., Mari, M., Morales, A., Fernandez-Checa, J.C., Direct effect of ceramide on the mitochondrial electron transport chain leads to generation of reactive oxygen species. Role of mitochondrial glutathione (1997) J Biol Chem, 272, pp. 11369-11377Garlid, K.D., Jabůrek, M., Jezek, P., Varecha, M., How do uncoupling proteins uncouple? (2000) Biochim Biophys Acta, 1459, pp. 383-389Gavino, V.C., Gavino, G., Leblanc, M.J., Tuchweber, B., An isomeric mixture of conjugated linoleic acids but not pure cis-9, trans-11-octadecadienoic acid affects body weight gain and plasma lipids in hamsters (2000) J Nutr, 130, pp. 27-29Gholam, P.M., Flancbaum, L., Machan, J.T., Charney, D.A., Kotler, D.P., Nonalcoholic fatty liver disease in severely obese subjects (2007) Am J Gastroenterol, 102, pp. 399-408Griinari, J.M., Corl, B.A., Lacy, S.H., Chouinard, P.Y., Nurmela, K.V., Bauman, D.E., Conjugated linoleic acid is synthesized endogenously in lactating dairy cows by Delta (9)-desaturase (2000) J Nutr, 130, pp. 2285-2291Haddad, R., Sparrapan, R., Eberlin, M.N., Desorption sonic spray ionization for (high) voltage-free ambient mass spectrometry (2006) Rapid Commun Mass Spectrom, 20, pp. 2901-2905Haddad, R., Sparrapan, R., Kotiaho, T., Eberlin, M.N., Easy ambient sonic-spray ionization-membrane interface mass spectrometry for direct analysis of solution constituents (2008) Anal Chem, 80, pp. 898-903Halade, G.V., Rahman, M.M., Fernandes, G., Effect of CLA isomers and their mixture on aging C57Bl/6J mice (2009) Eur J Nutr, 48, pp. 409-418Hissin, P.J., Hilf, R., A fluorometric method for determination of oxidized and reduced glutathione in tissues (1976) Anal Biochem, 74, pp. 214-226Jaudszus, A., Moeckel, P., Hamelmann, E., Jahreis, G., Trans-10, cis-12-CLA-caused lipodystrophy is associated with profound changes of fatty acid profiles of liver, white adipose tissue and erythrocytes in mice: Possible link to tissue-specific alterations of fatty acid desaturation (2010) Ann Nutr Metab, 57, pp. 103-111Jezek, P., Garlid, K.D., Mammalian mitochondrial uncoupling proteins (1998) Int J Biochem Cell Biol, 30, pp. 1163-1168Kennedy, A., Martinez, K., Schmidt, S., Mandrup, S., LaPoint, K., McIntosh, M., Antiobesity mechanisms of action of conjugated linoleic acid (2010) J Nutr Biochem, 21, pp. 171-179Konig, B., Spielmann, J., Haase, K., Brandsch, C., Kluge, H., Stangl, G.I., Effects offish oil and conjugated linoleic acids on expression of target genes of PPAR alpha and sterol regulatory elementbinding proteins in the liver of laying hens (2008) Br J Nutr, 100, pp. 355-363Kritchevsky, D., Tepper, S.A., Wright, S., Tso, P., Czarnecki, S.K., Influence of conjugated linoleic acid (CLA) on establishment and progression of atherosclerosis in rabbits (2000) J Am Coll Nutr, 19, pp. 472S-477SLin, H., Boylston, T.D., Chang, M.J., Luedecke, L.O., Shultz, T.D., Survey of the conjugated linoleic acid contents of dairy products (1995) J Dairy Sci, 78, pp. 2358-2365Moya-Camarena, S.Y., Heuvel, J.P.V., Blanchard, S.G., Leesnitzer, L.A., Belury, M.A., Conjugated linoleic acid is a potent naturally occurring ligand and activator of PPARalpha (1999) J Lipid Res, 40, pp. 1426-1433Nicholls, D.G., The bioenergetics of brown adipose tissue mitochondria (1976) FEBS Lett, 61, pp. 103-110Ohnuki, K., Haramizu, S., Ishihara, K., Fushiki, T., Increased energy metabolism and suppressed body fat accumulation in mice by a low concentration of conjugated linoleic acid (2001) Biosci Biotechnol Biochem, 65, pp. 2200-2204Ohnuki, K., Haramizu, S., Oki, K., Ishihara, K., Fushiki, T., A single oral administration of conjugated linoleic acid enhanced energy metabolism in mice (2001) Lipids, 36, pp. 583-587Ostrowska, E., Muralitharan, M., Cross, R.F., Bauman, D.E., Dunshea, F.R., Dietary conjugated linoleic acids increase lean tissue and decrease fat deposition in growing pigs (1999) J Nutr, 129, pp. 2037-2042Park, Y., Albright, K.J., Liu, W., Storkson, J.M., Cook, M.E., Pariza, M.W., Effect of conjugated linoleic acid on body composition in mice (1997) Lipids, 32, pp. 853-858Peters, J.M., Park, Y., Gonzalez, F.J., Pariza, M.W., Influence of conjugated linoleic acid on body composition and target gene expression in peroxisome proliferator-activated receptor alphanull mice (2001) Biochim Biophys Acta, 1533, pp. 233-242Rahman, M.M., Bhattacharya, A., Banu, J., Fernandes, G., Conjugated linoleic acid protects against age-associated bone loss in C57BL/6 female mice (2007) J Nutr Biochem, 18, pp. 467-474Rakhshandehroo, M., Hooiveld, G., Müller, M., Kersten, S., Comparative analysis of gene regulation by the transcription factor PPARalpha between mouse and human (2009) PLoS One, 4, pp. e6796Reznick, A.Z., Packer, L., Oxidative damage to proteins: Spectrophotometric method for the carbonyl assay (1994) Methods Enzymol, 233, pp. 357-363Ribot, J., Portillo, M.P., Picó, C., Macarulla, M.T., Palou, A., Effects of trans-10, cis-12 conjugated linoleic acid on the expression of uncoupling proteins in hamsters fed an atherogenic diet (2007) Br J Nutr, 97, pp. 1074-1082Roche, H.M., Noone, E., Sewter, C., Mc, B.S., Savage, D., Gibney, M.J., O'Rahilly, S., Vidal-Puig, A.J., Isomer-dependent metabolic effects of conjugated linoleic acid: Insights from molecular markers sterol regulatory element-binding protein-1c and LXRalpha (2002) Diabetes, 51, pp. 2037-2044Ryder, J.W., Portocarrero, C.P., Song, X.M., Cui, L., Yu, M., Combatsiaris, T., Galuska, D., Houseknecht, K.L., Isomer-specific antidiabetic properties of conjugated linoleic acid. Improved glucose tolerance, skeletal muscle insulin action, and UCP-2 gene expression (2001) Diabetes, 50, pp. 1149-1157Samec, S., Seydoux, J., Dulloo, A.G., Role of UCP homologues in skeletal muscles and brown adipose tissue: Mediators of thermogenesis or regulators of lipids as fuel substrate? (1998) FASEB J, 12, pp. 715-724Schild, L., Reinheckel, T., Wiswedel, I., Augustin, W., Short-term impairment of energy production in isolated rat liver mitochondria by hypoxia/reoxygenation: Involvement of oxidative protein modification (1997) Biochem J, 15, pp. 205-210Schönfeld, P., Wojtczak, L., Fatty acids as modulators of the cellular production of reactive oxygen species (2008) Free Radic Biol Med, 45, pp. 231-241Schoonjans, K., Staels, B., Auwerx, J., Role of the peroxisome proliferator-activated receptor (PPAR) in mediating the effects of fibrates and fatty acids on gene expression (1996) J Lipid Res, 37, pp. 907-925Semighini, C.P., Marins, M., Goldman, M.H.S., Goldman, G.H., Quantitative analysis of the relative transcript levels of ABC transporter Atr genes in Aspergillus nidulans by real-time reverse transcripition-PCR assay (2002) Appl Environ Microbiol, 68, pp. 1351-1357Simas, R.C., Catharino, R.R., Cunha, I.B.S., Cabral, E.C., Barrera-Arellano, D., Eberlin, M.N., Instantaneous characterization of vegetable oils via TAG and FFA profiles by easy ambient sonicspray ionization mass spectrometry (2010) Analyst, 135, pp. 735-744Takahashi, Y., Kushiro, M., Shinohara, K., Ide, T., Dietary conjugated linoleic acid reduces body fat mass and affects gene expression of proteins regulating energy metabolism in mice (2002) Comp Biochem Physiol B Biochem Mol Biol, 133, pp. 395-404Terpstra, A.H., Effect of conjugated linoleic acid on body composition and plasma lipids in humans: An overview of the literature (2004) Am J Clin Nutr, 79, pp. 352-361Tsuboyama-Kasaoka, N., Takahashi, M., Tanemura, K., Kim, H.J., Tange, T., Okuyama, H., Conjugated linoleic acid supplementation reduces adipose tissue by apoptosis and develops lipodystrophy in mice (2000) Diabetes, 49, pp. 1534-1542Tsuboyama-Kasaoka, N., Miyazaki, H., Kasaoka, S., Ezaki, O., Increasing the amount of fat in a conjugated linoleic acid-supplemented diet reduces lipodystrophy in mice (2003) J Nutr, 133, pp. 1793-1799Wang, Y.W., Jones, P.J., Conjugated linoleic acid and obesity control: Efficacy and mechanisms (2004) Int J Obes Relat Metab Disord, 28, pp. 941-955West, D.B., Delany, J.P., Camet, P.M., Blohm, F., Truett, A.A., Scimeca, J., Effects of conjugated linoleic acid on body fat and energy metabolism in the mouse (1998) Am J Physiol, 275, pp. R667-R672West, D.B., Blohm, F.Y., Truett, A.A., DeLany, J.P., Conjugated linoleic acid persistently increases total energy expenditure in AKR/J mice without increasing uncoupling protein gene expression (2000) J Nutr, 130, pp. 2471-2477World Health Organization, Programmes and Projects, Nutrition Topics, Controlling the Global Obesity Epidemic, , http://www.who.int/nutrition/topics/obesity/en, Accessed April 5, 2012Zhou, M., Diwu, Z., Panchuk-Voloshina, N., Haugland, R.P., A stable nonfluorescent derivative of resorufin for the fluorometric determination of trace hydrogen peroxide: Applications in detecting the activity of phagocyte NADPH oxidase and other oxidases (1997) Anal Biochem, 15, pp. 162-16

Galignani's messenger

17 août 18931893/08/17 (N24813)

Galignani's messenger

25 juillet 18931893/07/25 (N24790)