Insecticidal activity of the essential oils (EOs) isolated from Tagetes lucida, Lippia alba, Lippia origanoides, Eucalyptus citriodora, Cymbopogon citratus, Cymbopogon flexuosus, Citrus sinensis, Swinglea glutinosa, and Cananga odorata aromatic plants, grown in Colombia (Bucaramanga, Santander), and of a mixture of L. alba and L. origanoides EOs were evaluated on Aedes (Stegomyia) aegypti Rockefeller larvae. The EOs were extracted by microwave-assisted hydrodistillation and characterized by gas chromatography-mass spectrometry (GC-MS). The main components of the EOs were identified using their linear retention indices and mass spectra. The lethal concentrations (LCs) of the EOs were determined between the third and fourth instar of A. aegypti. LC50 was determined by probit analysis using mortality rates of bioassays. All essential oils tested showed insecticidal activity. The following values were obtained for C. flexuosus (LC50 = 17.1 ppm); C. sinensis (LC50 = 20.6 ppm); the mixture of L. alba and L. origanoides (LC50 = 40.1 ppm); L. alba (LC50 = 42.2 ppm); C. odorata (LC50 = 52.9 ppm); L. origanoides (LC50 = 53.3 ppm); S. glutinosa (LC50 = 65.7 ppm); T. lucida (LC50 = 66.2 ppm); E. citriodora (LC50 = 71.2 ppm); and C. citratus (LC50 = 123.3 ppm). The EO from C. flexuosus, with citral (geranial + neral) as main component, showed the highest larvicidal activity.

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A vicious cycle between oxidation and inflammation leads to complications in a growing number of disease states. Knowledge on tissue distribution of chemokines, mediators of inflammatory response, and paraoxonases, with antioxidant and anti-inflammatory actions, may be relevant. Using immunohistochemistry and quantitative real-time PCR we have investigated the distribution of PON1, 2 and 3, CCL2, 7, 8 and 12 and the chemokine receptor CCR2 protein and mRNA in 23 tissues from C57BL/6J mice. As expected, PON1, 2 and 3, CCL2, 7, 8 and 12 and CCR2 proteins were present in the vast majority of tissues investigated. Surprisingly, mRNA for these proteins was also expressed in most of these tissues suggesting local production and the ability to respond in situ to inflammatory stimuli. The wide distribution and expression of mRNA for paraoxonases and CC-chemokines suggest a systemic, probably coordinated, role in the overall inflammatory response.

BackgroundFatty acid synthase (FASN) is an enzyme synthesized by the liver and plays an important role in lipogenesis. The present study aimed to investigate whether serum FASN concentration may provide a direct link between HIV and/or HCV viral infections and lipid metabolic disorders commonly observed in HIV/HCV-infected patients.MethodsWe evaluated serum FASN concentration in 191 consecutive HIV-infected patients in the absence or presence of HCV co-infection. For comparison, 102 uninfected controls were included. Metabolic and inflammatory phenotype was also compared with respect to the presence of HCV co-infection.ResultsSerum FASN concentration was significantly higher in HIV-infected patients than in healthy participants and HCV co-infected patients showed higher levels than those without co-infection. Levels were also affected by treatment regimen, but marginally influenced by virological variables. Insulin concentration was the sole variable among metabolic parameters that demonstrated a significant correlation with serum FASN concentrations. Serum alanine aminotransferase (ALT) values correlated significantly with serum FASN concentration and provided the best discrimination with respect to the presence or absence of HCV co-infection. In multivariate analysis, only ALT, monocyte chemoattractant protein-1 (MCP-1) and the presence of antiretroviral treatment regimen significantly contributed to explain serum FASN concentration in HIV/HCV co-infected patients.ConclusionSerum FASN concentration is significantly increased in HIV-infected individuals. The release of FASN into the circulation is further enhanced in patients who are co-infected with HCV. Subsequent studies should explore the usefulness of this indicator to monitor the effect of viral infections on disease progression and survival.

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HIV infection itself may promote major changes in cholesterol distribution among HDL subpopulations that could be partially attenuated by current antiretroviral treatments. Further studies in larger populations are necessary to confirm the impact of HIV on lipoprotein composition and distribution.

Research on the molecular basis of the hepatic alterations associated to obesity is dependent on the availability of suitable animal models. Apolipoprotein E deficient mice (ApoE(-/-)) and LDL-receptor deficient mice (LDLr(-/-)) develop steatosis and steatohepatitis when given pro-atherogenic diets. However, previous data suggest that these two models are not completely interchangeable, and that their metabolic phenotype may partially differ in response to nutrient stimuli. The present study further investigates this question, by comparing changes in hepatic inflammation, lipoprotein metabolism, and their related gene expressions. LDLr(-/-) mice were more susceptible to the development of obesity and hepatic steatosis, while the ApoE(-/-) model increased the amount of macrophages and inflammatory nodules in the liver. These changes were accompanied by a differential expression of selected members of the MAPK family and PPARs in the liver.

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