Tolerance of a sulfidogenic sludge to trichloroethylene at microcosms level as a basis for a long-term operation of reactors designed for its biodegradation.

Trichloroethylene (TCE) is known as a toxic organic compound found as a pollutant in water streams around the world. The ultimate goal of the present work was to determine the TCE concentration that would be feasible to biodegrade on a long-term basis by a sulfidogenic sludge while maintaining sulfate reducing activity (SRA). Microcosms were prepared with sulfidogenic sludge obtained from a stabilized sulfidogenic UASB and amended with different TCE concentrations (100-300 µM) and two different proportions of volatile fatty acids (VFA) acetate, propionate and butyrate at COD of 2.5:1:1 and 1:1:1, respectively to evaluate the tolerance of the sludge. The overall results suggested that the continuous exposure of the microorganisms to TCE leads to inhibition of SRA; nonetheless, the SRA can be recovered after adequate supplementation of carbon sources and sulfate. The most suitable TCE concentration to operate on a long-term basis while preserving SRA was 26-35 mg L-1 (200-260 µM). A low level of expression of the mRNA of the sulfite reductase subunit alpha (dsrA) gene was obtained in the presence of the TCE and its intermediate products. This gene was associated to SRB belonging to the genera Desulfovibrio, Desulfosalsimonas, Desulfotomaculum, Desulfococcus, Desulfatiglans and Desulfomonas.

(-)-Epicatechin modulates the expression of myomiRs implicated in exercise response in mouse skeletal muscle.

The flavanol (-)-epicatechin has exercise-mimetic properties. Besides, several miRNAs play a role in modulating the adaptation of the muscle to different training protocols. However, notwithstanding all information, few studies aimed to determine if (-)-epicatechin can modify the expression of miRNAs related to skeletal muscle development and regeneration. Mice were treated for fifteen days by oral gavage with the flavanol (-)-epicatechin. After treatment, the quadriceps of the mice was dissected, and total RNA was extracted. The expression level of miR-133, -204, -206, -223, -486, and -491 was analyzed by qRT-PCR. We also used bioinformatic analysis to predict the participation of these miRNAs in different skeletal muscle signal transduction pathways. Additionally, we analyzed the level of the myogenic proteins MyoD and myogenin by Western blot and measured the cross-sectional area of muscle fibers stained with E&H. (-)-Epicatechin upregulated the expression of miR-133, -204, -206, -223, and -491 significantly, which was associated with an increase in the level of the myogenic proteins MyoD and Myogenin and an augment in the fiber size. The bioinformatics analysis showed that the studied miRNAs might participate in different signal transduction pathways related to muscle development and adaptation. Our results showed that (-)-epicatechin upregulated miRNAs that participate in skeletal exercise muscle adaptation, induced muscle hypertrophy, and increased the level of myogenic proteins MyoD and MyoG.

Identification of influenza A pandemic (H1N1) 2009 variants during the first 2009 influenza outbreak in Mexico City.

BACKGROUND: In March 2009, public health surveillance detected increased numbers of influenza-like illness presenting to hospitals in Mexico City. The aetiological agent was subsequently determined to be a novel influenza A (H1N1) triple reassortant, which has spread worldwide. As a consequence the World Health Organisation has declared the first Influenza pandemic of the 21st century. OBJECTIVES: To describe clinically and molecularly the first outbreak of influenza A pH1N1 (2009) during 1-5 May to establish a baseline of epidemiological data for pH1N1. Also, to monitor for the emergence of antiviral resistance, and mutations affecting virulence and transmissibility. STUDY DESIGN: Samples were collected from 751 patients with influenza-like symptoms throughout Mexico City and were tested for influenza A pH1N1 (2009) using real-time PCR. In the samples that were positive for influenza A pH1N1 (2009) fragments from the haemagglutinin (H1) and neuraminidase (N1) genes were sequenced. RESULTS: A total of 203/751 (27%) patients were positive for the pandemic H1N1 (2009) virus (53% male and 47% female). The 0-12-year-old group was the most affected 85/751 (42%). Sequence analysis showed five new variants of the pandemic H1N1 (2009) virus for NA: G249E (GQ292900), M269I (GQ292892), Y274H (GQ292913), T332A (GQ292933), N344K (GQ292882), and four variants for HA: N461K (GQ293006), K505R (GQ292989), I435V (GQ292995), I527N (GQ292997). CONCLUSIONS: We have provided a baseline of epidemiological data from the first outbreak of influenza A pH1N1 (2009) during 1-5 May in Mexico City. The sequencing of partial fragments of the HA and NA genes did not show the presence of previously described mutations affecting known sites of antiviral resistance in seasonal influenza A such as the H275Y (oseltamivir resistance), R293 or N295 etc.