Monitoring of a microbial community during bioaugmentation with hydrogenotrophic methanogens to improve methane yield of an anaerobic digestion process.

Methane production by microbial fermentation of municipal waste is a challenge for better yield processes. This work describes the characterization of a hydrogenotrophic methanogen microbial community used in a bioaugmentation procedure to improve the methane yield in a thermophilic anaerobic process, digesting the organic fraction of municipal solid waste. The performance of the bioaugmentation was assessed in terms of methane production and changes in the microbial community structure. The results showed that bioaugmentation slightly improved the cumulative methane yield (+ 4%) in comparison to the control, and its use led to an acceleration of the methanogenesis stage. We observed associated significant changes in the relative abundance of taxa and their interactions, using high throughput DNA sequencing of V3-16S rRNA gene libraries, where the abundance of the archaeal hydrogenotrophic genus Methanoculleus (class Methanomicrobia, phylum Euryarchaeota) and the bacterial order MBA08 (class Clostridia, phylum Firmicutes) were dominant. The relevant predicted metabolic pathways agreed with substrate degradation and the anaerobic methanogenic process. The purpose of the study was to evaluate the effect of the addition of hydrogenotrophic methanogens in the generation of methane, while treating organic waste through anaerobic digestion.

Seasonal and Spatial Variability of PM2.5 Concentration, and Associated Metal(loid) Content in the Toluca Valley, Mexico.

This study provides evidence of the seasonal and spatial variation of metal(lloid)s in particulate matter minor to 2.5 microns (PM2.5) in the Toluca Valley Metropolitan Area (TVMA), the fifth largest urban center in Mexico. Four sites were sampled between 2013 and 2014, which included urban and industrial areas, in the dry-cold (November-February) and dry-hot (March-May) seasons; PM2.5 was collected using high- and medium-volume samplers. Metal(lloid) concentrations in PM2.5 were analyzed using inductively coupled plasma‒mass spectrometry (ICP‒MS). The highest 24-hour PM2.5 concentration in the northern area was observed, and the PM2.5 concentrations were independent of the season. Five metal(lloid)s with a recovery percentage above 80% were considered to be reported (Co, Cr, Cu, Mn, and Sb). The maximum concentrations of metal(lloid)s were observed during the dry-cold season, and concentrations were up to one hundred or thousand fold with respect to the dry-hot season. The 24-hour PM2.5 and metal(lloid) concentrations exceeded national and international guidelines to protect population health.

pVHL suppresses Akt/ß-catenin-mediated cell proliferation by inhibiting 14-3-3ζ expression.

The mechanisms controlling degradation of cytosolic ß-catenin are important for regulating ß-catenin co-transcriptional activity. Loss of von Hippel-Lindau protein (pVHL) has been shown to stabilize ß-catenin, increasing ß-catenin transactivation and ß-catenin-mediated cell proliferation. However, the role of phosphoinositide 3-kinase (PI3K)/Akt in the regulation of ß-catenin signaling downstream from pVHL has never been addressed. Here, we report that hyperactivation of PI3K/Akt in cells lacking pVHL contributes to the stabilization and nuclear accumulation of active ß-catenin. PI3K/Akt hyperactivation is facilitated by the up-regulation of 14-3-3ζ and the down-regulation of 14-3-3ε, 14-3-3η and 14-3-3θ. Up-regulation of 14-3-3ζ in response to pVHL is important for the recruitment of PI3K to the cell membrane and for stabilization of soluble ß-catenin. In contrast, 14-3-3ε and 14-3-3η enhanced PI3K/Akt signaling by inhibiting PI3K and PDK1, respectively. Thus, our results demonstrated that 14-3-3 family members enhance PI3K/Akt/ß-catenin signaling in order to increase proliferation. Inhibition of Akt activation and/or 14-3-3 function strongly reduces ß-catenin signaling and decreases cell proliferation. Thus, inhibition of Akt and 14-3-3 function efficiently reduces cell proliferation in 786-0 cells characterized by hyperactivation of ß-catenin signaling due to pVHL loss.