A two-stage thermophilic anaerobic digestion process for the concurrent production of hydrogen and methane through the treatment of the source-sorted organic fraction of municipal solid waste was carried out over a long-term pilot scale experience. Two continuously stirred tank reactors were operated for about 1 year. The results showed that stable production of bio-hythane without inoculum treatment could be obtained. The pH of the dark fermentation reactor was maintained in the optimal range for hydrogen-producing bacteria activity through sludge recirculation from a methanogenic reactor. An average specific bio-hythane production of 0.65 m(3) per kg of volatile solids fed was achieved when the recirculation flow was controlled through an evaporation unit in order to avoid inhibition problems for both microbial communities. Microbial analysis indicated that dominant bacterial species in the dark fermentation reactor are related to the Lactobacillus family, while the population of the methanogenic reactor was mainly composed of Defluviitoga tunisiensis. The archaeal community of the methanogenic reactor shifted, moving from Methanothermobacter-like to Methanobacteriales and Methanosarcinales, the latter found also in the dark fermentation reactor when a considerable methane production was detected.
BackgroundMutations in the PARK2 gene encoding the protein parkin cause autosomal recessive juvenile parkinsonism (ARJP), a neurodegenerative disease characterized by dysfunction and death of dopamine (DA) neurons in the substantia nigra pars compacta. Since a neuroprotective therapy for ARJP does not exist, research efforts aimed at discovering potential targets for neuroprotection are critically needed.A previous study demonstrated that loss of parkin function or expression of parkin mutants associated with ARJP causesan accumulation of glutamate kainate receptors (KARs) in human brain tissues and an increase of KAR-mediated currents in neuronsin vitro. MethodsBased on the hypothesisthat such KAR hyper-activation may contribute to the death of nigralDA neurons, we investigated the effect of KAR antagonism on the DA neuron dysfunction and death that occur in the parkinQ311X mouse, a model of human parkin-induced toxicity. ResultsWe found that early accumulation of KARs occurs in the DA neurons of the parkinQ311X mouse model and that chronic administration of the KAR antagonist UBP310 prevents DA neuron loss. This neuroprotective effect was associated with rescue of the abnormal firing rate of nigral DA neurons and downregulation of GluK2, the key KAR subunit. ConclusionsThis study provides novel evidence ofa causal role of glutamate KARs in the DA neuron dysfunction and loss occurring in a mouse model of human parkin-induced toxicity. Our results support KAR as a potential target in the development of a neuroprotective therapy for ARJP.
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