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Introduction: The limited availability of fossil fuel sources, worldwide rising energy demands and anticipated climate changes attributed to an increase of greenhouse gasses are important driving forces for finding alternative energy sources. One approach to meeting the increasing energy demands and reduction of greenhouse gas emissions is by large-scale substitution of petrochemically derived transport fuels by the use of carbon dioxide-neutral biofuels, such as ethanol derived from lignocellulosic material., Results: This paper describes an integrated pilot-scale process where lime-treated wheat straw with a high dry-matter content (around 35% by weight) is converted to ethanol via simultaneous saccharification and fermentation by commercial hydrolytic enzymes and bakers' yeast (Saccharomyces cerevisiae). After 53 hours of incubation, an ethanol concentration of 21.4 g/liter was detected, corresponding to a 48% glucan-to-ethanol conversion of the theoretical maximum. The xylan fraction remained mostly in the soluble oligomeric form (52%) in the fermentation broth, probably due to the inability of this yeast to convert pentoses. A preliminary assessment of the distilled ethanol quality showed that it meets transportation ethanol fuel specifications. The distillation residue, which contained non-hydrolysable and non-fermentable (in)organic compounds, was divided into a liquid and solid fraction. The liquid fraction served as substrate for the production of biogas (methane), whereas the solid fraction functioned as fuel for thermal conversion (combustion), yielding thermal energy, which can be used for heat and power generation., Conclusion: Based on the achieved experimental values, 16.7 kg of pretreated wheat straw could be converted to 1.7 kg of ethanol, 1.1 kg of methane, 4.1 kg of carbon dioxide, around 3.4 kg of compost and 6.6 kg of lignin-rich residue. The higher heating value of the lignin-rich residue was 13.4 MJ thermal energy per kilogram (dry basis).

It is debated whether ecstasy use has neurotoxic effects on the human brain and what the effects are of a low dose of ecstasy use. We prospectively studied sustained effects (>2 weeks abstinence) of a low dose of ecstasy on the brain in ecstasy-naive volunteers using a combination of advanced MR techniques and self-report questionnaires on psychopathology as part of the NeXT (Netherlands XTC Toxicity) study. Outcomes of proton magnetic resonance spectroscopy (1H-MRS), diffusion tensor imaging (DTI), perfusion-weighted imaging (PWI), and questionnaires on depression, impulsivity, and sensation seeking were compared in 30 subjects (12M, 21.8+/-3.1 years) in two sessions before and after first ecstasy use (1.8+/-1.3 tablets). Interval between baseline and follow-up was on average 8.1+/-6.5 months and time between last ecstasy use and follow-up was 7.7+/-4.4 weeks. Using 1H-MRS, no significant changes were observed in metabolite concentrations of N-acetylaspartate (NAA), choline (Cho), myo-inositol (mI), and creatine (Cr), nor in ratios of NAA, Cho, and mI relative to Cr. However, ecstasy use was followed by a sustained 0.9% increase in fractional anisotropy (FA) in frontoparietal white matter, a 3.4% decrease in apparent diffusion (ADC) in the thalamus and a sustained decrease in relative regional cerebral blood volume (rrCBV) in the thalamus (-6.2%), dorsolateral frontal cortex (-4.0%), and superior parietal cortex (-3.0%) (all significant at p<0.05, paired t-tests). After correction for multiple comparisons, only the rrCBV decrease in the dorsolateral frontal cortex remained significant. We also observed increased impulsivity (+3.7% on the Barratt Impulsiveness Scale) and decreased depression (-28.0% on the Beck Depression Inventory) in novel ecstasy users, although effect sizes were limited and clinical relevance questionable. As no indications were found for structural neuronal damage with the currently used techniques, our data do not support the concern that incidental ecstasy use leads to extensive axonal damage. However, sustained decreases in rrCBV and ADC values may indicate that even low ecstasy doses can induce prolonged vasoconstriction in some brain areas, although it is not known whether this effect is permanent. Additional studies are needed to replicate these findings.