Bioethanol from Germinated Grains.

The most well-known way to produce bioethanol is by the enzymatic hydrolysis and fermentation of starch. In a new project “BioConcens” (2007) sponsored by DARCOF (DAnish Research Center for Organic Food and farming) one aim is to develop a combined ethanol and biogas production for use in organic farming using starch containing biomass. Natural enzymes from cereals will be used for hydrolysis of starch to glucose in accordance with technology in brewing technology. Commercial enzymes are often produced from gene-modified organisms and will therefore not be used in the suggested organic context or process. A preliminary study was performed in which grains of wheat, rye, and barley were germinated using traditional methods applied in malting for beer production. During malting the amylase enzymes present in the grain are activated (autoamylolytic effect). Three steps were applied in the malting process; steeping, germination, and drying of the grains. After malting the grains were milled and mixed with water to 13% DM, cooked at 57.5C for 2 hours (to activate the enzymes), and cooled to 30C before adding Bakers Yeast. The results of this study indicate that efficient hydrolysis of starch can be achieved by activation of autoamylolytic enzymes in cereal grains after a malting process. The ethanol yields obtained in the autoamylolytic hydrolysis was comparable (or slightly higher) to that of reference experiments using commercial enzymes (amylases). The highest ethanol yield was obtained with wheat (0.34 g/g DM grain), followed by barley (0.31 g/g DM grain), and rye (0.29 g/g DM grain)

Muscle fat content and abdominal adipose tissue distribution investigated by magnetic resonance spectroscopy and imaging in obese children and youths

The degree of fat deposition in muscle and its implications for obesity-related complications in children and youths are not well understood. One hundred and fifty-nine patients (mean age: 13.3 years; range: 6–20) with a body mass index (BMI) >90th percentile for age and sex were included. Muscle fat content (MFC) was measured in the psoas muscle by proton magnetic resonance spectroscopy. The patients were assigned to two groups: MFC <5% or ≥5%. Visceral adipose tissue volume (VAT) and subcutaneous adipose tissue volume (SAT) were measured by magnetic resonance imaging. The data were analysed to detect associations between MFC and BMI standard deviation scores, VAT and SAT, blood values, pubertal stages, and physical activity scores. The mean BMI standard deviation score (SDS) was 3.04 (range 1.32–5.02). The mean MFC was 8.9% (range 0.8–46.7), and 118 (74.2%) of 159 patients had an MFC ≥5%. Children with an MFC ≥5%, compared with children with an MFC <5%, had a higher BMI SDS (P=0.03), a higher VAT (P=0.04), and elevated intramyocellular lipid (IMCL) and extramyocellular lipid (EMCL) contents (both P<0.0001). SAT, SAT/VAT ratio, blood values, pubertal stages and physical activity scores did not differ between the two groups. Severely obese children and youths tend to have a high MFC, which is associated with elevated VAT, IMCL, and EMCL contents. An increased MFC may be associated with impaired metabolic processes, which may predispose these young people to obesity-related complications

Frontotemporal dementia caused by CHMP2B mutation is characterised by neuronal lysosomal storage pathology

Mutations in the charged multivesicular body protein 2B (CHMP2B) cause frontotemporal dementia (FTD). We report that mice which express FTD-causative mutant CHMP2B at physiological levels develop a novel lysosomal storage pathology characterised by large neuronal autofluorescent aggregates. The aggregates are an early and progressive pathology that occur at 3 months of age and increase in both size and number over time. These autofluorescent aggregates are not observed in mice expressing wild-type CHMP2B, or in non-transgenic controls, indicating that they are a specific pathology caused by mutant CHMP2B. Ultrastructural analysis and immuno- gold labelling confirmed that they are derived from the endolysosomal system. Consistent with these findings, CHMP2B mutation patient brains contain morphologically similar autofluorescent aggregates. These aggregates occur significantly more frequently in human CHMP2B mutation brain than in neurodegenerative disease or age-matched control brains. These data suggest that lysosomal storage pathology is the major neuronal pathology in FTD caused by CHMP2B mutation. Recent evidence suggests that two other genes associated with FTD, GRN and TMEM106B are important for lysosomal function. Our identification of lysosomal storage pathology in FTD caused by CHMP2B mutation now provides evidence that endolysosomal dysfunction is a major degenerative pathway in FTD