39 research outputs found

    Business development in renewable energy

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    This paper discusses how to foster development of renewable energy business. Factors that impede or enhance renewable energy in the EU 27 member states in the period 1998–2008 are analyzed. Nine factors are considered: population density, production output and energy sector output to indicate market conditions, public total expenditures, subsidies and environmental protection expenditures to indicate institutional conditions, R&D, share of students in population and venture capital to indicate firm’s resources. Scarce space for business development and vested energy interests are the main impediments. R&D and venture capital are main drivers. The US and EU support for R&D and venture capital in renewable energy are compared. The US support is larger and mainly based on R&D grants. It has generated large, innovative enterprises. The EU support is mainly based on price guarantees for renewable energy delivery to grid. It has generated many enterprises. Building capabilities through stakeholders’ networks in early phase of business development and clusters in the later phase is recommended

    Exploration of Shared Genetic Architecture Between Subcortical Brain Volumes and Anorexia Nervosa

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    In MRI scans of patients with anorexia nervosa (AN), reductions in brain volume are often apparent. However, it is unknown whether such brain abnormalities are influenced by genetic determinants that partially overlap with those underlying AN. Here, we used a battery of methods (LD score regression, genetic risk scores, sign test, SNP effect concordance analysis, and Mendelian randomization) to investigate the genetic covariation between subcortical brain volumes and risk for AN based on summary measures retrieved from genome-wide association studies of regional brain volumes (ENIGMA consortium, n = 13,170) and genetic risk for AN (PGC-ED consortium, n = 14,477). Genetic correlations ranged from − 0.10 to 0.23 (all p > 0.05). There were some signs of an inverse concordance between greater thalamus volume and risk for AN (permuted p = 0.009, 95% CI: [0.005, 0.017]). A genetic variant in the vicinity of ZW10, a gene involved in cell division, and neurotransmitter and immune system relevant genes, in particular DRD2, was significantly associated with AN only after conditioning on its association with caudate volume (pFDR = 0.025). Another genetic variant linked to LRRC4C, important in axonal and synaptic development, reached significance after conditioning on hippocampal volume (pFDR = 0.021). In this comprehensive set of analyses and based on the largest available sample sizes to date, there was weak evidence for associations between risk for AN and risk for abnormal subcortical brain volumes at a global level (that is, common variant genetic architecture), but suggestive evidence for effects of single genetic markers. Highly powered multimodal brain- and disorder-related genome-wide studies are needed to further dissect the shared genetic influences on brain structure and risk for AN

    Exploration of Shared Genetic Architecture Between Subcortical Brain Volumes and Anorexia Nervosa

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    Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect

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    Celiac disease is probably the best-understood immune-related disorder. The disease presents in the small intestine and results from the interplay between multiple genes and gluten, the triggering environmental factor(1). Although HLA class II genes explain 40% of the heritable risk, non-HLA genes accounting for most of the familial clustering have not yet been identified. Here we report significant and replicable association (P = 2.1 x 10(-6)) to a common variant located in intron 28 of the gene myosin IXB (MYO9B), which encodes an unconventional myosin molecule that has a role in actin remodeling of epithelial enterocytes(2,3). Individuals homozygous with respect to the at-risk allele have a 2.3-times higher risk of celiac disease ( P = 1.55 x 10(-5)). This result is suggestive of a primary impairment of the intestinal barrier in the etiology of celiac disease, which may explain why immunogenic gluten peptides are able to pass through the epithelial barrier
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