Enhancing synergies between European renewables and regional development policies

Renewable energy is key to decarbonising the European economy and mitigating climate change. For national and European Union policies to be successful, they need to be coherent and work together. We investigated whether EU regional development policies supported the deployment of renewable energy sources in a number of EU Member States. We find that regional policy is not well-aligned with the objective to extend renewables in the Czech Republic, Lithuania and Poland. There are inconsistencies between the two policies including: mismatches in renewables targets and respective cohesion policy allocations; mismatches in operationalization across energy and cohesion policies; insufficiently clear description of the relevance of EU Structural and Cohesion Funds in the National Renewable Energy Action Plans (NREAP); and a mismatch between the existing rhetorical commitment for integrating markets and grids, and substantial allocations in EU regional funds. These mismatches may impede the effective use of regional funding to support renewable energy sources

Delayed Gastric Emptying in Patients with Prader Willi Syndrome

Background: A 15 year old girl with Prader-Willi Syndrome (PWS) died of gastric rupture. Systematic literature research revealed seven case reports of PWS patients with acute gastric dilatation, two had a lethal course. The objective of this study was to determine if delayed gastric emptying in PWS patients might contribute to gastric dilatation. Methods: Gastric emptying was measured in eight patients with PWS by nucleotid scintigraphy after a standardized test meal. Results: Median age was 17.8 years (range 10.1-19.5). Median BMI of the male patients was 29.5 (range 18.4-34.8), of the female patients 28 (range 20.0-44.8). Half time of gastric emptying was delayed in five of the eight patients (median 78.5 minutes, range 59-134). Conclusion: Scintigraphic measurement of gastric emptying in eight PWS patients revealed delay in comparison to normal values. This might be a risk factor for gastric dilatation and rupture in patients with PW

Molecular evolution of the vesicle coat component βCOP in Toxoplasma gondii

Author Posting. © The Author(s), 2007. This is the author's version of the work. It is posted here by permission of Elsevier for personal use, not for redistribution. The definitive version was published in Molecular Phylogenetics and Evolution 44 (2007): 1284-1294, doi:10.1016/j.ympev.2007.02.031.Coatomer coated (COPI) vesicles play a pivotal role for multiple membrane trafficking steps throughout the eukaryotic cell. Our focus is on βCOP, one of the most well known components of the COPI multi-protein complex. Amino acid differences in βCOP may dictate functional divergence across species during the course of evolution, especially with regards to the evolutionary pressures on obligate intracellular parasites. A bioinformatic analysis of βCOP amino acid sequences was conducted for 49 eukaryotic species. Cloning and sequence analysis of the Toxoplasma gondii βCOP homologue revealed several amino acid insertions unique to T. gondii and one C-terminal insertion that is unique to apicomplexan parasites. These findings led us to investigate the possibility that βCOP experienced functional divergence during the course of its evolution. Bayesian phylogenetic analysis revealed a tree consistent with pan eukaryote distribution and long-branch lengths were observed among the apicomplexans. Further analysis revealed that kinetoplast βCOP underwent the most amount of change, leading to perhaps an overall change of function. In comparison, T. gondii exhibited subtle yet specific amino acid changes. The amino acid substitutions did not occur in the same places as other lineages, suggesting that TgβCOP has a role specific to the apicomplexans. Our work identifies forty-eight residues that are likely to be functionally important when comparing apicomplexan, kinetoplastid, and fungal βCOP.KMH is an Ellison Medical Foundation New Scholar in Infectious Disease; SLP was supported by an NIH training grant (NIH/NIAID/TMP T 32 7030); AGM was supported by the Marine Biological Laboratory’s Program in Global Infectious Diseases, also funded by the Ellison Medical Foundation

Decreased T cell reactivity to Epstein–Barr virus infected lymphoblastoid cell lines in multiple sclerosis

Objective: To investigate T cell and antibody immunity to Epstein-Barr virus (EBV) in multiple sclerosis (MS)

Prevalence and Predictors of Overweight and Insulin Resistance in Offspring of Mothers With Gestational Diabetes Mellitus

OBJECTIVE: Gestational diabetes mellitus (GDM) is associated with high birth weight in the offspring. This may lead to overweight and insulin resistance during childhood. The aim of the study was to assess the impact of GDM on overweight risk and insulin resistance in offspring. RESEARCH DESIGN AND METHODS: BMI measurements were collected at age 2, 8, and 11 years from 232 offspring of mothers with GDM (OGDM) and compared with those from 757 offspring of mothers with type 1 diabetes (OT1D) and 431 offspring of nondiabetic mothers (ONDM) born between 1989 and 2000. Insulin resistance (homeostasis model assessment of insulin resistance [HOMA-IR]) was determined at age 8 and 11 years in 751 children (74 OGDM). Overweight was defined as BMI percentile >or=90; insulin resistance was defined by HOMA-IR. RESULTS: Overweight prevalence was increased in OGDM compared with OT1D and to ONDM throughout childhood (age 11 years 31.1, 15.8, and 15.5%; P = 0.005). Maternal obesity was an important predictor of overweight risk in children (age 11 years odds ratio 7.0 [95% CI 1.8-27.7]; P = 0.006); birth size and maternal smoking during pregnancy were inconsistently associated with and treatment of GDM during pregnancy did not affect overweight risk. HOMA-IR was increased in OGDM compared with offspring of ONDM mothers (P = 0.01, adjusted for sex and age) and was associated with the child's BMI (P = 0.004). CONCLUSIONS: Overweight and insulin resistance in children is increased in OGDM compared with OT1D or ONDM. The finding that overweight risk is associated mainly with maternal obesity suggests that familial predisposition contributes to childhood growth in these offspring

Direct Substrate Delivery into Mitochondrial-Fission Deficient Pancreatic Islets Rescues Insulin Secretion

In pancreatic beta cells, mitochondrial bioenergetics control glucose-stimulated insulin secretion (GSIS). Mitochondrial dynamics are generally associated with quality control, maintaining the functionality of bioenergetics. By acute pharmacological inhibition of mitochondrial fission protein Drp1, we here demonstrate that mitochondrial fission is necessary for GSIS in mouse and human islets. We confirm that genetic silencing of Drp1 increases mitochondrial proton leak in MIN6 cells. However, our comprehensive analysis of pancreatic islet bioenergetics reveals that Drp1 does not control insulin secretion via its effect on proton leak but instead via modulation of glucose-fuelled respiration. Notably, pyruvate fully rescues the impaired insulin secretion of fission-deficient beta cells, demonstrating that defective mitochondrial dynamics solely impact substrate supply upstream of oxidative phosphorylation. The present findings provide novel insights in how mitochondrial dysfunction may cause pancreatic beta cell failure. In addition, the results will stimulate new thinking in the intersecting fields of mitochondrial dynamics and bioenergetics, as treatment of defective dynamics in mitochondrial diseases appears to be possible by improving metabolism upstream of mitochondria

Primary Dietary Intervention Study to Reduce the Risk of Islet Autoimmunity in Children at Increased Risk for Type 1 Diabetes: The BABYDIET study

OBJECTIVE: To determine whether delaying the introduction of gluten in infants with a genetic risk of islet autoimmunity is feasible, safe, and may reduce the risk of type 1 diabetes-associated islet autoimmunity. RESEARCH DESIGN AND METHODS: A total of 150 infants with a first-degree family history of type 1 diabetes and a risk HLA genotype were randomly assigned to a first gluten exposure at age 6 months (control group) or 12 months (late-exposure group) and were followed 3 monthly until the age of 3 years and yearly thereafter for safety (for growth and autoantibodies to transglutaminase C [TGCAs]), islet autoantibodies to insulin, GAD, insulinoma-associated protein 2, and type 1 diabetes. RESULTS: Adherence to the dietary-intervention protocol was reported from 70% of families. During the first 3 years, weight and height were similar in children in the control and late-exposure groups, as was the probability of developing TGCAs (14 vs. 4%; P = 0.1). Eleven children in the control group and 13 children in the late-exposure group developed islet autoantibodies (3-year risk: 12 vs. 13%; P = 0.6). Seven children developed diabetes, including four in the late-exposure group. No significant differences were observed when children were analyzed as per protocol on the basis of the reported first gluten exposure of the children. CONCLUSIONS: Delaying gluten exposure until the age of 12 months is safe but does not substantially reduce the risk for islet autoimmunity in genetically at-risk children

The role of clathrin in post-golgi trafficking in toxoplasma gondii

Apicomplexan parasites are single eukaryotic cells with a highly polarised secretory system that contains unique secretory organelles (micronemes and rhoptries) that are required for host cell invasion. In contrast, the role of the endosomal system is poorly understood in these parasites. With many typical endocytic factors missing, we speculated that endocytosis depends exclusively on a clathrin-mediated mechanism. Intriguingly, in Toxoplasma gondii we were only able to observe the endogenous clathrin heavy chain 1 (CHC1) at the Golgi, but not at the parasite surface. For the functional characterisation of Toxoplasma gondii CHC1 we generated parasite mutants conditionally expressing the dominant negative clathrin Hub fragment and demonstrate that CHC1 is essential for vesicle formation at the trans-Golgi network. Consequently, the functional ablation of CHC1 results in Golgi aberrations, a block in the biogenesis of the unique secretory microneme and rhoptry organelles, and of the pellicle. However, we found no morphological evidence for clathrin mediating endocytosis in these parasites and speculate that they remodelled their vesicular trafficking system to adapt to an intracellular lifestyle