185 research outputs found

    Transport af farligt gods

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    Formålet med projektet er at belyse risiko og konsekvenser ved vej- og jernbanetransport af farligt gods. Til denne brug er der udviklet modeller for uheldsfrekvenser , udslipssandsynligheder og konsekvenser for mennesker og miljø. De enkelte modeller er implementeret i et geografisk informationssystem (GIS)

    Fleshy Fruits in Liliflorous Monocots

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    Fleshy fruits occur in several monocot orders and families, and it is generally assumed that they have been derived from capsular fruits many times during the evolution of monocot lineages. Huber hypothesized in 1969 that most capsules in Asparagales are derived secondarily from berries and that this transformation was correlated with the evolution of phytomelan-coated seeds, a pivotal character in his circumscription of Asparagales as part of reclassifying Liliaceae s.l. Dahlgren and co-workers suggested several parallel derivations and reversals in this character, e.g., the transformation sequence trifollicular fruits → capsules → berries→ capsules→ berries. Mapping of fleshy fruits on a phylogeny based on molecular characters indicates that Asparagales do not have fleshy fruits as a basal character. Dahlgren\u27s cyclic character evolution hypothesis is not supported by the distribution of dry and fleshy fruits, and there is no obvious correlation between baccate fruits and phytomelaniferous seeds in Asparagales. Phytomelaniferous seeds are not an evident synapomorphy of Asparagales as presently circumscribed. The anatomy and development of different capsular and baccate fruits in selected genera are studied in an ongoing project to reveal homologies and establish an adequate fruit typology. Some observations of texture and dehiscence structures in dry and fleshy capsules and in typical berries from hypogynous and epigynous flowers are reported in this paper

    Risiko ved transport af farligt gods

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    Projektet ”Transport af farligt gods”, er næsten afsluttet. Slutrapporten publiceres i 1999. Den indeholder to risikomodeller for transporter af farligt gods: en model for jernbanetrafik og en model for vejtrafik. Disse modeller angiver risikoen for udslip af forskellige størrelser ved givne transporter. Endvidere angives modeller for konsekvenserne af givne udslip, dels hu-mane konsekvenser i form af fN-kurver for dødsfald, dels miljøkonsekvenser i form af jord-og grundvandsforurening og i form af forurening af overfladevand. Modellerne indlægges i et GIS, som kan anskueliggøre konsekvensernes geografiske fordeling totalt eller vise forskelle ved forskelligt rutevalg for en given transport

    Circulating Glucagon 1-61 Regulates Blood Glucose by Increasing Insulin Secretion and Hepatic Glucose Production

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    Glucagon is secreted from pancreatic a cells, and hypersecretion (hyperglucagonemia) contributes to diabetic hyperglycemia. Molecular heterogeneity in hyperglucagonemia is poorly investigated. By screening human plasma using high-resolution-proteomics, we identified several glucagon variants, among which proglucagon 1-61 (PG 1-61) appears to be the most abundant form. PG 1-61 is secreted in subjects with obesity, both before and after gastric bypass surgery, with protein and fat as the main drivers for secretion before surgery, but glucose after. Studies in hepatocytes and in b cells demonstrated that PG 1-61 dose-dependently increases levels of cAMP, through the glucagon receptor, and increases insulin secretion and protein levels of enzymes regulating glycogenolysis and gluconeogenesis. In rats, PG 1-61 increases blood glucose and plasma insulin and decreases plasma levels of amino acids in vivo. We conclude that glucagon variants, such as PG 1-61, may contribute to glucose regulation by stimulating hepatic glucose production and insulin secretion

    Thyroid Function and Body Weight: A Community-Based Longitudinal Study

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    OBJECTIVE: Body weight and overt thyroid dysfunction are associated. Cross-sectional population-based studies have repeatedly found that thyroid hormone levels, even within the normal reference range, might be associated with body weight. However, for longitudinal data, the association is less clear. Thus, we tested the association between serum thyrotropin (TSH) and body weight in a community-based sample of adult persons followed for 11 years. METHODS: A random sample of 4,649 persons aged 18-65 years from a general population participated in the DanThyr study in 1997-8. We included 2,102 individuals who participated at 11-year follow-up, without current or former treatment for thyroid disease and with measurements of TSH and weight at both examinations. Multiple linear regression models were used, stratified by sex and adjusted for age, smoking status, and leisure time physical activity. RESULTS: Baseline TSH concentration was not associated with change in weight (women, P = 0.17; men, P = 0.72), and baseline body mass index (BMI) was not associated with change in TSH (women, P = 0.21; men, P = 0.85). Change in serum TSH and change in weight were significantly associated in both sexes. Weight increased by 0.3 kg (95% confidence interval [CI] 0.1, 0.4, P = 0.005) in women and 0.8 kg (95% CI 0.1, 1.4, P = 0.02) in men for every one unit TSH (mU/L) increase. CONCLUSIONS: TSH levels were not a determinant of future weight changes, and BMI was not a determinant for TSH changes, but an association between weight change and TSH change was present

    New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

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    Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes
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