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Copenhagen, Denmark

The University of Copenhagen is the oldest university and research institution in Denmark. Founded in 1479 as a studium generale, it is the second oldest institution for higher education in Scandinavia after Uppsala University . The university has 23,473 undergraduate students, 17,398 postgraduate students, 2,968 doctoral students and more than 9,000 employees. The university has four campuses located in and around Copenhagen, with the headquarters located in central Copenhagen. Most courses are taught in Danish; however, many courses are also offered in English and a few in German. The university has several thousands of foreign students, of whom about half come from Nordic countries.The university is a member of the prestigious International Alliance of Research Universities , along with University of Cambridge, University of Oxford, Yale University, The Australian National University, and UC Berkeley, amongst others. The Academic Ranking of World Universities, compiled by Shanghai Jiao Tong University, saw the University of Copenhagen as the leading university in Scandinavia and ranked 39th best university in the world in 2014. It is ranked 45th in the 2014 QS World University Rankings and 13th in Europe. Moreover, in 2013, according to the University Ranking by Academic Performance, the University of Copenhagen is the best university in Denmark and the 25th university in the world. The university has had 8 alumni become Nobel laureates and has produced one Turing Award recipient. Wikipedia.

The morbidity and mortality of patients with the chronic Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia, polycythemia vera, and primary myelofibrosis are mainly caused by cardiovascular diseases, thrombohemorrhagic complications, and bone marrow failure because of myelofibrosis and leukemic transformation. In the general population, chronic inflammation is considered of major importance for the development of atherosclerosis and cancer. MPNs are characterized by a state of chronic inflammation, which is proposed to be the common denominator for the development of "premature atherosclerosis," clonal evolution, and second cancer in patients with MPNs. Chronic inflammation may both initiate clonal evolution and catalyze its expansion from early disease stage to the myelofibrotic burnt-out phase. Furthermore, chronic inflammation may also add to the severity of cardiovascular disease burden by accelerating the development of atherosclerosis, which is well described and recognized in other chronic inflammatory diseases. A link between chronic inflammation, atherosclerosis, and second cancer in MPNs favors early intervention at the time of diagnosis (statins and interferon-α2), the aims being to dampen chronic inflammation and clonal evolution and thereby also diminish concurrent disease-mediated chronic inflammation and its consequences (accelerated atherosclerosis and second cancer). © 2012 by The American Society of Hematology. Source

Borregaard N.,Copenhagen University
Immunity | Year: 2010

Neutrophils are produced in the bone marrow from stem cells that proliferate and differentiate to mature neutrophils fully equipped with an armory of granules. These contain proteins that enable the neutrophil to deliver lethal hits against microorganisms, but also to cause great tissue damage. Neutrophils circulate in the blood as dormant cells. At sites of infection, endothelial cells capture bypassing neutrophils and guide them through the endothelial cell lining whereby the neutrophils are activated and tuned for the subsequent interaction with microbes. Once in tissues, neutrophils kill microorganisms by microbicidal agents liberated from granules or generated by metabolic activation. As a final act, neutrophils can extrude stands of DNA with bactericidal proteins attached that act as extracellular traps for microorganisms. © 2010 Elsevier Inc. Source

Couchman J.R.,Copenhagen University
Annual Review of Cell and Developmental Biology | Year: 2010

Virtually allmetazoan cells contain at least one and usually several types of transmembrane proteoglycans. These are varied in protein structure and type of polysaccharide, but the total number of vertebrate genes encoding transmembrane proteoglycan core proteins is less than 10. Some core proteins, including those of the syndecans, always possess covalently coupled glycosaminoglycans; others do not. Syndecan has a long evolutionary history, as it is present in invertebrates, but many other transmembrane proteoglycans are vertebrate inventions. The variety of proteins and their glycosaminoglycan chains is matched by diverse functions. However, all assume roles as coreceptors, often working alongside high-affinity growth factor receptors or adhesion receptors such as integrins. Other common themes are an ability to signal through their cytoplasmic domains, often to the actin cytoskeleton, and linkage to PDZ protein networks. Many transmembrane proteoglycans associate on the cell surface with metzincin proteases and can be shed by them. Work with model systems in vivo and in vitro reveals roles in growth, adhesion, migration, and metabolism. Furthermore, a wide range of phenotypes for the core proteins has been obtained in mouse knockout experiments. Here some of the latest developments in the field are examined in hopes of stimulating further interest in this fascinating group of molecules. Copyright © 2010 by Annual Reviews. All rights reserved. Source

Astrup A.,Copenhagen University
American Journal of Clinical Nutrition | Year: 2014

Dairy products contribute important nutrients to our diet, including energy, calcium, protein, and other micro- and macronutrients. However, dairy products can be high in saturated fats, and dietary guidelines generally recommend reducing the intake of saturated fatty acids (SFAs) to reduce coronary artery disease (CAD). Recent studies question the role of SFAs in cardiovascular disease (CVD) and have found that substitution of SFAs in the diet with omega-6 (n-6) polyunsaturated fatty acids abundant in vegetable oils can, in fact, lead to an increased risk of death from CAD and CVD, unless they are balanced with n-3 polyunsaturated fat. Replacing SFAs with carbohydrates with a high glycemic index is also associated with a higher risk of CAD. Paradoxically, observational studies indicate that the consumption of milk or dairy products is inversely related to incidence of CVD. The consumption of dairy products has been suggested to ameliorate characteristics of the metabolic syndrome, which encompasses a cluster of risk factors including dyslipidemia, insulin resistance, increased blood pressure, and abdominal obesity, which together markedly increase the risk of diabetes and CVD. Dairy products, such as cheese, do not exert the negative effects on blood lipids as predicted solely by the content of saturated fat. Calcium and other bioactive components may modify the effects on LDL cholesterol and triglycerides. Apart from supplying valuable dairy nutrients, yogurt may also exert beneficial probiotic effects. The consumption of yogurt, and other dairy products, in observational studies is associated with a reduced risk of weight gain and obesity as well as of CVD, and these findings are, in part, supported by randomized trials. © 2014 American Society for Nutrition. Source

In this study, we report the results from the largest cohort to date of newly diagnosed adult immune thrombocytopenia patients randomized to treatment with dexamethasone alone or in combination with rituximab. Eligible were patients with platelet counts ≤25×10(9)/L or ≤50×10(9)/L with bleeding symptoms. A total of 133 patients were randomly assigned to either dexamethasone 40 mg/day for 4 days (n = 71) or in combination with rituximab 375 mg/m(2) weekly for 4 weeks (n = 62). Patients were allowed supplemental dexamethasone every 1 to 4 weeks for up to 6 cycles. Our primary end point, sustained response (ie, platelets ≥50×10(9)/L) at 6 months follow-up, was reached in 58% of patients in the rituximab + dexamethasone group vs 37% in the dexamethasone group (P = .02). The median follow-up time was 922 days. We found longer time to relapse (P = .03) and longer time to rescue treatment (P = .007) in the rituximab + dexamethasone group. There was an increased incidence of grade 3 to 4 adverse events in the rituximab + dexamethasone group (P = .04). In conclusion, rituximab + dexamethasone induced higher response rates and longer time to relapse than dexamethasone alone. This study is registered at http://clinicaltrials.gov as NCT00909077. Source

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