Danish Institute for Food and Veterinary Research

Copenhagen, Denmark

Danish Institute for Food and Veterinary Research

Copenhagen, Denmark
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Scapigliati G.,University of Tuscia | Buonocore F.,University of Tuscia | Randelli E.,University of Tuscia | Casani D.,University of Tuscia | And 19 more authors.
Fish and Shellfish Immunology | Year: 2010

Naïve sea bass juveniles (38.4 ± 4.5 g) were intramuscularly infected with a sublethal dose of betanodavirus isolate 378/I03, followed after 43 days by a similar boosting. This infection resulted in an overall mortality of 7.6%. At various intervals, sampling of fish tissues was performed to investigate: i) B and T lymphocyte content in organs and tissues; ii), proliferation of leucocytes re-stimulated in vitro with inactivated virus; iii) presence of serum antibody specific for betanodavirus; iv) expression of genes coding for the following immunoregulatory molecules involved in innate and acquired responses: type I IFN, Mx, IL-1, Cox-2; IL-10, TGF-β, TCRβ, CD4, CD8α, IgM, by using a quantitative PCR array system developed for sea bass. The obtained results showed a detectable increase of T cells and B cells in PBL during betanodavirus infection. Furthermore, leucocytes obtained from blood, head kidney, and gills showed a detectable "in vitro" increase in viability upon addition of inactivated viral particles, as determined by measuring intracellular ATP concentration. ELISA analysis of sera showed that exposure to nodavirus induced a low, but specific antibody titer measured 43 days after infection, despite the presence of measurable levels of natural antibody. Finally, a strong upregulation of genes coding for type I IFN, Mx, and IgM was identified after both infection and boosting. Interestingly, an upregulation of Cox-2 until boosting, and of TGF-β and IL-10 after boosting was also observed, while the other tested genes did not show any significant variations with respect to mock-treated fish. Overall, our work represents a first comprehensive analysis of cellular and molecular immune parameters in a fish species exposed to a pathogenic virus. © 2009 Elsevier Ltd. All rights reserved.


News Article | November 14, 2016
Site: news.europawire.eu

COPENHAGEN, 14-Nov-2016 — /EuropaWire/ — The Board of the University of Copenhagen has found the person to succeed Ralf Hemmingsen as leader of the university for the next five years. On 1 March 2017, the current Provost at the Technical University of Denmark, Henrik C. Wegener, will become Rector of the university. A total of 26 persons applied for the position. The University of Copenhagen’s new Rector knows about bacteria, infectious diseases – and about running a university. Henrik Wegener has a PhD in microbiology from the Royal Veterinary and Agricultural University, which merged with the University of Copenhagen in 2007. After his PhD degree he has, among other things, been Head of Research, Professor, Centre Director, Institute Director and, since 2011, Provost at the Technical University of Denmark in charge of research, research centres, collaboration agreements, international relations, etc. Henrik Wegener holds a Master of Public Administration and serves as one of the EU Commission’s top research advisers. “We’ve had a strong and broad field of applicants. The Board has chosen Henrik Wegener because he has both the professional and personal competences required, and because he has created excellent results throughout his career, both as a researcher and in leadership roles. Altogether, he has 18 years of leadership experience at all levels. He has been in charge of large-scale change processes, and is recognised for working through dialogue and involvement of the entire organisation, and for achieving the goals of the initiatives he launches. The University of Copenhagen will get a leader who has good knowledge of the university, but who also has an outsider’s new and refreshing view of the tasks ahead. And then he understands how a university can impact framework conditions for research as well as the importance of protecting the integrity of the university,” Nils Strandberg Pedersen says. Henrik Wegener is an internationally recognised researcher within food safety, antibiotic resistance and bacterial zoonoses, i.e. bacteria transferred from animals to humans. As a researcher he has been working with applied research at four sector research institutions: The Danish Veterinary Serum Institute, the Danish Zoonosis Centre, Denmark’s National Veterinary Institute and the Danish Institute for Food and Veterinary Research, all of which are now merged with the Technical University of Denmark. For a number of years he served as national expert to the World Health Organisation, WHO. As Provost at the Technical University of Denmark, he has had the overall responsibility for the university’s research activities.  In addition, he has extensive experience of collaboration with public and private sector players, nationally and internationally. “The University of Copenhagen is the most important university in Denmark. The university must continue to address society’s need for new knowledge and talented graduates. Quality of education and basic research at the highest international level should therefore still be top of the agenda. The university must be developed through a determined focus on high-level research, keen priorities, global recruitment of researchers as well as inspiring and demanding research-based teaching of an international standard. The same goes for the efforts to develop a professional and coherent administration in collaboration with staff and students. And then, of course, we will continue to focus on safeguarding the university’s external interests, and not least maintain our independence,” Henrik Wegener says.


Laurberg P.,Aarhus University Hospital | Cerqueira C.,Glostrup Hospital | Ovesen L.,Slagelse Hospital | Rasmussen L.B.,Danish Institute for Food and Veterinary Research | And 4 more authors.
Best Practice and Research: Clinical Endocrinology and Metabolism | Year: 2010

Depending on the availability of iodine, the thyroid gland is able to enhance or limit the use of iodine for thyroid hormone production. When compensation fails, as in severely iodine-deficient populations, hypothyroidism and developmental brain damage will be the dominating disorders. This is, out of all comparison, the most serious association between disease and the level of iodine intake in a population. In less severe iodine deficiency, the normal thyroid gland is able to adapt and keep thyroid hormone production within the normal range. However, the prolonged thyroid hyperactivity associated with such adaptation leads to thyroid growth, and during follicular cell proliferation there is a tendency to mutations leading to multifocal autonomous growth and function. In populations with mild and moderate iodine deficiency, such multifocal autonomous thyroid function is a common cause of hyperthyroidism in elderly people, and the prevalence of thyroid enlargement and nodularity is high. The average serum TSH tends to decrease with age in such populations caused by the high frequency of autonomous thyroid hormone production. On the other hand, epidemiological studies have shown that hypothyroidism is more prevalent in populations with a high iodine intake. Probably, this is also a complication to thyroid adaptation to iodine intake. Many thyroid processes are inhibited when iodine intake becomes high, and the frequency of apoptosis of follicular cells becomes higher. Abnormal inhibition of thyroid function by high levels of iodine is especially common in people affected by thyroid autoimmunity (Hashimoto's thyroiditis). In populations with high iodine intake, the average serum thyroid-stimulating hormone (TSH) tends to increase with age. This phenomenon is especially pronounced in Caucasian populations with a genetically determined high tendency to thyroid autoimmunity. A small tendency to higher serum TSH may be observed already when iodine intake is brought from mildly deficient to adequate, but there is at present no evidence that slightly elevated serum TSH in elderly people leads to an increase in morbidity and mortality. Conclusion: Even minor differences in iodine intake between populations are associated with differences in the occurrence of thyroid disorders. Both iodine intake levels below and above the recommended interval are associated with an increase in the risk of disease in the population. Optimally, iodine intake of a population should be kept within a relatively narrow interval where iodine deficiency disorders are prevented, but not higher. Monitoring and adjusting of iodine intake in a population is an important part of preventive medicine. © 2009 Elsevier Ltd. All rights reserved.


Elguindi J.,University of Arizona | Moffitt S.,University of Arizona | Hasman H.,Danish Institute for Food and Veterinary Research | Andrade C.,University of Arizona | And 2 more authors.
Applied Microbiology and Biotechnology | Year: 2011

The rapid killing of various bacteria in contact with metallic copper is thought to be influenced by the influx of copper ions into the cells, but the exact mechanism is not fully understood. This study showed that the kinetics of contact killing of copper surfaces depended greatly on the amount of moisture present, copper content of alloys, type of medium used, and type of bacteria. We examined antibiotic- and copper ion-resistant strains of Escherichia coli and Enterococcus faecium isolated from pig farms following the use of copper sulfate as feed supplement. The results showed rapid killing of both copper ion-resistant E. coli and E. faecium strains when samples in rich medium were spread in a thin, moist layer on copper alloys with 85% or greater copper content. E. coli strains were rapidly killed under dry conditions, while E. faecium strains were less affected. Electroplated copper surface corrosion rates were determined from electrochemical polarization tests using the Stern-Geary method and revealed decreased corrosion rates with benzotriazole and thermal oxide coating. Copper ion-resistant E. coli and E. faecium cells suspended in 0.8% NaCl showed prolonged survival rates on electroplated copper surfaces with benzotriazole coating and thermal oxide coating compared to surfaces without anti-corrosion treatment. Control of surface corrosion affected the level of copper ion influx into bacterial cells, which contributed directly to bacterial killing. © 2010 Springer-Verlag.


Biro E.,Semmelweis University | Kocsis K.,Semmelweis University | Nagy N.,Semmelweis University | Molnar D.,Semmelweis University | And 3 more authors.
Avian Pathology | Year: 2011

The effects of infectious bursal disease virus (IBDV) (strain F52/70) infection were studied by immunohistochemical methods on the splenic extracellular matrix (ECM). The major fibrillar components of the ECM, the type I and type III collagens and the main ECM organizing glycoproteins (laminin, tenascin and fibronectin) were monitored up to 11 days post-infection (d.p.i.). By 3 d.p.i., the collagens that form the basic scaffold of the antigen-trapping region of the spleen are destroyed, which is followed by deterioration of the glycoproteins. The ECM in the red pulp and the other regions of the white pulp (periarteriolar lymphatic sheath and germinal centre) seem to be normal. The reason for the significantly different pathological alterations in the ECM between the two regions of the spleen may be explained by the origin of the reticular cells. The reticular cells in the antigen-trapping zone and other splenic regions are of haemopoietic and mesenchymal origins, respectively. Possibly, the reticular cells of the haemopoietic origin are more susceptible for the IBDV infection than the mesenchymal ones. Development of the antigentrapping, B-cell-dependent zone of the splenic white pulp precedes that of the periarteriolar lymphatic sheath and germinal centre, which suggests that this region may contribute to B-cell maturation. Damage of the ECM in the antigen-trapping zones results in impairment of tissue organization, which may contribute to the permanent immunosuppression. © 2011 Houghton Trust Ltd.

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