Allgemein

2nd Research Workshop ›Technologies and Resources‹

We cordially invite all members of the University to join the 2nd Research Workshop
›Technologies and Resources‹ which will be held on September 29, 2017 from 14:00-19:00.

This event will take place in the CBBM building.

The aim of this workshop is to share technologies and resources to intensify collaboration and strenghten our university as an excellent centre of science and research.

Please send us an e-mail for registration at: jeanette.erdmann@uni-luebeck.de or marina.ladewig@uni-luebeck.de. We very welcome poster presentatios.

10 Years Anniversary – time to remember

Today, ten years ago, our most often cited (1710 times) paper “Genomewide association analysis of coronary artery disease” was published in the New England Journal of Medicine.

Together with the papers from R. McPherson and A. Helgadottir, as well as the famous WTCCC paper – all published in Summer 2007 – this was the starting shot for a decade of fascinating science to understand, or to be more precise, to partly understand the genetics of coronary artery disease and myocardial infarction (for those who are interested in more details please see recent reviews by Visscher et al. (2017) and Khera & Kathiresan (2017)). There is still a lot to learn.

Please read the full story on our blog.

PhD position in bioinformatics available

The University Medical Center Schleswig-Holstein is one of the largest university hospitals in Europe with more than 80 clinics and institutes. It offers outstanding medical treatment and excellence in research and education with nearly 12,500 employees, 2,600 patient beds and more than 100,000 hospitalized patients, 240,000 outpatient cases and more than 3,000 births a year. We provide top research at the interface of medicine, science, and technology and maintain research co-operations with universities all over the world.

The Institute for Cardiogenetics was founded in January 2013.

Scientists working at this institution are nationally and internationally well-recognized for their success in the field of cardiovascular genomics. Cardiovascular diseases, including coronary artery disease (CAD) and myocardial infarction (MI), are among the leading causes of mortality worldwide. Over the last five years, we identified most of the known coronary artery disease risk variants by genome-wide association studies (GWAS) and whole-exome as well as whole-genome sequencing in families (Erdmann et al. Nature Genetics 2009, Schunkert et al. Nature Genetics 2011, Erdmann et al. Nature 2013).

The primary aim of our institute is identifying further cardiovascular risk variants using GWAS as well as next-generation-sequencing and understanding the underlying pathomechanisms. We have already established several mouse and zebrafish models as well as in-vitro assays and standardized phenotyping methods in our group.

The „Institute for Cardiogenetics“ (ICG, www.cardiogenetics-luebeck.de) (Head: Prof. Dr. Jeanette Erdmann) at the University of Lübeck, Germany, is seeking for an outstanding Ph.D. student with a research interest in the field of cardiovascular genetics.

Your role:

  • Establishing/maintenance of next-generation sequencing pipelines for whole-exome, whole-genome as well as panel sequencing data for large-scale population as well as family data
  • Annotation of genetic variants by making use of state-of-the-art bioinformatics methods and publicly available/in-house transcriptomic/RNA-seq data.
  • Presentation of scientific results at conferences, meetings, seminars
  • Writing of publications under guidance of supervisors
  • Contributing to supervision of master students

Your profile:

  • You hold a master’s degree in bioinformatics or another relevant specialization
  • You have appropriate programming skills in R, Perl or Python
  • You are experienced using Linux systems including shell programming
  • You have a strong background in molecular biology/genetics
  • You are experienced in handling computational clusters, genetic databases such as Ensembl and/or Web Application Frameworks (Play! or Django) would be a plus
  • Record of prior publications
  • Personal qualities such as good teamwork attitude, multitasking ability, and communication skills (excellent in written and oral English and German language and excellent communication skills) are also essential.

What we offer:

This is a fixed-term position for 2 years, with the possibility of extension. Weekly working time is 65% of a full-time position (currently 38,50 hours per week). Working part-time is possible. Salary will be, depending on qualifications, according to the German salary scale E13 TV-L. The preferred starting date is 01.12.2017.

The UKSH has been certified as a family-friendly institution and is committed to further improve the compatibility of work and family life. The University Medical Center Schleswig-Holstein is an equal opportunity employer. People with disabilities will be given preference in case of equal qualifications.

Your Application should include:

  • Letter of motivation describing previous achievements and your research interest and why you are suitable for this position (maximum 1-2 pages)
  • CV including list of publications, reports, certificates
  • Transcripts
  • Names, e-mail addresses, and telephone numbers for at least two academic references/recommendation letters

Additional Information:

For more details on the position, please contact Prof. Dr. Jeanette Erdmann, phone: 0451 3101 8300, E-mail: jeanette.erdmann@uni-luebeck.de. Questions on administrative aspects can be addressed to Bea Roßteutscher via e-mail: karriere@uksh.de.

We are looking forward to your application. Please submit your application until o5.11.2017 indicating your earliest possible starting date as well as the reference number 20170835.219.CL.

Please apply via our online portal: www.uksh.de/Bewerbung.html?nr=20170835

More information on the University Medical Center Schleswig-Holstein can be obtained online at

www.uksh.de/karriere.

Universitätsklinikum Schleswig-Holstein
Human Resource Management | Recruiting Center

HIWI position available

Das Institut für Kardiogenetik sucht zum 01.Oktober 2017 eine studentische Hilfskraft zur Mitarbeit in einem Industrieprojekt für 49 Stunden pro Monat für zunächst ein Jahr.

Der Tätigkeitsbereich umfasst die Vorhersage von 3D Proteinstrukturen und deren Validierung/Auswertung nach vorgegebenem Protokoll unter Betreuung eines wissenschaftlichen Mitarbeiters.

Es sind keine Vorkenntnisse im Bereich Computerchemie oder Programmierung erforderlich.

Die Bezahlung richtet sich nach den üblichen Stundensätzen der Universität zu Lübeck für studentische Hilfskräfte. Die Arbeitszeit kann im Rahmen der üblichen Bürozeiten am Institut flexibel gestaltet werden.

Sie sind verlässlich, können selbständig und konzentriert arbeiten, sind vertraut im Umgang mit MS-Office-Anwendungen, sind kommunikativ und können sich gut in ein bestehendes Team einfügen, dann richten Sie bitte ihre Bewerbung per E-Mail an:

Dr. rer. nat. Stephanie Tennstedt

stephanie.tennstedt@uni-luebeck.de

Rückfragen gerne telefonisch unter der folgenden Telefonnummer: +49 451 3101 8322

GfH Poster Award 2016 for Ingrid Braenne

The best scored abstracts, which could not be selected for oral presentation, competed for the 3 GfH Poster Awards 2016.

Ingrid Braenne from the IIEG was selected for her poster entitled: Novel coronary artery disease loci identified by studying the pleiotropic effects of coxibs.

The award is dedicated to recognize excellent research presentations of young investigators. Congratulations to Ingrid.

IMG_9727 IMG_9726

Zebrafish platform

Zebrafish (Danio rerio) has been established as a model for dyslipidemia or atherosclerosis due to the remarkable similarities with humans in lipid and lipoprotein metabolism. In contrast to mice, zebrafish show lipoprotein oxidation and dyslipidemia after feeding with a high cholesterol diet even without any genetic intervention; this makes the zebrafish an attractive model for atherosclerosis research.
In Spring 2014 we started to establish a platform to study atherosclerosis in zebrafish in close collaboration with the Fraunhofer Research Institution for Marine Biotechnology.
The main intended use of the zebrafish platform is to investigate the early signs of atherosclerosis. The techniques involved in the study include the following:
– Breeding, maintenance, and exposure of zebrafish to a HCD or control diet
– Quantifying of lipid deposits in zebrafish larvae at different time points after Oil Red O staining
– Confocal imaging and conformation of lipid deposits
– Cholesterol and triglyceride measurements of zebrafish plasma samples
– Dissection of different zebrafish organs, including the heart, liver, aorta, eyes, brain, skin, kidney, and liver
– Quantitative RT-PCR analyses
– Use of microinjection technique for knock down/out or transgenesis of genes associated with cardiovascular disease

Nexilin and dilated cardiomyopathy

Cardiomyopathy, a disease of the heart muscle, is one of the most common causes of heart failure in Western countries. The European Society of Cardiology (ESC) differentiates a primary or secondary form of cardiomyopathy. The primary cardiomyopathy cannot be attributed to a specific cause, such as high blood pressure, heart valve disease, coronary artery diseases or congenital heart defects. Secondary cardiomyopathy is due to specific causes and often associated with diseases involving other organs including the heart itself.
The majority of DCM cases are due to mutations in previously reported or still unknown genes rather than environmental triggers including viral infection and autoimmunity. Nexilin (NEXN) is one of these genes recently identified by our group to play a pivotal role in DCM. Furthermore, another group could reveal a functional role for NEXN in hypertrophic cardiomyopathy (HCM).
Admittedly, the molecular mechanisms leading to the initiation and development of this, often fatal disease are still unknown. In this project, we aim to provide new insights into the pathogenic mechanisms using a mammalian cardiac knockout model to more accurately recapitulate the pathology of the human DCM.
In addition, comprehensive investigations of the Nexilin protein interaction network will further emphasize the physiological relevance of Nexilin in heart development.

Abcc6 and coronary artery calcification

Coronary artery calcification is one of the determinant cardiovascular risk factor for CAD/MI, which leads to increased morbidity and mortality in western countries. Our group have reported the heritability of CAC and worked intensively on genetic predisposition of certain laboratory inbred strains to calcification. These mice were used later on to understand the underlying pathological processes. Based on quantitative trait locus (QTL) analysis, fine mapping and ultrafine mapping strategies Abcc6 was finally identified as causal gene for dystrophic cardiac calcification in mice within the Dyscalc1 major locus on mouse chromosome 7. Interestingly, mutations in ABCC6 were also identified from other research groups to cause calcification in two human rare disorders pseudoxanthoma elasticum (PXE) and general arterial calcification of infancy (GACI).
Abcc6 encodes for an Abc-transporter, which is expressed mainly in liver. We and other PXE/GACI scientific researchers work together at international level to understand the underlying pathological mechanisms and identify the substrate (s) transported by this membrane transporter. Very recently our group demonstrated that dystrophic calcification shares many features with osteogenic processes and identified Runx2 as determinant osteogenic transcription factor enhancing calcification in mice deficient for Abcc6 via increased transcription of its downstream gene osteopontin. Furthermore and using gene transfer approach our group worked together with the research group of Prof. Le Saux in Hawaii as well as the research group of Prof. Varadi in Budapest, Hungary to demonstrate for the first time that a low hepatic level of the functional Abcc6 rescue calcification in mice.

Gucy1a3 and coagulation/atherosclerosis

ucy1a3 encodes for the 1 subunit of the soluble guanylate cyclase (sGC), where nitric oxide binds to increase the levels of cGMP. Gucy1a3 has been associated to CAD in GWAS studies as well as in family studies.
This gene is involved in the regulation of vasodilation, inhibition of platelet adhesion and aggregation and neurotransmission. Mice lacking Gucy1a3 present a reduction in artery relaxation, an abrogation of agonist-induced platelet aggregation and hypertension.
In this project we aim to backcross the Gucy1a3-KO animals to Ldlr-KO background and induce atherosclerosis after feeding the animals with a standard or high fat diet. Studies are on going to reveal the role of Gucy1a3 in atherosclerosis as well as lipid metabolism.
Results from mice we have been able to identify a reduction in plaque size and in collagen content, a reduction in total cholesterol and Ldl levels and hypertension in the Double-KO animals. Present studies include the final characterization of the atherosclerotic plaque, expression analysis in several tissues, a deeper lipid analysis and the study of macrophages, endothelial and smooth muscle cells.

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