No. 15/ December 11, 2003

Dr. Ron McKay to Receive Max-Delbrück Medal in Berlin

Honoured for his “outstanding contributions to stem cell research”

“For his outstanding contributions to stem cell research” Dr. Ronald McKay from the National Institute of Neurological Disorders and Stroke (NINDS), Bethesda, USA has received the Max Delbrück Medal in a ceremony at the Charité University Hospital in Berlin/Germany. „Using the power of genomics and genetics Dr. McKay analyzed the development and the function of stem cells in the mouse and human nervous system. His work was fundamental for our understanding of the control of proliferation and differentiation of these cells. He showed that stem cells can generate synaptically active neurons and applied this knowledge to clinical models of neurodegenerative diseases”, remarked Prof. Björn Wallmark (Ernst Schering Research Foundation) in his address before the Organizing Committee of the Berlin Lecture on Molecular Medicine.

No. 14/October 25, 2003

Health Benefits of the Mediterranean Diet: Myth or Reality?

Rapid changes in our life-styles have gone hand-in-hand with changes in eating habits. People are not exercising enough and typically over-eat, particularly fatty foods. This has led to an increase in overweight and obesity worldwide, so that epidemiologists speak of an epidemic affecting more than 250 million people. Overweight and obesity are major risk factors for cardiovascular diseases. “Physicians urge their patients to reduce weight and make healthier food choices guided by the traditional Mediterranean diet”, Prof. Anthony Kafatos from the University of Crete School of Medicine, Heraklion, Greece pointed out at the 3rd International Symposium on Obesity and Hypertension at the Communications Center of the Max Delbrück Center for Molecular Medicine (MDC) in Berlin on October 25, 2003. “This means: fruits, vegetables, bread, pulses, olive oil, cheese, milk, eggs, fish and a little red wine”, he said.

No. 13/25.October 2003

A More Specific Treatment for Obese Patients with Hypertension in the Future?

New discoveries from basic research could possibly result in more targeted treatment of hypertension and diabetes in the case of greatly overweight (obese) patients in the future. Excess weight and obesity are the main risk factors for hypertension and cardiovascular diseases as well as diabetes type 2. There are not yet any standardized recommendations for the treatment of hypertension in the obese, as up to now extensive clinical studies have not dealt with this question. The treatment for reducing blood pressure in these patients is therefore strongly influenced by existing accompanying diseases. Frequently so-called angiotensin converting enzyme-inhibitors (ACE-inhibitors), diuretics and calcium channel blockers are used as the initial treatment.

No. 12/October 25, 2003

DASH - A diet to reduce high blood pressure

Overweight and obesity are a major risk factor for ill health, especially high blood pressure (hypertension) and diabetes. In the US more than 50 million American adults or 30 per cent are obese and more than 100 million or 60 per cent are overweight. “One consequence of this epidemic is an increase in the prevalence of hypertension”, said Professor George A. Bray from the Louisiana State University Medical Center, Pennington Biomedical Research Center in Baton Rouge/USA. “If obesity could be prevented or effectively treated, hypertension could be reined in, and the need for pharmacologic intervention for hypertension would be reduced”, he told researchers and clinicians attending the 3rd International Symposium on Obesity and Hypertension at the Communications Center of the Max Delbrück Center for Molecular Medicine (MDC) in Berlin/Germany on October 25, 2003.

No. 11/October 23, 2003

Obesity - A Worldwide Epidemic affecting more than 250 Million People - High Blood Pressure Direct Result of Excess Weight

Obesity is currently recognized as a worldwide epidemic affecting more than 250 million people. It is a major risk factor for cardiovascular diseases including hypertension. More than half of the people who are obese, also have hypertension. People with a body mass index of more than 25 kg/m2 (bodyweight in kilogram divided twice by body height in meters) are regarded as being obese. Accordingly, about ten million obese people in Germany are considered to be also hypertensive. These facts were pointed out by Prof. Arya Sharma (McMaster University, Hamilton, Ontario, Canada) and Prof. Friedrich Luft (Franz Volhard Clinic, Charité, Universitätsmedizin Berlin, Berlin-Buch Campus in the Helios Clinic and Max Delbrück Center for Molecular Medicine, MDC, Berlin-Buch), the organizers of the 3rd Symposium on Obesity and Hypertension, at the beginning of the meeting on Thursday at MDC`s Communications Center.

No. 10/15. October 2003

How prions infect nerve cells – immune cells serve as vehicle.

The Creutzfeldt Jacob Disease (CJD) is an infectious disease, which is triggered by prion proteins. In the advanced stage the pathogens destroy the brain. Yet it is evident that the brain is not directly infected in every case. Prions mostly gain entry into the body via the peripheral areas - presumably via the gastro-intestinal tract – and multiply in the organs of the immune system: in the lymph nodes, the spleen and in the pharyngeal tonsils. Unfortunately the prions are assisted in becoming established in these lymphatic organs by a further component of the immune system, the complement system, as Prof. Adriano Aguzzi from the University Hospital Zürich/Switzerland was able to prove some time ago. However the mechanism of prion transfer from the immune system to the nervous system is still unknown. Evidently prions, which have become established in the spleen, manage to infect peripheral nerve cells via a further group of immune cells, the so-called follicular dendritic cells (FDCs). This has now been demonstrated in animal experiments by Prof. Aguzzi and his colleagues Dr. Marco Prinz and Dr. Mathias Heikenwalder in collaboration with Dr. Martin Lipp from the Max-Delbrück-Center for Molecular Medicine (MDC) Berlin-Buch. The journal Nature has published their findings online in advance on 15th October 2003 ( |


3rd International Symposium on Obesity and Hypertension

(3. Internationales Symposium zu Übergewicht und Bluthochdruck)

Thursday 23rd October – Saturday 25th October 2003

Max Delbrück Communications Center (MDC.C)

Robert-Rössle-Str. 10

13125 Berlin, Germany

No. 8/August 18, 2003

From hydras to humans - only few signaling pathways control the development of living beings

Over the past five to ten years, biologists have gained increasingly deeper insights into biochemical and molecular networks regulating the development of living beings, from the fertilized egg to complete organisms containing billions of cells and different organs. “We established that from hydras (freshwater polyps) to humans only a handful of signaling pathways control this development”, commented Prof. Walter Birchmeier, Research Group Leader at the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch. He added, “the signaling paths fit in precisely with each other, preventing any maldevelopment or tumor formation”. Together with Natalia Soshnikova, a PhD student from his research group, he has now been able to demonstrate in mice that two particular signaling pathways are required for the formation of limb. “Both signaling pathways are equally important and depend on each other. If one of them is missing, limbs cannot form”, commented the researchers. At the same time, they succeeded in tracking the timely sequence and the associated formation of the limbs (axis formation). The research by Natalia Soshnikova, Dr. Dietmar Zechner und Prof. Birchmeier carried out in collaboration with researchers in the USA and Japan, has now been published in the renowned journal Genes and Development (Vol. 16, No. 17, August 15, 2003, pp. 1963-1968) and online

No. 7/27 July 2003

Discovery of molecular cause of arterial calcification in early infancy

These infants are already born with arterial calcification and only have a short life expectancy. Most of them die in early infancy. Geneticists from Germany, the USA, Australia, Italy and the United Kingdom have now discovered the molecular cause for this rare arterial calcification in babies. Tests of DNA samples of eleven affected infants and their parents showed that they carried mutations in the gene, containing the building instructions for an enzyme, responsible for the formation of a natural agent preventing calcification. The agent is inorganic pyrophosphate, a modified format of which is also added to toothpastes to inhibit the formation of tartar. The full activity of the enzyme in healthy infants prevents any calcification of vascular walls. Where the enzyme is not formed due to the genetic defect or where it is inactive, this results in serious calcification and thus vasoconstriction with, in most cases, deadly consequences for infants because of an inadequate blood supply to the heart. The disease is recessively hereditary, i.e. the gene mutation is passed onto the infants from their father and their mother. The research work of Dr. Frank Rutsch, University Clinic of Pediatrics, Münster, Germany, and Prof. Robert Terkeltaub, University of California, San Diego, USA, and the Research Group of Dr. Peter Nürnberg, Charité and Max-Delbrück-Center for Molecular Medicine (MDC) Berlin-Buch*, a National Research Center of the Helmholtz-Association, has now been initially published online by the journal Nature Genetics under

No. 6/July 8, 2003

Genetic tests identify men at risk from sudden cardiac death and allow life-saving therapy for young men

Genetic tests in patients at risk from sudden cardiac death prompt implantation of defibrillators, devices which can terminate otherwise deadly arrhythmias. “This is an example of how molecular genetics is already proving helpful in identifying high risk patients and allowing suitable treatment to be given“, stated Professor Ludwig Thierfelder, Executive Medical Director of the Franz Volhard Clinic for Cardiovascular Diseases of the Charité, Humboldt University of Berlin, Berlin-Buch Campus/Helios Klinikum Berlin. He also heads a research group at the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, a national research laboratory of the Helmholtz Association. Professor Thierfelder has been collaborating with researchers of the Memorial University of St. John´s, Newfoundland, Canada since 1996. In their search for the disease causing mutation responsible for an inherited cardiac disorder (arrhythmogenic right ventricular cardiomyopathy; ARVC), they discovered that numerous patients from Newfoundland families who had died suddenly, carried an identical chromosomal defect on chromosome 3p25. In several cases, the defibrillators could terminate ventricular fibrillation, thus saving the life of the young men affected by ARVC.

No. 5 /June 17, 2003

Nephrologist Friedrich C. Luft Receives Prestigious Awards in Milan and Berlin

Friedrich C. Luft, MD, a Professor of Medicine at the Medical Faculty of the Charité, Humboldt University of Berlin, Campus-Buch, Helios Klinikum-Berlin, Germany, has been awarded the Björn Folkow Prize at this year’s meeting of the European Society of Hypertension in Milan, Italy. The prestigious award was for his important contributions to the molecular and clinical approaches to hypertension research. This award was for lifetime achievements and included a lectureship. Björn Folkow, MD, PhD was Professor of Physiology at the University of Göteborg, Sweden. Folkow described fundamentally important modifications in the blood vessel wall in patients with hypertension. At this year’s World Congress of Nephrology meeting in Berlin, Prof. Luft also received the “Anthony Raine Award” from the International Society of Nephrology. That award, which also includes a lectureship, is in memory of Anthony Raine, Professor of Nephrology at the St. Bartholomew's & the Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, University of London, UK. Raine was a nephrologist who devoted his career to cardiovascular issues in patients with chronic renal diseases.

Nr. 4/ June 15, 2003

The Difference between Touch and Pain no longer such a Mystery

Scientists of the Max Delbrück Center in Berlin unveil a new mechanism for touch receptors

The ability to read Braille, crack a safe, or enjoy a kiss is due to specific sensory receptors in the skin of humans. Animals also possess such sensors for touch and pain called mechanoreceptors. Both senses are of vital importance for both animals and humans. However, up until now very little was known about how these receptors function and what makes them so specific for touch or pain. Dr. Jung-Bum Shin from the research group of Dr. Gary Lewin working in the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, a national research laboratory in Berlin (Germany) has thrown new light onto this problem. The findings of Dr. Shin have been published online by the prestigious Journal Nature Neuroscience*. They provide the first evidence that in vertebrates (mice) certain ion channels - in this case – a calcium channel which is required specifically for the function of a touch sensing mechanoreceptor. The neuroscientist assume that similar receptors also exist in humans.


Berlin-Buch Congress on Biotechnology 2003

Friday, June 13 - Saturday, June 14, 2003

Max Delbrück Communications Center (MDC.C)

No. 3/April 16, 2003

Discovering how blood cells develop

MDC researchers investigate key molecular pathways

One of the fundamental processes of biology is the conversion of information encoded by genes into proteins, the universal building blocks and driving force of life. Initially, the genetic information stored in DNA is copied into transportable messenger-RNA (mRNA). mRNAs pass the information on to ribosomes, the protein factories in cells. The latter assemble the proteins from a series of individual building blocks, so-called amino acids, using the mRNA as a template. The transmission of information from messenger-RNA into specific sequences of amino acids is termed „translation“. For the majority of genes, however, the individual steps controlling translation have remained a mystery. Dr. Cornelis F. Calkhoven and Dr. Christine Müller from the research group headed by Dr. Achim Leutz of the Max-Delbrück-Center for Molecular Medicine (MDC) Berlin-Buch, in collaboration with researchers from the Clinical Research Institute in Montreal/Canada, have now unraveled a novel regulatory mechanism for translation which plays a key role in the formation of a variety of blood cells. Their investigations have now been published in the renowned scientific journal Genes and Development (Vol. 17, No. 8, April 15, 2003)*.

No.2/April 9, 2003

Bazooka delivers a surprise

New information about cell motility in the fruit fly (Drosophila)

Many cells, in certain phases of development, leave their site of origin, migrate in a predetermined way within the organism and reattach themselves to new sites. These fundamental processes are of critical importance for both embryonic development and for functioning of mature tissues. If these very precisely regulated processes get out of control diseases can develop affecting the cardiovascular and nervous systems, as well as causing tumour formation. Therefore scientists also investigate just how tumour cells are able to migrate and form metastases.

No.1/January 2, 2003

MDC Scientists discover a second gene for serotonin synthesis

What makes sure that we are in a good mood, regulates our sleep, appetite, blood pressure and our gut motility ? It’s the hormone serotonin. But what happens if the body is no longer able to make any more serotonin? This is the question that has been investigated by scientists at the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch in collaboration with researchers at the Free University (FU) of Berlin und the Humboldt University of Berlin (HUB). Their research has led to the discovery of a new gene, the product of which is responsible for serotonin synthesis in the brain. Working with mice, they switched off the gene that produces the enzyme tryptophan hydroxylase, which is responsible for serotonin synthesis. Result: the production of serotonin in the gut was halted, but not that in the brain. The results of this work have now been published by Dr. Diego J. Walther and Dr. Michael Bader in the prestigious American journal „Science“ (Vol. 299, No. 5603,*.