Press releases

FRANKFURT. Since first being awarded in 1901, most Nobel Prizes for science have gone to the USA, the United Kingdom, Germany and France. An empirical study by Professor Claudius Gros from the Institute for Theoretical Physics at the Goethe University in Frankfurt has now shown that the Nobel Prize productivity in these countries is primarily determined by two factors: a long-term success rate, and periods during which each country has been able to win an especially large number of Nobel Prizes.

For the study, Nobel Prizes for physics, chemistry and medicine were assigned proportionately, since up to three scientists can share the prize. The success rates were calculated on the basis of population figures. For France and Germany, the periods of increased scientific creativity occurred around 1900, whereas for the USA it occurred in the second half of the 20^th century.

“The US era is approaching its end,” states Claudius Gros. “Since its zenith in the 1970s, US Nobel Prize productivity has already declined by a factor of 2.4.” According to his calculations, a further decline is foreseeable. “Our model predicts that starting in 2025 the productivity of the USA will be below that of Germany, and from 2028, below that of France as well.”

With a nearly constant, very high success rate per capita, Great Britain occupies a special position with regard to Nobel Prizes. It remains uncertain, however, whether Great Britain will be able to maintain this success, especially in view of the increasing industrialization of research.

“National research advancement can undoubtedly also be successful independent of Nobel Prize productivity,“ Claudius Gros stresses. “Especially because new areas of research such as the computer sciences – a typical US domain – are not included.” It therefore remains open whether the decline in Nobel Prize productivity is cause for concern, or merely an expression of a new orientation toward more promising research fields.  

A chart to download can be found at: www.uni-frankfurt.de/71881831

Chart: Claudius Gros, Goethe University

Publication:
Claudius Gros: An empirical study of the per capita yield of science Nobel Prizes: Is the US era coming to an end?, in: Royal Society Open Science (2018) http://rsos.royalsocietypublishing.org/content/5/5/180167

Claudius Gros: Pushing the complexity barrier: diminishing returns in the sciences, in: Complex Systems 21, 183 (2012). https://arxiv.org/abs/1209.2725

Further information: Prof. Claudius Gros, Department for Theoretical Physics, Faculty of Physics, Riedberg Campus, Tel.:+49(0)69 798-47818, gros07@itp.uni-frankfurt.de.

FRANKFURT. How new blood vessels form in mammals, for example during development or after injury, was so far not known exactly. Scientists at the Goethe University have now been able to shed light on this process. They have shown that single cells in the innermost layer of blood vessels proliferate after injury and in so doing make a significant contribution to the formation of new vessels.

Observation in the living organism – and especially in the heart – of how new blood vessels form is not possible in mammals. That is why only endpoints can ever be seen, i.e. that new veins and arteries have formed and of what type of cells they consist. However, little is known to date about the actual process of new vessel formation, although this knowledge could contribute in future to remedying tissue damage, such as occurs in diabetes or following an ischemia-induced heart attack.

That is the reason why Professor Stefanie Dimmeler and her fellow researchers at the Institute of Cardiovascular Regeneration of Goethe University Frankfurt have studied the fate of single cells in the innermost vascular layer, i.e. the endothelial cells, during development and after tissue damage in what are known as Confetti mice. In these models, the researchers can mark specific cell types and distinguish between them with the help of fluorescent proteins. In the models used, only endothelial cells fluoresced in three different colors. Since the cells continue to fluoresce when they divide, single endothelial cells and their “progeny” can be tracked. In so doing, the scientists sought to answer the question of whether cell division in the formation of new blood vessels, as known from zebrafish, takes place more or less randomly or whether specific cells divide again and again to produce new vessels.

Clonal expansion after a heart attack

In damaged heart tissue following a heart attack, the researchers were able to observe that certain cells had divided repeatedly. They also detected this cell division, which is referred to as clonal expansion, in damaged tissue in skeletal muscles caused by ischemia. To do so, they analyzed the fluorescence in endothelial cells in tissue slices taken from the damaged areas. They found the ratio of clonally expanding cells – between 30 and 50 percent - very surprising. “But perhaps we’re even underestimating the ratio of clonal expansion,” presumes Dimmeler. “Because after all we haven’t conducted a three-dimensional analysis but instead identified the fluorescing cells in two-dimensional tissue slices.” In addition, further experiments showed that the vessels formed through clonal expansion are also supplied with blood and thus able to function.

In new-born models, by contrast, Professor Dimmeler and her team did not observe any clonal expansion in the formation of new vessels in the retina. It would therefore seem that the growth of blood vessels during normal development results from the random multiplication and integration of cells. This result coincides with observations in zebrafish, in which what is known as “cell mixing” also plays an important role in the formation of new blood vessels during development.

Cell profiling

The researchers were keen to characterize the dividing cells more precisely and to this purpose they analyzed which genes are transcribed in single examples of the clonally expanding endothelial cells. “Surprisingly, we found a large number of gene products that are typical for the transition from an endothelial to a mesenchymal cell,” says Dimmeler. This transition, or EndMT process, is a contributor in many pathogenic processes, such as scarring or arteriosclerosis. In endothelial cells, the gene products typical for EndMT do not, however, mirror a transition but instead presumably just an intermediate stage that enables the cells to detach themselves from the cell assembly in order to multiply.

Clonal expansion as possible therapy for heart attack patients

Dimmeler and her team now want to find out what happens with the clonally expanded cells in the long term, since at present they are only able to track their fate for about two months. “We want to know what has happened to these cells after a year and whether the new blood vessels are just as good as the old ones in the long term,” says Dimmeler.  

Is clonal expansion different in older patients? This is another question she finds fascinating. “It might be that clonal expansion is no longer that efficient in older people, which is why a lot of damaged tissue dies off after a heart attack and forms scar tissue which cannot be reactivated through the formation of new blood vessels,” says Dimmeler. “If we manage to characterize the clonally expanding cells more precisely, we will hopefully find ways to re-stimulate this process.”

Original publication:

Clonal Expansion of Endothelial Cells Contributes to Ischemia-Induced Neovascularization. Manavski, Y., Lucas, T., Glaser, S. F., Dorsheimer, L., Gunther, S., Braun, T., Rieger, M. A., Zeiher, A. M., Boon, R. A. & Dimmeler, S. Circulation research 122, 670-677, (2018).

DOI: 10.1161/CIRCRESAHA.117.312310.

Further information: Professor Stefanie Dimmeler, Institute of Cardiovascular Regeneration, University Hospital Frankfurt, Tel.: +49(0)69-6301-7440; Email: Dimmeler@em.uni-frankfurt.de

FRANKFURT. What difference does it make to the Earth’s water resources if we can limit global warming to 1.5°C instead of 2°C? A research group led by Goethe University Frankfurt has simulated these scenarios with global hydrological models. An important result: High flows and thus flood hazards will increase significantly over an average of 21 percent of the global land area if the temperature rises by 2°C. On the other hand, if we manage to limit the rise in global warming to 1.5°C only 11 percent of the global land area would be affected.

According to the Paris Agreement on climate change of December 2015, the increase in global average temperature should be kept well below 2°C compared to pre-industrial levels, if possible even below 1.5°C. To find out what the two scenarios mean specifically in terms of reducing risks for the global freshwater system, the Federal Ministry of Education and Research commissioned a study which has now been published and is intended for inclusion in the forthcoming special report by the Intergovernmental Panel on Climate Change (IPCC) on global warming of 1.5°C.

As the research group led by Professor Petra Döll from the Department of Physical Geography at Goethe University Frankfurt reports in the current issue of “Environmental Research Letters”, it used two global hydrological models for the analysis, which were “fed” with a new type of climate simulations, known as HAPPI simulations. These are more suitable than previous types of simulations for quantifying the risks of the two long-term climate goals. By calculating seven indicators, risks for humans, freshwater organisms and vegetation were characterized.

“If we compare four groups of countries with different per-capita incomes, those countries with a low or lower middle income would profit most from a limitation of global warming to 1.5°C in the sense that the increase in flood risk in those countries would remain far lower than at 2°C,” explains Petra Döll, first author of the study. Countries with a high income would profit most of all from the fact that rivers and land would dry out far less in the dry months of the year.

Professor Döll performed the study in cooperation with the Potsdam Institute for Climate Impact Research and Climate Analytics in Berlin. She is an expert on water and has been investigating the potential impacts of climate change on the Earth’s freshwater systems for twenty years.

A picture can be downloaded under: http://www.uni-frankfurt.de/71631166

Caption: Access to clean water is a major challenge facing many people, such as this boy in the semi-arid Northeast Region of Brazil. Photo: Petra Döll.

Publication: Petra Döll, Tim Trautmann, Dieter Gerten, Hannes Müller Schmied, Sebastian Ostberg, Fahad Saaed und Carl-Friedrich Schleussner: Risks for the global freshwater system at 1.5 ◦C and 2 ◦C global warming, in: Enviromental Research Letters 13 (2018) 044038, https://doi.org/10.1088/1748-9326/aab792

Further information: Professor Petra Döll, Department of Physical Geography, Faculty of Geosciences and Geography, Riedberg Campus, Tel.: +49(0)69-798-40219, p.doell@em.uni-frankfurt.de

FRANKFURT. Harold James, Princeton University, will hold the Visiting Professorship of Financial History at Goethe University Frankfurt’s House of Finance this year. The professorship is endowed by Metzler Bank and Friedrich Flick Förderungsstiftung.

Harold James is Claude and Lore Kelly Professor in European Studies, Professor of History and International Affairs, and Director of the Program in Contemporary European Politics and Society at Princeton University. Furthermore Professor Harold James holds the position of Official Historian at the International Monetary Fund. His research focuses on Economics and Financial History and Modern European History. James was educated at Cambridge University (Ph.D. in 1982) and a Fellow of Peterhouse for eight years before joining Princeton University in 1986. In 2004 he was awarded the Helmut Schmidt Prize for Economic History, and in 2005 the Ludwig Erhard Prize for writing about economics.

James’ publications include a study of the interwar depression in Germany (“The German Slump”, 1986), an analysis of the changing character of national identity in Germany (“A German Identity 1770-1990” 1989), and a study on “International Monetary Cooperation Since Bretton Woods” (1996). He was a co-author of a history of Deutsche Bank (1995) which won the Financial Times Global Business Book Award in 1996, and he wrote the book “The Deutsche Bank and the Nazi Economic War Against the Jews” (2001). Furthermore he published “The End of Globalization: Lessons from the Great Depression” (2001); “Europe Reborn: A History 1914-2000” (2003); “The Roman Predicament: How the Rules of International Order Create the Politics of Empire” (2006), and “Family Capitalism: Wendels, Haniels and Falcks”. His most recent works are “The Globalization Cycle” (2009); “Making the European Monetary Union” (2012), and “The Euro and the Battle of Economic Ideas (with Markus K. Brunnermeier and Jean-Pierre Landau)” (2016).

During his stay in Frankfurt, Harold James will deliver a CFS Presidential Lecture on 28 May. Also, he will give a seminar in the Ph.D. program of the University’s Graduate School GSEFM at the House of Finance on the topic “Thinking About Financial History”. On 8 June 2018, James will give the keynote address in an international research conference on “Lehman – 10 Years After” which he co-organizes together with Bernd Rudolph, LMU.

Professor James is the fourth holder of the Visiting Professorship of Financial History. In the context of this professorship, distinguished international experts in banking and financial history are invited to share their research insights and methods with researchers, students and the interested public in Frankfurt. Cooperation partners are the Research Center SAFE at the House of Finance and the Institut für Bank- und Finanzgeschichte. Previous Visiting Professors were Benjamin Friedman, Harvard University (2015), Caroline Fohlin, Emory University, Atlanta (2016) and Hans-Joachim Voth, University of Zurich (2017). The Visiting Professorship was initially endowed by Metzler Bank and Edmond de Rothschild Group in 2014 on the occasion of Goethe University’s centennial.

Information: Ursula Maßner, House of Finance, Faculty of economics and business administration, Westend Campus, Phone +49 (0)69 798 30091, E-Mail massner@hof.uni-frankfurt.de

FRANKFURT. One of the most significant impairments of the quality of life after a chemotherapy is infertility. Researchers of the Goethe University and the University Tor Vergata in Rome have now identified the mechanism of chemotherapy-induced infertility in females.

Many chemotherapeutics act by damaging the DNA. Since cancer cells divide more often than most normal cells, they react more sensitive to DNA damaging agents. One exception are oocytes. To prevent birth defects they initiate a cellular death program if DNA damage is detected. This process, called apoptosis, is triggered in oocytes by the protein p63. Oocytes contain a high concentration of an oocyte-specific isoform of p63 which plays a key role as a quality control factor in causing infertility.

In contrast to men who produce new sperm cells throughout their life women are born with a finite number of oocytes. When this pool is depleted menopause starts. This pool of oocytes can be depleted prematurely by chemotherapy resulting in early menopause. This results not only in infertility but also in hormone-based problems such as osteoporosis.

Scientists in the laboratory of Prof Volker Dötsch at the Institute for Biophysical Chemistry of Goethe University have now deciphered the mechanism leading to premature loss of the oocyte pool caused by treatment with chemotherapy. In non-damaged oocytes p63 exists in an inactive form. DNA damage caused by chemo- or radiotherapy results in the modification of p63 with phosphate groups which triggers a conformational change to the active form. Active p63 starts the cell death program which leads to the elimination of the oocyte. The scientists describe in the online edition of the journal „Nature Structural and Molecular Biology“ the molecular details of this activation mechanism and the enzymes responsible for it.

These results open new opportunities for developing a therapy for preserving oocytes of female cancer patients treated with chemotherapeutics. In experiments with mouse ovaries inhibiting the identified enzymes saved the oocytes from cell death despite treatment with chemotherapeutics.

Publication: Tuppi M., Kehrloesser S., Coutandin D.W. et al. Oocyte DNA damage quality control requires consecutive interplay of CHK2 and CK1 to activate p63, in: Nature Structural and Molecular Biology. DOI: 10.1038/s41594-018-0035-7