Unravelling the genetics of fungal fratricide

Press Releases   •   Oct 15, 2018 12:38 BST

Selfish genes are genes that are passed on to the next generation but confer no advantage on the individual as a whole, and may sometimes be harmful. Researchers at Uppsala University have, for the first time, sequenced (or charted) two selfish genes in the fungus Neurospora intermedia that cause fungal spores to kill their siblings.

New knowledge about retrovirus-host coevolution

Press Releases   •   Oct 08, 2018 20:00 BST

Retroviruses have colonised vertebrate hosts for millions of years by inserting their genes into host genomes, enabling their inheritance through generations as endogenous retroviruses (ERVs). Researchers from Uppsala University now provide new knowledge about the long-term associations of retroviruses and their hosts by studying ERV variation and segregation in wild and domestic rabbit populations. The findings are being published in Proceedings of the National Academy of Sciences (PNAS).

Retroviruses, such as HIV in humans, must become part of the host cell’s nuclear DNA to produce new viruses. Over timescales of millions of years, retroviral infiltrations of germ cells have been inherited by the host’s offspring as ERVs, which make up large parts of vertebrate genomes today.

The researchers used recent technological advances for population-based analyses of whole genomes derived from wild and domestic hosts, which offer new insights into ERV-host genome variation. As a model, the researchers studied European rabbits, which diverged into two subspecies on the Iberian Peninsula about one million years ago and were domesticated in southern France about 1,000 years ago.

“By studying whole genome sequences from related host populations compared to the genome of a single individual, we can identify new ERVs to better understand retrovirus-host coevolution,” says Daniel Rivas, lead author of the study.

Using data from hundreds of individuals from many rabbit populations, the researchers were able to identify previously unknown retroviral insertions, as well as determine the spread of those that existed in the reference genome. The ERV diversity mostly follows rabbit divergence and the results indicate substantial variation across ERV insertions in different rabbit populations. This new knowledge sheds light on how ERVs spread in host populations, and how that spread correlates with the evolution of the host species.

“The abundance and segregating variation we uncover from host populations demonstrate the genomic ERV record as a remarkable source for an evolutionary perspective on retrovirus-host associations,” says Patric Jern, who headed the study.

Rivas Carillo S.D., Pettersson M.E., Rubin C.J. and Jern P. (2018) Whole-genome comparison of endogenous retrovirus segregation across wild and domestic host species populations. Proceedings of the National Academy of Sciences (USA), DOI: 10.1073/pnas.1815056115

For more information please contact:

Patric Jern, Science for Life Laboratory, Department of Medical Biochemistry and Microbiology,
e-mail: Patric.Jern@imbim.uu.se

Uppsala University -- quality, knowledge, and creativity since 1477
World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

Retroviruses have colonised vertebrate hosts for millions of years by inserting their genes into host genomes, enabling their inheritance through generations as endogenous retroviruses (ERVs). Researchers from Uppsala University now provide new knowledge about the long-term associations of retroviruses and their hosts by studying ERV variation and segregation in wild and domestic rabbits.

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Artificial enzymes convert solar energy into hydrogen gas

Press Releases   •   Oct 04, 2018 10:02 BST

In a new scientific article, researchers at Uppsala University describe how, using a completely new method, they have synthesised an artificial enzyme that functions in the metabolism of living cells. These enzymes can utilize the cell’s own energy, and thereby enable hydrogen gas to be produced from solar energy.

Hydrogen gas has long been noted as a promising energy carrier, but its production is still dependent on fossil raw materials. Renewable hydrogen gas can be extracted from water, but as yet the systems for doing so have limitations.

In the new article, published in the journal Energy and Environmental Science, an interdisciplinary European research group led by Uppsala University scientists describe how artificial enzymes convert solar energy into hydrogen gas. This entirely new method has been developed at the University in the past few years. The technique is based on photosynthetic microorganisms with genetically inserted enzymes that are combined with synthetic compounds produced in the laboratory. Synthetic biology has been combined with synthetic chemistry to design and create custom artificial enzymes inside living organisms.

“We’ve now been able to use the method we developed to produce enzymes that use the cell’s own energy to produce hydrogen gas,” says Adam Wegelius, a PhD student at the Department of Chemistry – Ångström Laboratory, Uppsala University.

Senior Lecturer Gustav Berggren and Professor Peter Lindblad of the same department have been jointly leading the research.

“Evolution has already developed and refined a tool for capturing sunlight through photosynthesis. And by introducing our artificial enzyme into photosynthetic cyanobacteria we can directly benefit from this efficient process, thus producing hydrogen gas from solar energy. We’ve developed a completely new method, which allows us to go beyond the solutions offered by evolution and nature, in our development of artificial enzymes” Berggren says.

The article, “Generation of a functional, semisynthetic [FeFe]-hydrogenase in a photosynthetic microorganism”, was published in Energy and Environmental Science and is available at dx.doi.org/10.1039/C8EE01975D.

For more information, contact:
Gustav Berggren, tel.: +46 73 633 2698, email: gustav.berggren@kemi.uu.se
Peter Lindblad, tel.: +46 70 425 0498, email: peter.lindblad@kemi.uu.se
Adam Wegelius, tel.: +46 70 393 7119, email: adam.wegelius@kemi.uu.se

Uppsala University -- quality, knowledge, and creativity since 1477
World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

In a new scientific article, researchers at Uppsala University describe how, using a completely new method, they have synthesised an artificial enzyme that functions in the metabolism of living cells. These enzymes can utilize the cell’s own energy, and thereby enable hydrogen gas to be produced from solar energy.

Read more »

​World speed record for polymer simulations

Press Releases   •   Oct 04, 2018 08:34 BST

Star polymers are within the most topologically entangled macromolecules. With a simulation over a hundred times faster than earlier studies, it is demonstrated that the mean square displacement scales with a power law 1/16 in time, instead of the previously assumed zero. It suggests that star polymer motion is the result of two linear relaxations coinciding in time.

New study shows cells produce specialised protein factories under stress

Press Releases   •   Oct 03, 2018 12:15 BST

Prevailing dogma in biological research holds that the cell’s protein factories, the ribosomes, function the same way in all cells and in all conditions. In an international study with participation from Weill Cornell Medicine and Uppsala University, published today in the journal Cell Reports, the researchers show that this is a truth that seems to not hold true.

Most functions in a cell are controlled by proteins. They are formed inside the cells in special protein factories called ribosomes. Different cells, i.e. in different tissues, need different sets of proteins and there are several ways that a cell can control how they are produced. However, it has long been an established “truth” that the composition and function of the ribosomes are the same in all cells and in all conditions.

This truth is now being disputed and in the present study the researchers show that E. coli bacteria can form specialised ribosomes that influence which proteins are produced.

“We exposed the bacteria to stress conditions by reducing the nutrient levels and found that a certain type of ribosome was produced in larger amounts. We could also link the increase in this type of ribosome to an activation of the cells’ general stress response,” says Theresa Vincent, group leader at the Department of Immunology, Genetics and Pathology, who participated in the study together with Professor Scott Blanchard at Weill Cornell Medicine in New York.

A ribosome consists of a large number of molecules that are all encoded by genes in the cell. In the study the researchers could show that variations in the DNA sequence in one of these genes gives rise to the specialised ribosomes.

“Our results support the finding that specialised ribosomes exist, that they are a result of natural gene variations and that they can control gene activity and the production of proteins. Since it has previously been believed that ribosomes have a passive role during the production of proteins, their importance in for instance diseases has not been investigated. But specialised ribosomes also exist in animal cells and it is warranted to study if and how the gene variations behind those ribosomes affect the function of the cells.”


Contact:
Theresa Vincent, email: theresa.vincent@igp.uu.se tel: +1-3478039171.

http://www.igp.uu.se/forskning/neuroonkologi/theresa-vincent/

Chad M. Kurylo, Matthew M. Parks, Manuel F. Juette, Boris Zinshteyn, Roger B. Altman, Jordana K. Thibado, C. Theresa Vincent, Scott C. Blanchard (2018) Endogenous rRNA Sequence Variation Can Regulate Stress Response Gene Expression and Phenotype, Cell Reports, Open Access, DOI: https://doi.org/10.1016/j.celrep.2018.08.093

Uppsala University -- quality, knowledge, and creativity since 1477
World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

Prevailing dogma in biological research holds that the cell’s protein factories, the ribosomes, function the same way in all cells and in all conditions. In an international study with participation from Weill Cornell Medicine and Uppsala University, published today in the journal Cell Reports, the researchers show that this is a truth that seems to not hold true.

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Well established theories on patterns in evolution might be wrong

Press Releases   •   Sep 27, 2018 13:23 BST

How do the large-scale patterns we observe in evolution arise? A new paper in the journal Evolution by researchers at Uppsala University and University of Leeds argues that many of them are a type of statistical artefact caused by our unavoidably recent viewpoint looking back into the past. As a result, it might not be possible to draw any conclusions about what caused the enormous changes in diversity we see through time.

The diversity of life through time shows some striking patterns. For example, the animals appear in the fossil record about 550 million years ago, in an enormous burst of diversification called the “Cambrian Explosion”. Many groups of organisms appear to originate like this, but later on in their evolutionary history, their rates of diversification and morphological change seem to slow down. These sorts of patterns can be seen both in the fossil record, and also in reconstructions of past diversity by looking at the relationships between living organisms, and they have given rise to a great deal of debate.

Do organisms have more evolutionary flexibility when they first evolve? Or do ecosystems get “filled up” as more species evolve, giving fewer opportunities for further diversification later on? In their new paper, Graham Budd and Richard Mann make the provocative argument that these patterns may be largely illusory, and that we would still expect to see them even if rates of evolutionary change stay the same on average through time.

Biologists and palaeontologists use statistical models called “birth-death models” to model how random events of speciation and extinction give rise to patterns of diversity. Just as one can roll a dice five times and get five sixes or none, the outcomes of these random models are very variable. These statistical fluctuations are particularly important at the origin of a group, when there are only a few species. It turns out that the only groups that survive this early period are those that happen to diversify quickly – all the others go extinct. As is it exactly those groups that go on to be the large successful groups we see living today, and that fill most of the fossil record, it follows that they are likely to show this rapid pattern of diversification at their origin – but only because they are a biased subset of all groups. Later in their history, when such groups are diverse, statistical fluctuations have much less effect, and therefore their rate of evolution appears to slows down to the background average.

As a result, the patterns we discover by analyzing such groups are not general features of evolution as a whole, but rather represent a remarkable bias that emerges by only studying groups we already know were successful. This bias, called “the push of the past”, has indeed been known about theoretically for about 25 years, but it has been almost completely ignored, probably because it was assumed to be negligible in size. However, Budd and Mann show that the effect is very large, and can in fact account for much of the variation we see in past diversity, especially when we combine it with the effects of the great “mass extinctions” such as the one that killed off the dinosaurs some 66 million years ago. Because the resulting patterns are an inevitable feature of the sorts of groups available for us to study, Budd and Mann argue, it follows that we cannot perceive any particular cause of them: they simply arise from statistical fluctuation.

The push of the past is an example of a much more general type of pattern called “survivorship bias” which can be seen in many other areas of life, for example in business start-ups and finance and the study of history. In all these cases, failure to recognize the bias can lead to highly misleading conclusions. Budd and Mann argue that the history of life itself is not immune to such effects, and that many traditional explanations for why diversity changes through time may need to be reconsidered – a viewpoint that is bound to prove controversial.

For more information, please contact: Graham Budd, professor at the Department of Earth Sciences, Palaeobiology, Uppsala University, tel: +4618-471 2762, email: Graham.Budd@pal.uu.se

Article reference:
Graham E. Budd, Richard P. Mann (2018) History is written by the victors: The effect of the push of the past on the fossil record, Evolution
https://doi.org/10.1111/evo.13593

Uppsala University -- quality, knowledge, and creativity since 1477
World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

How do the large-scale patterns we observe in evolution arise? A new paper in the journal Evolution by researchers at Uppsala University and University of Leeds argues that many of them are a type of statistical artefact caused by our unavoidably recent viewpoint looking back into the past.

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Genetic risk: Should researchers let people know?

Press Releases   •   Sep 24, 2018 08:10 BST

Should researchers inform research participants, if they discover genetic disease risks in the participants? Yes, many would say, if the information is helpful to the participants. However, the value of complex genetic risk information for individuals is uncertain. In a PhD thesis from Uppsala University, Jennifer Viberg Johansson suggests that this uncertainty needs to be acknowledged by both geneticists and ethicists.

One of the reasons people participate in large genetic studies is the comprehensive health check that researchers often include to collect data. These studies inform participants about their blood pressure, lung function and the results of different blood tests. In the future, people could also be offered information about genetic risks. Jennifer Viberg Johansson’s PhD thesis explores factors that researchers should consider before offering these kinds of results.

According to Jennifer Viberg Johansson, providing genetic risk information may not be as helpful to individuals as one may think. Knowing your genetic make-up is not the same as knowing your own probability for disease. In addition, the kind of genetic risk information you would get when participating in research is less “personalised” than results from a genetic test you would do in a hospital to confirm suspicions that you might be at risk, or have a genetic disorder. Instead, you are given results that are not connected to any symptoms.

Genetic risk information is complex and can be difficult to understand. Jennifer Viberg Johansson has studied how participants in the Swedish population study, SCAPIS, understand genetic risk information, and what kind of information they would like to receive. It turns out that participants think of genetic risk as something that could explain who they are, or where they are from, but also as affecting their future life. To them, learning about genetic risk represents an opportunity to plan their lives and take appropriate precautions to prevent disease.

Answering whether research participants want genetic risk information or not is more complex. Jennifer Viberg Johansson found that people’s willingness to receive genetic risk information could be influenced by the way the question is asked. Risk research has shown that people interpret probabilities in different ways, depending on the outcome and consequences. Her work points in the same direction: probability is not an essential component in peoples’ decision-making in cases where there are ways to prevent disease.

Jennifer Viberg Johansson found that people have difficulties making sense of genetic risk when it is presented in the traditional numeric sense. Having a 10% or 50% risk of developing a condition is hard to interpret. Instead, people tend to understand genetic risk as a binary concept: you either have risk, or not. She suggests that we need to keep this in mind when conducting genetic counselling. According to her, genetic counselling needs to be tailored to people’s often binary perceptions of risk.

“Communicating risk is difficult, and requires that genetic counsellors understand how different people understand the same figures in different ways,” says Jennifer Viberg Johansson.

Facts about SCAPIS: The SCAPIS (Swedish CArdioPulmonary bioImage Study) research programme is a population study involving extensive measurements of 30,000 Swedes aged 50–64. The aim of the project is to find risk markers that allow prediction of who is at risk of cardiopulmonary disease, and prevention of this disease before it occurs. The study is a collaboration among six university hospitals in Sweden, funded primarily by the Swedish Heart-Lung Foundation.

Jennifer Viberg Johansson (2018) Individual Genetic Research Results - Uncertainties, Conceptions, and Preferences, Uppsala: Acta Universitatis Upsaliensis

For more information, please contact: Jennifer Viberg Johansson, Department of Public Health and Caring Sciences, Centre for Research Ethics & Bioethics (CRB), email: jennifer.viberg@crb.uu.se  tel: + 46 70-5755981

Uppsala University -- quality, knowledge, and creativity since 1477
World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

Should researchers inform research participants, if they discover genetic disease risks in the participants? The value of complex genetic risk information for individuals is uncertain. In a PhD thesis from Uppsala University, Jennifer Viberg Johansson suggests that this uncertainty needs to be acknowledged by both geneticists and ethicists.

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Bravery cells found in the hippocampus

Press Releases   •   Sep 07, 2018 10:00 BST

Why do some people comfortably walk between skyscrapers on a high-wire or raft the Niagara Falls in a wooden barrel whereas others freeze on the mere thought of climbing off escalators in a shopping mall? In a new study, scientists have found that a certain type of cells in the hippocampus play a key role.

People are very different when it comes to trying dangerous or exhilarating things. Even siblings can show dramatic differences in risk-taking behaviour. The neural mechanisms that drive risk-taking behaviour are largely unknown. However, scientists from the Department of Neuroscience of Uppsala University in Sweden and the Brain Institute of the Federal University of Rio Grande do Norte in Brazil have found that some cells in the hippocampus play a key role in risk taking behaviour and anxiety.

In an article published in the journal Nature Communications the authors show that neurons known as OLM cells, when stimulated, produce a brain rhythm that is present when animals feel safe in a threatening environment (for example, when they are hiding from a predator but aware of the predator's proximity). The study, produced by Drs. Sanja Mikulovic, Ernesto Restrepo, Klas Kullander and Richardson Leao among others, showed that anxiety and risk-taking behaviour can be controlled by the manipulation of OLM cells. To find a pathway that quickly and robustly modulates risk-taking behaviour is very important for treatment of pathological anxiety since reduced risk-taking behaviour is a trait in people with high anxiety levels.

Adaptive (or normal) anxiety is essential for survival because it protects us from harm. Unfortunately, in a large number of people, anxiety can be dysfunctional and severely interfere with daily life. In these cases, doctors often rely on antidepressants to help patients recover from the dysfunctional state. However, these drugs act in the entire brain and not only in the areas where it is needed and may therefore have severe side-effects. Thus, to act in a single brain region and in a very specific group of cells to control anxiety may be a major breakthrough in treating anxiety and associated disorders like depression. Another interesting finding in the study is that OLM cells can also be controlled by pharmacological agents. In the past, the same group of scientists have found that OLM cells were the ‘gatekeepers’ of memories in the hippocampus and that these cells were very sensitive to nicotine.

‘This finding may explain why people binge-smoke when they are anxious’, says Dr. Richardson Leao, researcher at the Brain Institute of the Federal University of Rio Grande do Norte and Uppsala University.

The participation of the hippocampus in emotions is much less studied than its role in memory and cognition. In 2014, for example, the Nobel prize was awarded for the discovery of “place cells” that represent a biological GPS and underlie the memories of where we are located in our surroundings. In the past decade, scientists have started to appreciate the role of the hippocampus also in regulating emotions.

‘It is fascinating how different regions of the same brain structure control distinct behaviours and how they interact with each other. Identifying specific circuits that underlie either cognitive or emotional processes is crucial for the general understanding of brain function and for more specific drug development to treat disorders’, says Dr. Sanja Mikulovic, Uppsala University.

The discovery of these neurons and their role in anxiety and risk-taking may open a path for the development of highly efficient anxiolytics and antidepressants without common side-effects, such as apathy.

For more information, please contact:

Klas Kullander, Professor at the Department of Neuroscience, Uppsala University tel: + 46 18-471 45 19, + 46 70-846 7524, email: klas.kullander@neuro.uu.se
Richardson Leao, Research Assistant, Department of Neuroscience, Uppsala University, email: Richardson.Leao@neuro.uu.se

Ventral hippocampal OLM cells control type 2 theta oscillations and response to predator odor, Nature Communications, DOI: 10.1038/s41467-018-05907-w

Uppsala University -- quality, knowledge, and creativity since 1477
World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

Why do some people comfortably walk between skyscrapers on a high-wire or raft the Niagara Falls in a wooden barrel whereas others freeze on the mere thought of climbing off escalators in a shopping mall? In a new study, scientists have found that a certain type of cells in the hippocampus play a key role.

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How sleep loss may contribute to adverse weight gain

Press Releases   •   Aug 23, 2018 08:43 BST

In a new study, researchers at Uppsala University now demonstrate that one night of sleep loss has a tissue-specific impact on the regulation of gene expression and metabolism in humans. This may explain how shift work and chronic sleep loss impairs our metabolism and adversely affects our body composition. The study is published in the scientific journal Science Advances.

Epidemiological studies have shown that the risk for obesity and type 2 diabetes is elevated in those who suffer from chronic sleep loss or who carry out shift work. Other studies have shown an association between disrupted sleep and adverse weight gain, in which fat accumulation is increased at the same time as the muscle mass is reduced – a combination that in and of itself has been associated with numerous adverse health consequences. Researchers from Uppsala and other groups have in earlier studies shown that metabolic functions that are regulated by e.g. skeletal muscle and adipose tissue are adversely affected by disrupted sleep and circadian rhythms. However, until now it has remained unknown whether sleep loss per se can cause molecular changes at the tissue level that can confer an increased risk of adverse weight gain.

In the new study, the researchers studied 15 healthy normal-weight individuals who participated in two in-lab sessions in which activity and meal patterns were highly standardised. In randomised order, the participants slept a normal night of sleep (over eight hours) during one session, and were instead kept awake the entire night during the other session. The morning after each night-time intervention, small tissue samples (biopsies) were taken from the participants’ subcutaneous fat and skeletal muscle. These two tissues often exhibit disrupted metabolism in conditions such as obesity and diabetes. At the same time in the morning, blood samples were also taken to enable a comparison across tissue compartments of a number of metabolites. These metabolites comprise sugar molecules, as well as different fatty and amino acids.

The tissue samples were used for multiple molecular analyses, which first of all revealed that the sleep loss condition resulted in a tissue-specific change in DNA methylation, one form of mechanism that regulates gene expression. DNA methylation is a so-called epigenetic modification that is involved in regulating how the genes of each cell in the body are turned on or off, and is impacted by both hereditary as well as environmental factors, such as physical exercise.

“Our research group were the first to demonstrate that acute sleep loss in and of itself results in epigenetic changes in the so-called clock genes that within each tissue regulate its circadian rhythm. Our new findings indicate that sleep loss causes tissue-specific changes to the degree of DNA methylation in genes spread throughout the human genome. Our parallel analysis of both muscle and adipose tissue further enabled us to reveal that DNA methylation is not regulated similarly in these tissues in response to acute sleep loss,” says Jonathan Cedernaes who led the study.

“It is interesting that we saw changes in DNA methylation only in adipose tissue, and specifically for genes that have also been shown to be altered at the DNA methylation level in metabolic conditions such as obesity and type 2 diabetes. Epigenetic modifications are thought to be able to confer a sort of metabolic “memory” that can regulate how metabolic programmes operate over longer time periods. We therefore think that the changes we have observed in our new study can constitute another piece of the puzzle of how chronic disruption of sleep and circadian rhythms may impact the risk of developing for example obesity,” notes Jonathan Cedernaes.

Further analyses of e.g. gene and protein expression demonstrated that the response as a result of wakefulness differed between skeletal muscle and adipose tissue. The researchers say that the period of wakefulness simulates the overnight wakefulness period of many shift workers assigned to nightwork. A possible explanation for why the two tissues respond in the observed manner could be that overnight wakefulness periods exert a tissue-specific effect on tissues’ circadian rhythm, resulting in misalignment between these rhythms. This is something that the researchers found preliminary support for also in this study, as well as in an earlier similar but smaller study.

“In the present study we observed molecular signatures of increased inflammation across tissues in response to sleep loss. However, we also saw specific molecular signatures that indicate that the adipose tissue is attempting to increase its capacity to store fat following sleep loss, whereas we instead observed signs indicating concomitant breakdown of skeletal muscle proteins in the skeletal muscle, in what’s also known as catabolism. We also noted changes in skeletal muscle levels of proteins involved handling blood glucose, and this could help explain why the participants’ glucose sensitivity was impaired following sleep loss. Taken together, these observations may provide at least partial mechanistic insight as to why chronic sleep loss and shift work can increase the risk of adverse weight gain as well as the risk of type 2 diabetes,” says Jonathan Cedernaes.

The researchers have only studied the effect of one night of sleep loss, and therefore do not know how other forms of sleep disruption of circadian misalignment would have affected the participants’ tissue metabolism.

“It will be interesting to investigate to what extent one or more nights of recovery sleep can normalise the metabolic changes that we observe at the tissue level as a result of sleep loss. Diet and exercise are factors that can also alter DNA methylation, and these factors can thus possibly be used to counteract adverse metabolic effects of sleep loss,” says Jonathan Cedernaes.


For more information, please contact:
Jonathan Cedernaes, M.D., Ph.D. at the Neuroscience Department, Uppsala University. Tel.: +1-312-866-0125, email: jonathan.cedernaes@neuro.uu.se

Cecilia Yates, Press information officer at the Neuroscience Department, Uppsala University. Tel.: +46 704 334 801, email: cecilia.yates@neuro.uu.se

Citation: Cedernaes et al. Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans. Science Advances. 2018;4:eaar8590. (in press)

The researchers are supported by among others AFA Försäkring, the Novo Nordisk Foundation, the Swedish SciLifeLab (e.g. WABI and the Swedish metabolomics center), the Swedish Brain Foundation, the Swedish Research Council, and the Åke Wiberg Foundation.

Uppsala University -- quality, knowledge, and creativity since 1477
World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

In a new study, researchers at Uppsala University now demonstrate that one night of sleep loss has a tissue-specific impact on the regulation of gene expression and metabolism in humans. This may explain how shift work and chronic sleep loss impairs our metabolism and adversely affects our body composition. The study is published in the scientific journal Science Advances.

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Catastrophic floods can trigger human resettlement away from rivers

Press Releases   •   Aug 22, 2018 19:00 BST

A new study by researchers at Uppsala University, published in the journal Science Advances, uses satellite nighttime light data to reveal how flood protection shapes the average distance of settlements from rivers.

Flooding is one of the most damaging natural hazards, and its negative impacts have markedly increased in many regions of the world in recent decades. In the period 1980–2014, floods generated economic losses exceeding USD 1 trillion and caused more than 226,000 casualties. The increasing trend of global flood losses has mainly been attributed to the increasing exposure of people and assets due to rising populations in flood-prone areas.

To understand (spatiotemporal) changes in flood risk, one needs to determine the way in which humans adapt and respond to flood events. For example, societies can cope with floods by reinforcing structural flood protection, implementing early warning systems and building codes, or by moving away from flood-prone areas.

By using satellite nighttime light data, a group of researchers at Uppsala University has been able to discern the relationship between long-term changes in human proximity to rivers (that is, the average distance of human settlement from rivers) and the occurrence of catastrophic flood events, with reference to different levels of structural flood protection (for example, levees and reservoirs/dams). This type of analysis has not been feasible previously because traditional census data are typically aggregated at administrative levels and available on decadal time scales. Thus, census data do not provide useful information needed to explore these relationships.

By focusing on the occurrence of catastrophic flood events (inferred from flood damage) in 16 countries across the globe, with different hydroclimatic and socioeconomic contexts as well as different levels of structural flood protection, the research group found that flood fatalities and economic losses on the country scale are both positively correlated with changes in human proximity to rivers. However, such tendencies are reduced when high levels of flood protection are in place.

More detailed analysis in four hotspot areas confirms these tendencies. Catastrophic flood events may trigger changes in human proximity to rivers.

“We found that societies with low protection levels tend to resettle further away from the river after catastrophic flood events, and that the decrease in human settlements close to the river may have contributed to reduced exposure to future flood events. Conversely, societies with high protection levels show no significant changes in human proximity to rivers,” says Johanna Mård, researcher at the Department of Earth Sciences, Uppsala University.

Societies with high protection levels continue to rely heavily on structural measures, reinforcing flood protection and quickly resettling in flood-prone areas after a flooding event. Although they will be protected from frequent flooding, total protection is not possible, and therefore they remain exposed to low-probability but catastrophic-impact events.

The study reveals interesting aspects of human adaptation to flood risk and offers key insights for comparing different risk reduction strategies. The analysis indicates that flood occurrences can trigger decreasing human proximity to rivers but mainly if societies do not strongly rely on structural protective measures. In addition, this study provides a framework that can be used to further investigate human response to floods, which is relevant as the urbanisation of floodplains continues and puts more people and economic assets at risk.

For more information, please contact:

Johanna Mård, Researcher at the Department of Earth Sciences, Uppsala University, Uppsala, Sweden, johanna.maard@geo.uu.se +46 18 471 3095

Giuliano Di Baldassarre, Professor at the Department of Earth Sciences, Uppsala University, Uppsala, Sweden, Giuliano.dibaldassarre@geo.uu.se 

Johanna Mård, Giuliano Di Baldassarre and Maurizio Mazzoleni (2018) Nighttime light data reveal how flood protection shapes human proximity to rivers, Science Advances, DOI: 10.1126/sciadv.aar5779 

This work was supported by Formas and the European Research Council within the project HydroSocialExtremes led by Giuliano Di Baldassarre, Director of the Centre of Natural Hazards and Disaster Science (www.cnds.se).

Uppsala University -- quality, knowledge, and creativity since 1477
World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

A new study by researchers at Uppsala University, published in the journal Science Advances, uses satellite nighttime light data to reveal how flood protection shapes the average distance of settlements from rivers.

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About Uppsala University

Uppsala University -- quality, knowledge, and creativity since 1477

World-class research and outstanding education of global benefit to society, business, and culture.
Uppsala University is one of northern Europe's highest ranked academic institutions. www.uu.se

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