Integrative Molecular Phenotyping
INTEGRATIVE MOLECULAR
PHENOTYPING
WHEELOCK LABORATORY
DEPARTMENT OF MEDICAL
BIOCHEMISTRY AND BIOPHYSICS
WHEELOCK LABORATORY
DEPARTMENT OF MEDICAL
BIOCHEMISTRY AND BIOPHYSICS
WHEELOCK LABORATORY
DEPARTMENT OF MEDICAL
BIOCHEMISTRY AND BIOPHYSICS
WHEELOCK LABORATORY
DEPARTMENT OF MEDICAL
BIOCHEMISTRY AND BIOPHYSICS
WHEELOCK LABORATORY
DEPARTMENT OF MEDICAL
BIOCHEMISTRY AND BIOPHYSICS
WHEELOCK LABORATORY

KI News

Updated: 1 hour 42 min ago

Rare ‘DNA and RNA jitters’ may explain random mutations

Fri, 13/03/2015 - 20:20
In a new study being published in Nature, researchers present a possible explanation to how seemingly random errors are made in the molecular machinery that copies DNA and produces proteins in a living cell. In a flicker of a second, DNA or RNA bases sometimes make the slightest change to mimic a different base. These rare ‘jitters’ seems to appear at about the same frequency as the DNA copying machinery makes mistakes or the ribosome incorporates new amino acids, which might make them the basis of random changes that drive evolution and diseases like cancer. The molecular process to copy DNA in a living cell is amazingly fast and accurate when it comes to pairing up the correct bases – G with C and A with T – into each new double helix. The ribosome is a high-throughput machinery producing proteins based on a RNA triple matching. These machineries work by recognizing the shape of the right base pair combinations, and discarding those that do not fit together correctly. Yet for approximately every 10,000 to 100,000 bases copied, a mistake is made that if uncorrected will be immortalized in the genome as a mutation. For decades, researchers have wondered how these seemingly random errors are made. Sophisticated technique By using a sophisticated technique called NMR relaxation dispersion, a team of researchers from Duke University and Karolinska Institutet could witness DNA bases making the slightest of changes – shifting a single atom from one spot to another or simply getting rid of it altogether – to temporarily mimic the shape of a different base. These ‘quantum jitters’ are exceedingly rare and only flicker into existence for a thousandth of a second, and also appears at about the same frequency that the DNA copying machinery makes mistakes or the ribosome adds the wrong amino acid. According to the researchers, it seems like structure of DNA is inherently tailored to allow mistakes to happen at a certain level. Without these errors life would not have evolved. On the other hand, with too many jitters our genes would mutate out of control.  Participating in this study from Karolinska Institutet did Dr. Katja Petzold, Principal investigator at the Department of Medical Biochemistry and Biophysics. Study leader has been Dr. Hashim Al-Hashimi from Duke University. The investigation was funded by an NIH grant and an Agilent Thought Leader Award. This news article is partly a rewrite from a press release issued by Duke University. Learn more about this research on the Futurity website Publication Visualizing transient Watson–Crick-like mispairs in DNA and RNA duplexes Isaac J. Kimsey, Katja Petzold, Bharathwaj Sathyamoorthy, and Hashim M. Al-Hashimi Nature, online 11 March 2015, doi:10.1038/nature14227

Brain training and healthy lifestyle may slow down cognitive decline

Thu, 12/03/2015 - 10:10
A comprehensive programme providing elderly people at risk of dementia with healthy eating guidance, exercise, brain training, and management of metabolic and vascular risk factors appears to slow down cognitive decline, according to a new randomised controlled trial lead from Karolinska Institutet. The study, which is published in The Lancet, is based on data from 1260 people from Finland and is the largest of its kind ever. In the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) study, Swedish and Finnish scientist assessed the effects on brain function of a comprehensive intervention aimed at addressing some of the most important risk factors for age-related dementia, such as high body-mass index and heart health. 1260 people from across Finland, aged 60–77 years, were included in the study, with half randomly allocated to the intervention group, and half allocated to a control group, who received regular health advice only. All of the study participants were deemed to be at risk of dementia, based on standardised test scores.  The intensive intervention consisted of regular meetings over two years with physicians, nurses, and other health professionals.  Participants were given comprehensive advice on maintaining a healthy diet, exercise programmes including muscle and cardiovascular training, brain training exercises, and management of metabolic and vascular risk factors through regular blood tests, and other means. After two years, study participants’ mental function was scored using a standard test, the Neuropsychological Test Battery (NTB), where a higher score corresponds to better mental functioning. Even more striking Overall test scores in the intervention group were 25 percent higher than in the control group. For some parts of the test, the difference between groups was even more striking; for executive functioning (the brain’s ability to organise and regulate thought processes) scores were 83 percent higher in the intervention group, and processing speed was 150 percent higher.  Based on a pre-specified analysis, the intervention appeared to have no effect on patients’ memory.  However, based on post-hoc analyses, there was a difference in memory scores between the intervention and control groups. The study was led by Professor Miia Kivipelto, MD, PhD, at Karolinska Institutet’s Department of Neurobiology, Care Sciences and Society, also affiliated to the Aging Research Centre in Stockholm as well as the National Institute for Health and Welfare in Helsinki, Finland and University of Eastern Finland. Funding bodies were, amongst others, the Academy of Finland, La Carita Foundation, Alzheimer Association, Alzheimer’s Research and Prevention Foundation, Juho Vainio Foundation, Novo Nordisk Foundation, Finnish Social Insurance Institution, Ministry of Education and Culture, Salama bint Hamdan Al Nahyan Foundation, and Axa Research Fund, EVO grants, Swedish Research Council, Swedish Research Council for Health, Working Life, and Welfare, and af Jochnick Foundation (full list in the article). This news article is based on a press release from The Lancet. Publication  A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial Tiia Ngandu, Jenni Lehtisalo, Alina Solomon, Esko Levälahti, Satu Ahtiluoto, Riitta Antikainen, Lars Bäckman, Tuomo Hänninen, Antti Jula, Tiina Laatikainen, Jaana Lindström, Francesca Mangialasche, Teemu Paajanen, Satu Pajala, Markku Peltonen, Rainer Rauramaa, Anna Stigsdotter-Neely, Timo Strandberg, Jaakko Tuomilehto, Hilkka Soininen, and Miia Kivipelto The Lancet, Published Online March 12, 2015 http://dx.doi.org/10.1016/ S0140-6736(15)60461-5

Karolinska Institutet launches a MOOC in e-health

Wed, 11/03/2015 - 08:08
Karolinska Institutet is now launching a massive open online course (MOOC) in the subject e-health. The course is being delivered via the international education group edX. Karolinska Institutet has been offering a master's programme in e-health for the past five years and will now also be offering a MOOC in the field of e-health (health informatics). In simple terms, the subject is about building bridges between medicine and technology and making information management in health and social care both safe and effective. The idea of the course is to offer students from all over the world an introduction to the field of e-health and its opportunities and challenges from different perspectives. The MOOC will give students an understanding of what health informatics is, and how it works. “IT projects in the healthcare sector require substantial expertise regarding the needs of the medical sector, as well as an understanding of the strengths and weaknesses of the technology. E-health can improve many aspects of the healthcare sector, but more insight is needed into the inherent problems of this area. We will be providing this knowledge in the course”, says course coordinator Professor Sabine Koch. The e-health MOOC begins on the 22 April 2015. Read more about the MOOC in eHealth.

How blood group O protects against malaria

Tue, 10/03/2015 - 07:07
It has long been known that people with blood type O are protected from dying of severe malaria. In a study published in Nature Medicine, a team of Scandinavian scientists explains the mechanisms behind the protection that blood type O provides, and suggest that the selective pressure imposed by malaria may contribute to the variable global distribution of ABO blood groups in the human population. Malaria is a serious disease that is estimated by the WHO to infect 200 million people a year, 600,000 of whom, primarily children under five, fatally. Malaria, which is most endemic in sub-Saharan Africa, is caused by different kinds of parasites from the plasmodium family, and effectively all cases of severe or fatal malaria come from the species known as Plasmodium falciparum. In severe cases of the disease, the infected red blood cells adhere excessively in the microvasculature and block the blood flow, causing oxygen deficiency and tissue damage that can lead to coma, brain damage and, eventually death. Scientists have therefore been keen to learn more about how this species of parasite makes the infected red blood cells so sticky. It has long been known that people with blood type O are protected against severe malaria, while those with other types, such as A, often fall into a coma and die. Unpacking the mechanisms behind this has been one of the main goals of malaria research. A team of scientists led from Karolinska Institutet in Sweden have now identified a new and important piece of the puzzle by describing the key part played by the RIFIN protein. Using data from different kinds of experiment on cell cultures and animals, they show how the Plasmodium falciparum parasite secretes RIFIN, and how the protein makes its way to the surface of the blood cell, where it acts like glue. The team also demonstrates how it bonds strongly with the surface of type A blood cells, but only weakly to type O. Conceptually simple Principal investigator Mats Wahlgren, a Professor at Karolinska Institutet’s Department of Microbiology, Tumour and Cell Biology, describes the finding as “conceptually simple”. However, since RIFIN is found in many different variants, it has taken the research team a lot of time to isolate exactly which variant is responsible for this mechanism. “Our study ties together previous findings”, said Professor Wahlgren. “We can explain the mechanism behind the protection that blood group O provides against severe malaria, which can, in turn, explain why the blood type is so common in the areas where malaria is common. In Nigeria, for instance, more than half of the population belongs to blood group O, which protects against malaria.” The study was financed by grants from the Swedish Foundation for Strategic Research, the EU, the Swedish Research Council, the Torsten and Ragnar Söderberg Foundation, the Royal Swedish Academy of Sciences, and Karolinska Institutet. Except Karolinska Institutet, co-authors of the study are affiliated to Stockholm University, Lund University, Karolinska University Hospital, and the national research facility SciLifeLab in Sweden, and to the University of Copenhagen in Denmark and University of Helsinki in Finland. Mats Wahlgren is a shareholder and board member of drug company Dilaforette AB, which is working on an anti-malaria drug. The company was founded with support from Karolinska Development AB, which helps innovators with patent-protected discoveries reach the commercial market. Publication RIFINs are Adhesins Implicated in Severe Plasmodium falciparum Malaria Suchi Goel, Mia Palmkvist, Kirsten Moll, Nicolas Joannin, Patricia Lara, Reetesh Akhouri, Nasim Moradi, Karin Öjemalm, Mattias Westman, Davide Angeletti, Hanna Kjellin, Janne Lehtiö, Ola Blixt, Lars Ideström, Carl G Gahmberg, Jill R Storry, Annika K. Hult, Martin L. Olsson, Gunnar von Heijne, IngMarie Nilsson and Mats Wahlgren  Nature Medicine, AOP 9 March 2015, doi: 10.1038/nm.3812

New findings on ‘key players’ in brain inflammation

Fri, 06/03/2015 - 09:09
Inflammation is a natural reaction of the body’s immune system to an aggressor or an injury, but if the inflammatory response is too strong it becomes harmful. Inflammatory processes occur in the brain in conjunction with stroke and neurological diseases such as Alzheimer’s and Parkinson’s disease. Researchers from Lund University and Karolinska Institutet in close collaboration with University of Seville have presented new findings about some of the ‘key players’ in inflammation. In the long term, these findings could lead to new treatments.  One of these key players is a receptor called TLR4. The receptor plays such an important role in the body’s innate immune system that the researchers who discovered it were awarded the 2011 Nobel Prize in Physiology or Medicine. The other key player is a protein called galectin-3, which is absent in healthy brains but present in a brain suffering ongoing inflammation. Researchers have now demonstrated that galectin-3 is secreted by microglial cells, a type of immune cell in the brain. The protein binds to the TLR4 receptor and amplifies the reactions that lead to inflammation. More galectin-3 is produced and binds to the immune cells, and the immune response is further intensified in a self-sustaining process. Various different methods The study, which is published in the journal Cell Reports, demonstrates the importance of the link between the two ‘key players’ using various different methods and in laboratory tests, animal experiments and human trials. The researchers have shown that mice genetically modified to be incapable of synthesising galectin-3 show a lower inflammatory response and less brain damage after model mimicing a heart attack. Mice with a model of Parkinson’s disease also suffer less brain damage if they do not have the gene for galectin-3. Researchers also observed the interaction between galectin-3 and TLR4 in the brains of people who died of a stroke. First study-author Miguel Angel Burguillos is currently working at Queen Mary University of London, but carried out the work on galectin-3 and TLR4 during his time as a postdoctoral fellow at Lund University and Karolinska Institutet. The research in Lund has been led by Tomas Deierborg and at Karolinska Institutet by Bertrand Joseph. The University of Seville also participated in the research. This work has been supported by the A.E. Berger Foundation, the Bergvall Foundation, the Crafoord Foundation, the G & J Kock Foundation, the Gyllenstiernska Krapperup Foundation, Lars Hierta Memorial Foundation, Proyecto de Excelencia from Junta de Andalucia, the Royal Physiographic Society in Lund, Spanish Ministerio de Ciencia y Tecnología, the Swedish Childhood Cancer Society, the Swedish Parkinson Foundation, the Swedish Research Council, the Swedish Strategic Research Area MultiPark at Lund University, the Swedish National Stroke Foundation, and the Wiberg foundation. Read more about the study on the website of Queen Mary University of London Publication Microglia-secreted Galectin-3 acts as a Toll-Like Receptor-4 ligand and contributes to microglial activation  Miguel Burguillos, Martina Svensson, Tim Schulte, Antonio Boza-Serrano, Albert Garcia-Quintanilla, Edel Kavanagh, Martiniano Santiago, Nikenza Viceconte, Maria Jose Oliva-Martin, Ahmed Osman, Emma Salomonsson, Lahouari Amar, Annette Persson, Klas Blomgren, Adnane Achour, Elisabet Englund, Hakon Leffler, Jose Luis Venero, Bertrand Joseph, Tomas Deierborg Cell Report, online 5 March 2015, DOI: http://dx.doi.org/10.1016/j.celrep.2015.02.012  

Helping researchers onto the commercial market

Wed, 04/03/2015 - 09:09
Taking a good idea from the lab to the market can seem an insurmountable task. But help is at hand. Gustaf Öqvist Seimyr and Mattias Nilsson Benfatto at KI’s Marianne Bernadotte Centre have been supported by KI Innovations all the way from the drawing board to a pitch for venture capitalists at SEB. ​“Nervous? No, to be honest, we were so well-prepared,” says Gustaf Öqvist Seimyr. He and Mattias Nilsson Benfatto have developed a method for discovering dyslexia in primary school children. “We felt that we simply had to bring our results out into the schools, which is where they’ll be of benefit,” says Dr Öqvist Seimyr. First of all, they were required to fill out an IDF (invention disclosure form) presenting their idea; then KI Innovations helped them investigate whether it was possible to patent and protect the product. Then followed market research and commercial development with consultant, until it was at last time for the dreaded pitch. A meeting was arranged in November with investors invited by SEB. Five minutes meeting “You get about five minutes and have to follow a set format,” says Dr Öqvist Seimyr. “But it went fine.” According to Åsa Kallas, project manager at KI Innovations, most researchers are not accustomed to launching their ideas as commercial projects. “They’re often focused on lab data to start with, and less on business, of course.” KI Innovations gives them the opportunity to pitch their ideas in a way that investors expect, she adds. “We’ve brought presentations down from 10 minutes to about a minute, even to a 30-second elevator pitch,” says her colleague Christian Krog Jensen, business developer and experienced board member. Work strictly confidentially No one need feel nervous about coming to KI Innovations, he says. “We’re very approachable and good at fishing out the gems,” he says. “We work strictly confidentially and protect the researchers who work with us from dodgy investors.” The entire process can take 18 months, depending on the project. “Can commercialising your research make you rich?” Yes. And no. “Sure, I daresay the odd fortune is made in the end. But most people just want to get their research out to the patients,” says Christian Krog-Jensen.   Text: Jonas Fredén Foto: Gustav Mårtensson

Human gene identified for tolerance to an environmental hazard

Wed, 04/03/2015 - 09:09
Studies conducted at the Karolinska Institutet and Uppsala University in Sweden show that some indigenous groups in the Andes of northern Argentina have increased resistance to arsenic. The researchers also identified the gene that underlies the altered metabolism and protects against exposure to arsenic. This study is the first to show that some humans have genetically adapted to a polluted environment. Arsenic occurs naturally in the bedrock in many places in the world and is one of the most potent carcinogens in our environment. People are exposed mainly through drinking water and food, especially rice and various rice products. People living in the Argentinean Andes have likely been exposed to high levels of arsenic in drinking water for thousands of years. The present study shows that residents who live in this region today have a clearly higher frequency of gene variants that enable the body to efficiently handle arsenic by methylating and excreting a less-toxic arsenic metabolite. By contrast, people who lack the protective gene variant produce a more-toxic arsenic metabolite if they are exposed to arsenic. Other communities in neighboring areas without the same historical arsenic exposure have significantly lower frequencies of the protective gene variant. These researchers have identified changes in the main gene for arsenic metabolism, AS3MT, as the cause of the altered metabolism. Their results suggest that people have adapted to arsenic via an increase in the frequency of protective variants of AS3MT. This study is a striking example of how humans have been able to adapt to local, sometimes harmful, environmental conditions. Those who survived the exposure to arsenic lived longer and had more children; thus, the protective gene variants are very common in some regions of the Andes today. Only a few such examples have previously been described in man. Particularly tolerant to environmental toxicants “Our study shows that there are not only extra-susceptible individuals, but also individuals who are particularly tolerant to environmental toxicants. This phenomenon is probably not unique to arsenic, but also applies to other toxicants in food and the environment, to which humans have been exposed for a long time. The results also highlight the necessity to be observant and not base health risk assessments for chemicals on data from people who may have strong genetic tolerance to the particular chemical", says Karin Broberg, researcher at the Institute of Environmental Medicine at Karolinska Institutet. “Only few other studies have found evidence of local adaptation in humans; for instance adaptation to high altitude conditions and the malaria parasite. This study adds another example of how humans have adapted, in a relatively short time, to tolerate an environmental stressor that they encountered when they settled in a new area", says Carina Schlebusch, researcher at the Department of Ecology and Genetics at Uppsala University. The researchers will now study whether other populations with historical arsenic exposure show an equivalent adaptation, and examine if other toxic substances in the environment can result in increased frequency of genetic variants that provide resistance in humans. This study was supported bySwedish Council for Working Life and Social Research, the Erik Philip Sörensen’s Foundation, EU’s Sixth Framework Programme, the Wenner-Gren Foundations, the Swedish Research Council Formas, and the Swedish Research Council for Science. Genotyping was performed by the SNP&SEQ Technology Platform in Uppsala, which is a part of the national research facility Science for Life Laboratory. Principal investigators are Karin Broberg at Karolinska Institutet, and Mattias Jakobsson at Uppsala University.  Read more about arsenic at IMM’s Risk Web View our press release about this research Publication  Human adaptation to arsenic-rich environments Carina M Schlebusch, Lucie M Gattepaille, Karin Engström, Marie Vahter, Mattias Jakobsson, Karin Broberg Molecular Biology & Evolution, online 3 March 2015, doi: doi: 10.1093/molbev/msv046

Government decides to return human remain

Mon, 02/03/2015 - 12:12
The government has decided to comply with the requests of New Zealand and French Polynesia and return the human crania – three from the former nation and seven from the latter – currently being held by Karolinska Institutet. Now that this decision has been taken, KI can inform the recipients that the crania are to be returned and ask how they would like the handover to be effected. “And then we’ll act accordingly,” says Olof Ljungström at the Unit for medical history and heritage. Karolinska Institutet spent last year preparing the matter of the repatriation of human remains to New Zealand. KI has also been working on drawing up a comprehensive inventory of its collections of non-European material, especially that of indigenous populations over and above the individuals from New Zealand.  Included in the 300-plus non-European individuals are three large collections from Ancient Egypt, pre-conquest Peru and Bronze Age Siberia, as well as a hundred or so crania of various origins. No request has as yet been made for the return of these remains. KI’s cranium collection also contains about 250 Swedish individuals. The remaining 200 or so skulls come from elsewhere in Europe.   More on KI News: "KI debates controversial name"   Read more in a pressrelease from the Swedish Government: "Remains at Karolinska Institutet to be returned"

Bariatric surgery affects risk of pregnancy complications

Thu, 26/02/2015 - 08:08
Bariatric surgery has both a positive and negative influence on the risk of complications during subsequent pregnancy and delivery, concludes a new study from Karolinska Institutet. The results, which are published in the New England Journal of Medicine, indicate that maternal health services should regard such cases as risk pregnancies. Pregnant women with obesity run a higher risk of developing complications during pregnancy and risks of fetal/infant complications are also higher. There has been a sharp rise in the number of women becoming pregnant after bariatric surgery; in 2013 almost 8,000 such operations were performed in Sweden, 80 per cent of which were on women. “The effects of bariatric surgery on health outcomes such as diabetes and cardiovascular disease have been studied, but less is known about the effects on pregnancy and perinatal outcomes,” says the study’s lead author, Kari Johansson, PhD, from the Department of Medicine in Solna. “Therefore we wanted to investigate if the surgery influenced in any way the risk of gestational diabetes, preterm birth, stillbirth, if the baby was small or large for its gestational age, congenital malformations and neonatal death.” Using data from nationwide Swedish health registries, the researchers identified 596 pregnancies to women who had given birth after bariatric surgery between 2006 and 2011. These pregnancies were then compared with 2,356 pregnancies to women who had not been operated upon but who had the same body mass index (BMI, weight divided by height squared) as the first group prior to surgery. Large for gestational age What researchers found was that the women who had undergone surgery were much less likely to develop gestational diabetes – 2% compared to 7% – and give birth to large babies. Just over 22% of women in the comparison group had babies that were large for gestational age, and barely 9% of the operated women. On the other hand, the operated women were twice as likely to give birth to babies who were small for gestational age, and the pregnancies were also of shorter duration. “Since bariatric surgery followed by pregnancy has both positive and negative effects, these women, when expecting, should be regarded as risk pregnancies,” says Dr Johansson. “They ought to be given special care from the maternal health services, such as extra ultrasound scans to monitor fetal growth, detailed dietary advice that includes checking the intake of the necessary post-surgery supplements.” The study was financed by the Swedish Research Council, The Obesity Society, Karolinska Institutet and the Stockholm County Council.  Senior authors of this study are Olof Stephansson and Martin Neovius, both affiliated to the Department of Medicine, Solna.     View our press release about this research Publication Outcomes of Pregnancy in Women with Prior Bariatric Surgery Kari Johansson, Sven Cnattingius, Ingmar Näslund, Nathalie Roos, Ylva Trolle-Lagerros, Fredrik Granath, Olof Stephansson, & Martin Neovius New England Journal of Medicine online 26th February 2015

Junior researcher posts now open to more applicants

Fri, 20/02/2015 - 14:14
Karolinska Institutet is now calling for a second round of applications for junior researcher posts as part of its “career ladder” programme. This time, following criticism from the first round, more people than before will be able to apply. At the start of 2014, the Board of Research announced a career ladder for junior researchers involving three levels of appointment: assistant professor (four years), a two-year extension of existing assistant professorships, and senior researcher (five years). In response to the negative comments that some junior researchers made about how the first round of applications was organised, the Board of Research held discussions with the Junior Faculty, an interest group for postdoc researchers at KI who have not yet been given permanent employment in preparation for this second round. Several amendments to the process have been made: “Firstly, we’ve changed the eligibility criteria,” says Birgitta Henriques Normark, vice dean of recruitment. “Beforehand, applicants were not allowed to be permanently employed at KI. This exclusion condition we’ve now removed. But as regards the four-year assistant professorships, applicants may not already hold that post.” “We consider this a very important improvement that makes it possible for more junior researchers at KI to apply for the posts,” Gonçalo Castelo-Branco, chair of the Junior Faculty. Discussions have also been held since the first round of advertisements on the extended assistant professorships. The Board of Research has decided to advertise this type of post again, a decision that has been welcomed by the Junior Faculty. “In most cases, four years isn’t enough time for assistant professors to amass the experience needed to qualify for the next step in their career and compete for positions with more established researchers,” says Dr Castelo-Branco. There is a possibility that the position of assistant professor might be extended, even if it does not happen this year. “We’re working on it being six years instead,” says Professor Henriques Normark. “We and the Junior Faculty both think that this would be for the better.” On top of this, the Junior Faculty might also want the funding for the positions to be supplemented with proper financial support for the completion of a research programme in order to make the post attractive for top-level national and international junior researchers. But according to Professor Henriques Normark the money is lacking to attach such a financial rucksack to the position. The recruitment drive has been announced to attract leading junior researchers to KI. The advertisements are to be published on 20 February on the KI website, in the journals Science and Nature, and on ResearchGate and universitetsjobb.se. The application deadline is 20 March.   Text: Karin Söderlund Leifler Photo: Gustav Mårtensson   The positions advertised Up to ten assistant professorships, 1 million kronor a year for four years. Up to ten positions of senior researcher (two-year extension of existing assistant professorships), 1 million kronor per year for two years. Up to six positions of senior researcher, 1.2 million a year for five years. Find more about the career positions on ki.se.  

New brain mapping reveals unknown cell types

Fri, 20/02/2015 - 08:08
Using a process known as single cell sequencing, scientists at Karolinska Institutet have produced a detailed map of cortical cell types and the genes active within them. The study, which is published in the journal Science, marks the first time this method of analysis has been used on such a large scale on such complex tissue. The team studied over three thousand cells, one at a time, and even managed to identify a number of hitherto unknown types. “If you compare the brain to a fruit salad, you could say that previous methods were like running the fruit through a blender and seeing what colour juice you got from different parts of the brain,” says Sten Linnarsson, senior researcher at the Department of Medical Biochemistry and Biophysics. “But in recent years we’ve developed much more sensitive methods of analysis that allow us to see which genes are active in individual cells. This is like taking pieces of the fruit salad, examining them one by one and then sorting them into piles to see how many different kinds of fruit it contains, what they’re made up of and how they interrelate.” The knowledge that all living organisms are built up of cells is almost 200 years old. Since the discovery was made by a group of 19th century German scientists, we have also learnt that the nature of a particular body tissue is determined by its constituent cells, which are, in turn, determined by which genes are active in their DNA. However, little is still known about how this happens in detail, especially as regards the brain, the body’s most complex organ. Large-scale single-cell analysis  In the present study, the scientists used large-scale single-cell analysis to answer some of these questions. By studying over three thousand cells from the cerebral cortex in mice, one at a time and in detail, and comparing which of the 20,000 genes were active in each one, they were able to sort the cells into virtual piles. They identified 47 different kinds of cell, including a large proportion of specialised neurons, some blood vessel cells and glial cells, which take care of waste products, protect against infection and supply nerve cells with nutrients. With the help of this detailed map, the scientists were able to identify hitherto unknown cell types, including a nerve cell in the most superficial cortical layer, and six different types of oligodendrocyte, which are cells that form the electrically insulating myelin sheath around the nerve cells. The new knowledge the project has generated can shed more light on diseases that affect the myelin, such as multiple sclerosis (MS). “We could also confirm previous findings, such as that the pyramidal cells of the cerebral cortex are functionally organised in layers,” says Jens Hjerling-Leffler, who co-led the study with Dr Linnarsson. “But above all, we have created a much more detailed map of the cells of the brain that describes each cell type in detail and shows which genes are active in it. This gives science a new tool for studying these cell types in disease models and helps us to understand better how brain cell respond to disease and injury.” Approximately 20 micrometres There are estimated to be 100 million cells in a mouse brain, and 65 billion in a human brain. Nerve cells are approximately 20 micrometres in diameter, glial cells about 10 micrometres. A micrometre is equivalent to a thousandth of a millimetre. The study was carried out by Sten Linnarsson’s and Jens Hjerling-Leffler’s research groups at the Department of Medical biochemistry and Biophysics, in particular by Amit Zeisel and Ana Muños Manchado. It also involved researchers from Karolinska Institutet’s Department of Oncology-Pathology, and Uppsala University. The study was financed with grants from several bodies, including the European Research Council, the Swedish Research Council, the Swedish Cancer Society, the EU’s Seventh Framework Programme, the Swedish Society of Medicine, the Swedish Brain Fund, Karolinska Institutet’s strategic programme for neuroscience (StratNeuro), the Human Frontier Science Program, the Åke Wiberg Foundation and the Clas Groschinsky Memorial Fund. View our press release about this study More about the Linnarsson lab More about the Hjerling-Leffler lab Publication Cell types in the mouse cortex and hippocampus revealed by single-cell RNA-seq Amit Zeisel, Ana B. Muñoz Manchado, Simone Codeluppi, Peter Lönnerberg, Gioele La Manno, Anna Juréus, Sueli Marques, Hermany Munguba, Liqun He, Christer Betsholtz, Charlotte Rolny, Gonçalo Castelo-Branco, Jens Hjerling-Leffler, and Sten Linnarsson Science online 19 February 2015, DOI: 10.1126/science.aaa1934

Brichos protein may prevent brain damage in Alzheimer’s

Mon, 16/02/2015 - 17:17
Researchers at Karolinska Institutet and the universities in Lund and Cambridge have found that fragments from the human Brichos protein have the ability to prevent neuronal and brain damage caused by amyloid-beta in Alzheimer’s disease. The findings are being published in the journal Nature Structural and Molecular Biology. Studies on brain tissue from mice show that the Alzheimer’s disease-peptide amyloid-beta (A-beta) degrades oscillations of the neuronal network in the gamma-frequency band (30-80 Hz), which are important for memory and learning. However, in the current study researchers show that in the presence of Brichos this degradation was completely prevented. The team also studied A-beta in test tubes with and without Brichos, and found that the preventive effects are associated with a highly specific function of this protein. Brichos was found to bind to aggregated forms of A-beta, thereby blocking the surfaces that would otherwise be responsible for generation of neurotoxic activity and cell death. The contributing scientists from Karolinska Institutet were Jenny Presto, Firoz Roshan Kurudenkandy, Henrik Biverstål, Lisa Dolfe, Janne Johansson, and André Fisahn. The study was funded by, amongst other organizations, the chiff Foundation, the Swedish Research Council, the Crafoord Foundation, the Swedish Alzheimer Foundation, the Frances and Augustus Newman Foundation the European Research Council, the Strategic Program in Neurosciences at the Karolinska Institute, the Swiss National Science Foundation, and the Wellcome Trust. Publikation The molecular chaperone Brichos breaks the catalytic cycle that generates toxic Aβ oligomers Samuel I. A. Cohen, Paolo Arosio, Jenny Presto, Firoz Roshan Kurudenkandy, Henrik Biverstål, Lisa Dolfe, Christopher Dunning, Xiaoting Yang, Birgitta Frohm, Michele Vendruscolo, Jan Johansson, Christopher M. Dobson, André Fisahn, Tuomas P. J. Knowles, and Sara Linse Nature Structural & Molecular Biology, advance online publication 16 February 2015, doi: 10.1038/nsmb.2971

Queen Silvia visits Karolinska Institutet in Huddinge

Mon, 16/02/2015 - 16:16
Last Friday the King of Sweden visited Karolinska Institutet in Solna. On Monday 16 February, Queen Silvia came to visit the department of neurobiology, care sciences and society (NVS) at Karolinska Institutet in Huddinge. The queen was welcomed by the board member and head of the department of neurobiology, care sciences and society professor Maria Eriksdotter, in conjunction with a meeting of the board of the Silviahemmet Foundation. She also met representatives from the department in the research areas focused on ageing and dementia disorders. All of the NVS courses and study programmes were presented at the meeting, including the new online master's course in dementia care for physicians that KI offers in collaboration with the Silviahemmet Foundation. The title of “Silvia Doctor” is offered upon completion of the course, as are the titles “Silvia Nurse” or “Silvia Nursing Assistant” after similar study programmes for nurses and nursing assistants. During the queen's visit there was also a presentation of the ongoing production of the online master's course for occupational therapists and physiotherapists focusing on dementia care, which is conducted in collaboration with the Silviahemmet Foundation. The queen also visited a class where she met physiotherapy students and she concluded her visit with a lunch at the NVS. Text: Pia Hellsing Photo: Ulf Sirborn  

KI debates controversial name

Mon, 16/02/2015 - 15:15
When new buildings were erected on KI’s Solna campus in the early 1990s, a laboratory, a street and an auditorium were named after Anders Retzius and his son Gustaf Retzius. A debate is now raging over whether these names should be kept or changed. Both father and son were famous anatomists in the 19th century scientific community and are two of the leading figures in the university’s history. As part of their anatomical research, they collected crania from around the world in the interests of racial science. Many of these countries have now asked to have the skulls returned and KI has been criticised for not handling the matter promptly enough. Last spring, a doctoral student at the Department of Neuroscience raised the issue of Retzius’s problematic links to eugenics in a letter to the vice-chancellor, and suggested that the name be removed from the various places around KI that honour it. Olof Ljungström at the medical history and cultural heritage unit prepared the background material for the university’s reply. We can’t acquit 19th century anatomists of racial science, we can’t whitewash them and simply erase it from the history books. “History needs to be written differently to how it was before,” he says. “The proposer asks, in a way, the right questions. Enough information is available on Retzius for him to start asking questions. If Retzius’s name disappears, people won’t be able to ask such questions any more in this way.” The issue is not a new one, and Olof Ljungström thinks that it will probably return even if the name is removed. “We can’t acquit 19th century anatomists of racial science, we can’t whitewash them and simply erase it from the history books. On the other hand, if we only base our decision on what to do in this situation on what’s problematic, it won’t be the perfect way out either. A working synthesis must include both aspects.” No decision on the name has yet been taken. “We’re planning an open seminar on the question, after which we’ll be considering the naming issue,” says University Director Per Bengtsson. “We must take into account the associations a name has, even if this is by no means the complete picture of who Retzius was.” A decision was taken last autumn on several activities for discussing the history of eugenics and racial science at Karolinska Institutet, including an internal seminar at the neuroscience department this spring. “We’re also planning an international symposium, possibly in 2016, on human museum specimens and how they relate to racial science,” says Eva Åhrén at the medical history and cultural heritage unit.   Text: Karin Söderlund Leifler Photo: Gunnar Ask

The King of Sweden visits Karolinska Institutet

Fri, 13/02/2015 - 14:14
On Friday 13 February, the King of Sweden visited Karolinska Institutet. The aim was to learn more about the university’s innovation system, select research areas and the new internet-based global MOOC:s that was launched at KI in 2014. The King was greeted by Vice-Chancellor Anders Hamsten at the entrance to the Aula Medica building and introduced to researchers and teachers who gave a presentation of a few important areas of research. Among other subjects, KI’s innovation system – which offers expert skills within entrepreneurship and business development was discussed. The system is to ensure that innovations and ideas within the field of biomedicine are available and at the disposal of the health services. The King also got to see how large-scale methods have revolutionised research and diagnostics on certain hereditary diseases. He was also given a presentation on the field of regenerative medicine, and of MOOC:s, Massive Open Online Courses. This autumn, KI was the first university in Sweden to offer these open, free-of-charge online courses, and thus earned a position as an important actor on the global education arena.

Promising results for new Alzheimer therapy

Fri, 13/02/2015 - 09:09
Scientists at Karolinska Institutet have evaluated a new Alzheimer’s therapy in which the patients receive an implant that stimulates the growth of a certain type of nerve cell. The results, which are published in the journal Alzheimer's & Dementia, suggest that the introduction of a nerve growth factor can prevent neuronal degradation in Alzheimer’s patients. Patients with Alzheimer’s disease suffer a selective and early breakdown of so-called cholinergic nerve cells, which require a specific nerve growth factor (NGF) – essentially a group of proteins necessary for cell growth and survival – to function. As NGF levels decline, the cholinergic nerve cells begin to degrade and the patient’s condition slowly deteriorates. In an attempt to curb the breakdown of the cholinergic nerve cells, researchers at Karolinska Institutet’s Centre for Alzheimer’s Research and their colleagues at Karolinska University Hospital’s neurosurgery clinic and the Danish biotech company NsGene introduced NGF directly into the brains of Alzheimer’s patients. To do this, they used NGF-producing cell capsules, placing them in the basal fore-brain where the cholinergic cells reside using precision stereotactic surgery. There the capsules, which can easily be removed, release NGF to the surrounding cells in order to prevent their degradation. Presence of specific markers  The study now published in Alzheimer’s & Dementia is based on data from six Alzheimer’s patients. To gauge whether the NGF release had any effect on the cholinergic nerve cells, the researchers assayed the presence of specific markers of functioning cholinergic cells. This cell system communicates using acetylcholine, which in turn produces an enzyme called ChAT (pronounced Cat) that is found both inside and outside the cells. The team therefore developed a method enabling them to measure ChAT in the cerebral spinal fluid for the first time. “Our results show that when the patients received NGF, there was a significant increase in ChAT in the CSF,” says Dr Taher Darreh-Shori, one of the researchers involved in the study. “The patients that exhibited this increase were also those that responded best to the treatment. Our PET scans also showed an increase in cholinergic cell activity and metabolism in the brain.” Retardation of memory impairment In addition, the researchers were able to detect a retardation of memory impairment over time compared with untreated patients. While all this suggests that cholinergic functionality improved in the Alzheimer’s patients who had received NGF therapy, the team adds the caveat that far-reaching conclusions should not be drawn from the results: “The results are promising, but must be treated with circumspection as only a few patients participated in the study,” says principal investigator Professor Maria Eriksdotter. “So our findings will have to be substantiated in a larger controlled study using more patients.” The NGF-producing cell capsule method (Encapsulated cell biodelivery) was developed by NsGene. The paper’s first authors are doctoral students Azadeh Karami and Helga Eyjolfsdottir. The study was financed by grants from several sources, including the Foundation Olle Engkvist Byggmästare, Åke Wiberg’s Foundation, Åhlén Foundation, the Dementia Fund, the Odd Fellows, the King Gustaf V and Queen Victoria Free Mason Foundation, Karolinska Institutet’s strategic research programme in neuroscience (StratNeuro), the Swedish Research Council and Swedish Brain Power (for a full list of financiers see the published article). View our press release about this study Publication Changes in CSF cholinergic biomarkers in response to cell therapy with NGF in patients with Alzheimer’s disease Karami, A., H. Eyjólfsdóttir, S. Vijayaraghavan, G. Lind, P. Almqvist, A. Kadir, B. Linderoth, N. Andreasen, K. Blennow, A. Wall, E. Westman, D. Ferreira, M. Kristoffersen-Wiberg, L. O. Wahlund, Seiger, Å. , A. Nordberg, L. Wahlberg, T. Darreh-Shori, M. Eriksdotter Alzheimer’s & Dementia, uncorrected proof online 9 February 2015, doi 10.1016/j.jalz.2014.11.008

New knowledge on cell differentiation mechanisms

Thu, 12/02/2015 - 20:20
The international FANTOM5 consortium, including scientists from Karolinska Institutet, has made major strides toward resolving common mechanisms in cell differentiation. In a new study published in the journal Science, they describe more than 400 stages of cell maturation in 33 different cell types in mouse and human. The FANTOM5 is led from the research institute RIKEN in Japan, and gathers scientists from 114 institutions around the world. In this large-scale project, scientists have created an atlas that shows which different genes that are used in virtually all cell types that humans are composed of. The atlas was launched in March 2014, and attracted attention worldwide. In the current study, the team has made an effort to map the transcriptional changes that occur when cells differentiate from one cell type to another cell type, both during cell development and in response to stresses or infection. Researchers investigated differentiation time series in 19 human and 14 mouse cell types, in total more than 400 stages of cell maturation. The technology used made it possible to see exactly where the genes are ‘read’ from the DNA, and to find the regulatory switches called ‘enhancers’ that are responsible for activating the reading of genes in the appropriate cells at the correct time point. Shared patterns The team found that just after the cells start to differentiate or react to stimuli, there are shared patterns in gene and enhancer activity between all the studied cells types. Enhancers are activated in the first 15 minutes after stimuli. At 30 to 100 minutes, the enhancers activate a specific type of regulatory genes (transcription factors), which in turn have the ability of activated other genes and over time forming a cascade of changes. These patterns were shared across all the studied cells, but the individual genes and enhancer that made up the patterns were specific to each cell type. This indicates that the team has found underlying rules for how cells differentiate that applies to all mammals, knowledge which may be an important part of the puzzle in understanding how the human body works in health and disease. The FANTOM5 consortium is led by Professor Yoshihide Hayashizaki at RIKEN, and  includes over 500 scientists from more than 20 countries over the whole world. The researchers from Karolinska Institutet who are members of the consortium are Andreas Lennartsson, Michelle Rönnerblad and Carsten Daub at the Department of Biosciences and Nutrition, and Peter Arner, Anna Ehrlund and Niklas Mejhert at the Department of Medicine, Huddinge. FANTOM5 was made possible through a grant from the Japanese Ministry of Education, Culture, Sports, Science and Technology, while the EU and a number of other research funders have also contributed. View a press release from RIKEN about this research Publication Transcribed enhancers lead waves of coordinated transcription in transitioning mammalian cells Erik Arner, Carsten Daub, Kristoffer Vitting-Seerup, Robin Andersson et al, Berit Lilje, Finn Drablos, Andreas Lennartsson, Michelle Rönnerblad et al. Science, online 12 February 2015, doi: 10.1126/science.1259418 List of all FANTOM publications

KI News special report: vice-chancellor of KI meets the new hospital director Melvin Samsom

Thu, 12/02/2015 - 14:14
The one has been vice-chancellor of KI for two years, the other CEO of Karolinska University Hospital for just four months. Here in an interview they talk about the challenges they share and about integrating research and education with academic healthcare and innovation. What are the main challenges facing the partnership between KI and the university hospital? Anders Hamsten: In general, it’s about how we’re to integrate the university and the university hospital more effectively. This is our main challenge, and one that can be broken down into different parts. One important part is the issue of leadership. In both organisations we talk a great deal about the importance of good leadership, academic leadership for knowledge-intensive, complex organisations. It’s also important to nurture a common leadership that works in both environments. Another part of the challenge is organisational: to harmonise our respective structures so that they dovetail better. And then, of course, we have the issues of financing all our joint activities, and to work together to improve the quality of academic healthcare. Another part of the challenge is organisational: to harmonise our respective structures so that they dovetail better. Melvin Samsom: I’d prefer to start at the other end: what are the options and possibilities available to us? KI and the university hospital together are uniquely endowed: such a renowned university next to such a large university hospital on two campuses. If we can coordinate our strategies, we will be in a strong position to drive the development of future healthcare systems, amongst other things. We both agree that our partnership is not operating at its optimum, and there is much to be gained by improving it. Resources will always be in short supply, but there is a lot we can improve using what we currently have at our disposal. One example is to take the areas in which KI excels and make them areas in which the university hospital also excels, so that we can benefit more from each other. Another important issue is the brand. To much of the world, both our organisations are “Karolinska”. It’s a powerful brand that we should take great of. In which areas should the two organisations integrate more? Anders Hamsten: In all core operations. As I see it, there are four areas: research, education, academic healthcare and, as the fourth point, innovation, implementation and knowledge dissemination. But to achieve this, we need to work with a fifth area: a common infrastructure. This is now being built up at both KI and the university hospital, and it’s something of a challenge to make sure that it’s designed in a way that favours our collaboration. What else does the infrastructure include? Melvin Samsom: It’s easy to think of material investments, but most of all I want to emphasise the importance of soft infrastructure: the people. The new environments being built are, of course, important, and we have a desperate need for new IT systems, but it’s still more important to find the right people – people who are in sync with us and how we’re changing. This has been one of the pivotal questions of our conversations: how can we get the right people in the right place? The ones who can tackle the four areas that Anders mentioned: academic healthcare, research, education and innovation. I know that this hasn’t always been the case at the hospital and that healthcare has been our main focus. This, however, will change over the coming years. What will happen to your education programmes? Anders Hamsten: One interesting question is to identify the most suitable clinical learning environments for our students: how relevant they are to our different programmes, what highly specialised care is done there, what the mix of the major disease categories looks like, what supervisory resources are available, and so on. Since the patient flow changes quite quickly, this will be a challenge. Melvin Samsom: We need to look at it from the students’ vantage point. The educational world is changing rapidly, and it’s now possible to study at universities in different countries by distance. Young people don’t want an education that assumes they’ll stay working in the same field until they retire. Do we offer the flexibility they’re looking for? Another question is: do we have the right patient groups at the university hospital for their education? What other caregivers need to be engaged to give the students proper clinical experience? Is it harder now to combine healthcare production with education and research? Melvin Samsom: I’d say it is. It’s more expensive to treat patients at a university hospital than in other places, and since we’re publicly financed, we need to justify why this is the case and why a patient has to be treated at this higher cost instead of somewhere else. Sometimes it’s because we’re the only ones with the competence. It can also be because the treatment of that patient group is closely linked to education or research. Uncertainty about the magnitude of this extra cost and what we get for it easily causes problems when healthcare is to be combined with education and research. Anders Hamsten: And to that I’d like to add the question of leadership. Not only the leadership of our respective organisations, whereby we both want to reinforce the academic leadership, but also political leadership, which must help to ensure that the university hospital receives the resources it needs. Without them, both healthcare and the education of the next generation of medical staff will suffer. Our political leaders must be explicit in making it clear that the university hospital plays a special role amongst all the hospitals and specialist clinics in the Stockholm region. KI and the university hospital must remain mutually critical, in a constructive sense. Melvin Samsom: Patient flows are changing, and the university hospital will be changing its patient mix. We will be focusing on more complex, academic healthcare that we have had, the kind of healthcare that demands close collaboration with research and education. We need to look critically at which patients require treatment at the university hospital and which can be treated more cheaply elsewhere. Because of this we have to cooperate in a more organised way with a network of other caregivers operating around us. You seem to agree on most things. Is there anything you don’t see eye to eye on? Melvin Samsom: It’s true that we’ve found much common ground. The fact that we have similar backgrounds – we’re both clinicians, researchers and managers – has no doubt helped to make it easy for us to agree. I think we have very similar ideas about our common goal. But of course then, when the job has to get done, lots of questions will crop up along the way that we’ll have different opinions about. Which is good. KI and the university hospital must remain mutually critical, in a constructive sense. It’s through such criticism that academic environments advance. Text: Anders Nilsson Photo: Gustav Mårtensson

New edition of Medical Science

Thu, 12/02/2015 - 14:14
Once every year a selection of the best articles are translated into English and collected in an English issue of Medicinsk Vetenskap. Order your issue of Medical Science 2015 and read articles about cooling treatments, obesity, cardiac care and many other things.  Browse the 2015 issue of Medical Science Order the 2015 issue of Medical Science The magazine Medical Science       A cool treatment saves the brain Are you a shiverer? Then you cope better with the cold. But without protective mechanisms, the body’s core temperature quickly drops and there is a risk of frostbite. At the same time, a body that is cooled down copes better without oxygen, something researchers can utilise to save lives.

One scientist, many hats – meet researcher Gabrielle Paulsson-Berne

Thu, 12/02/2015 - 14:14
The duties and roles one has to combine at work tend to increase over the years, as does the scope of one’s spheres of responsibility. Often it’s wonderful, but sometimes it gets too much. As atherosclerosis researcher Gabrielle Paulsson-Berne knows. Like most of her senior colleagues, she has several hats to juggle in her work at KI. It’s great being a multitasker. And frustrating. And essential. Fifteen years ago, Dr Paulsson-Berne was the one most au fait with her research group’s lab at the CMM (Centre for Molecular Medicine); today, as senior research associate, she rarely even finds time to take part in the experiments. These days she is a researcher, a supervisor, a deputy group leader, a course coordinator, a teacher and a member of various committees and networks at KI. Amongst other things. She usually has to delegate her lab work to postdocs and doctoral students. “Although last Monday I made time for it. It’s a special feeling to meet three or four people early in the morning and then to spend all day in the lab. It’s nice to see how just how much my fingers remember!” Researches the affects of atherosclerosis Dr Paulsson-Berne researches into how the immune system affects atherosclerosis, and has teamed up with vascular surgeons at the university hospital to create BIKE, a biobank containing surgically removed plaque (accumulations of matter that constrict the arteries) from patients with atherosclerosis. “From each of the samples we’ve gathered data on 20,000 genes, on whether they’re turned on or off. We’re now following up the leads we’ve found there in the search for mechanisms involved in the process of plaque spread.” Started the biomedicine Master's programme In 2007 she was in charge of setting up the “Frontiers in translational medicine” course on the newly started biomedicine Master’s programme, and she has been course coordinator ever since. The course is held every autumn semester, and her intention was to spend more time in the spring on her research. But things haven’t quite turned out that way. “Putting together a major course is a complex thing. Arranging such a large schedule, recruiting teachers, updating the course contents, pedagogical development…all this has to take place between courses.” All the general work she has to do with her research team also competes with her own research. This includes arranging its seminar series, organising the internal structures it needs to operate, being the senior backbone, the glue, that holds the team together over time while junior researchers do their time and then move on, etc. Dr Paulsson-Berne has been with the group since it started; she was recruited as a postdoc in the mid-1990s. Likes doing different things “The difficult thing is having time for everything. But I like doing many different things, and it seems as if all of us seniors at KI are multitaskers. There are many of us who just can’t help taking on new tasks – it’s fun and rewarding to have a finger in many pies. You learn so much, gain a huge contact network, and meet people from all over the world. I’d say that many of us would find it boring to do the same thing all the time. “But then the university is dependent on us multitaskers. We’re the ones who get insight into what’s going on elsewhere in the organisation, who discover points of convergence, and make different areas of the university cross-fertilise each other. Being a multitasker is also a way of surviving in the university environment. Sticking to just one thing makes you very vulnerable.” She goes on: “But it’s easy to take on too many duties. Because they’re fun and important, because I appreciate being asked, and because, like many of my colleagues, I’m an inveterate time optimist. I’m also a team person, you see. There’s no way I could sit on my own. KI is a wonderful crucible of enthusiastic nerds from all over the world. There’s something seductive in that.” Text: Anders Nilsson Photo: Gunnar Ask

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