KI News

An international team of researchers led from Karolinska Institutet and Science for Life Laboratory have found a new way of halting the growth of breast cancer cells. In their study, which is published in Nature Communications, the researchers explore a new way to starve cancer cells from their molecular energy source. They hope that their discoveries can be further developed into a new way of treating breast cancer, and possibly other types of cancer. Breast and prostate cancer are the most common forms of cancer in Sweden, and the number of cases is increasing yearly. Often, these tumours use hormones, such as oestrogen or testosterone, to drive their growth, and thus normal treatments aim to block the activity of these hormones. While modern treatments are often successful, cancers can also become resistant to these treatments and develop new ways of propagating. In the current study, the researchers confirmed that hormone-driven breast cancer cells use a newly discovered protein, NUDT5, to produce energy in the cell nucleus. This nuclear energy source provides energy for the expression of genes that drive cancer growth. In the next stage of their research, they developed a molecule able to block NUDT5 activity and thus deprive the cancer cells of their means of nuclear energy production. They demonstrated that this new molecule can stop the growth of breast cancer cells in isolated laboratory experiments. Can hopefully help improve treatment options The original purpose of the project was to understand the biological function of NUDT5, but this has now shifted and the aim is to progress NUDT5 inhibitors towards clinical testing where these molecules can hopefully help improve treatment options for cancer patients. “They’re exciting findings, but the path ahead is long since we still know very little about how NUDT5 operates,” says Professor Thomas Helleday at the Department of Medical Biochemistry and Biophysics, Karolinska Institutet. The study was led by researchers at Karolinska Institutet and SciLifeLab in association with colleagues from Stockholm and Uppsala universities and a team of Spanish researchers. Its main sources of funding were the Torsten Söderberg and Ragnar Söderberg foundations and the Knut and Alice Wallenberg Foundation. Publication “Targeted NUDT5 inhibitors block hormone signaling in breast cancer cells” Page BDG, Valerie NCK, Wright RHG, Wallner O, Isaksson R, Carter M, Rudd SG, Loseva O, Jemth A-S, Almlöf I, Font-Mateu J, Llona-Minguez S, Baranczewski P, Jeppsson F, Homan E, Almqvist H, Axelsson H, Regmi S, Gustavsson A-L, Lundbäck T, Scobie M, Strömberg K, Stenmark P, Beato M, Helleday T Nature Communications, online 17 January 2018, doi: 10.1038/s41467-017-02293-7

Researchers at Karolinska Institutet report that cholesterol metabolites cause specific immune cells in the large intestine to move, which lies behind the formation of the immune system's important lymphoid tissue in the intestine. The study, published in the journal Immunity, paves the way for a new possible treatment for patients with inflammatory bowel disease. Inflammatory bowel disease is a common and severe disease that has no cure. Normally, the immune cells of the gut accumulate and communicate with each other in the lymphoid tissue. But, for those who have autoimmune inflammatory bowel disease, such as ulcerative colitis, the lymphoid tissue can react to the body's own cells and cause chronic inflammation. Hitherto, it has not been known which signals control the formation of the lymphoid tissue in the large intestine. But, now scientists at Karolinska Institutet have discovered that cholesterol metabolites, called oxysterols, stimulate specific immune cells in the large intestine, called innate lymphoid cells (ILCs), to form lymphoid tissue in both health and in disease. “We have discovered that ILCs use a surface protein called GPR183 to sense the oxysterols, which attracts ILCs to specific sites in the large intestine where lymphoid tissue is formed,” says Tim Willinger, researcher at Karolinska Institutet’s Department of Medicine in Huddinge, who has led the study. “Our findings are relevant to humans because inflammatory lymphoid tissue contributes to tissue damage in inflammatory bowel disease. We have discovered that patients with ulcerative colitis have higher levels of oxysterol-producing enzymes than healthy controls. The results indicate that oxysterols and GPR183 are involved in ulcerative colitis,” he says. One way to treat inflammatory bowel disease could, therefore, be to attempt to inhibit GPR183 or oxysterol production. “This treatment option is attractive, because GPR183 belongs to a group of molecules that are excellent targets for drug treatment,” says Dr Willinger. The study was financed by a Junior Investigator Research Grant from the Center for Innovative Medicine (CIMED) from Karolinska Institutet/Stockholm County Council. Publication ”Oxysterol sensing through the receptor GPR183 promotes the lymphoid tissue-inducing function of innate lymphoid cells and colonic inflammation”. Johanna Emgård, Hana Kammoun, Bethania García-Cassani, Julie Chesné, Sara M. Parigi, Jean-Marie Jacob, Hung-Wei Cheng, Elza Evren, Srustidhar Das, Paulo Czarnewski, Natalie Sleiers, Felipe Melo-Gonzalez, Egle Kvedaraite, Mattias Svensson, Elke Scandella, Matthew R. Hepworth, Samuel Huber, Burkhard Ludewig, Lucie Peduto, Eduardo J. Villablanca, Henrique Veiga-Fernandes, João P. Pereira, Richard A. Flavell, Tim Willinger. Immunity, online 16 January 2018.

The failure of drugs such as SSRIs, used to treat depression, can be a result of genetic variations in patients. Variations within the gene that encodes the CYP2C19 enzyme results in extreme differences in the levels of escitalopram achieved in patients, according to a new study published in The American Journal of Psychiatry. Prescribing the dose of escitalopram based on a patient’s specific genetic constitution would greatly improve therapeutic outcomes. The study was conducted at Karolinska Institutet in association with researchers at Diakonhjemmet Hospital in Oslo. Pharmaceutical treatment of depression commonly makes use of selective serotonin reuptake inhibitors (SSRIs) of which escitalopram is the most frequently administered clinically. However, escitalopram therapy is currently limited by the fact that some patients do not respond well to the drug, while others develop adverse reactions requiring discontinuation of treatment. In order to individualise drug therapy, researchers are attempting to establish genetic biomarkers that can predict an individual’s response to drugs. In a recent study, it was discovered that variation in the gene encoding the enzyme responsible for escitalopram metabolism (CYP2C19) is very important in this respect. Individuals with a variant of the gene promoting increased enzyme expression had blood levels of escitalopram too low to impact the depression symptoms, whereas patients with a defective CYP2C19 gene reached drug levels which were too high. Overall, one third of the 2,087 study participants achieved escitalopram blood levels that were either too high or too low. Many patients switched to other drugs Interestingly, the researchers found that 30 per cent of the patients carrying gene variants causing excessive or inadequate enzyme levels switched to other drugs within one year, in contrast with only 10 to 12 per cent of patients carrying the common gene. “Our study shows that genotyping of CYP2C19 could be of considerable clinical value in individualising doses of escitalopram so that a better all-round antidepressive effect could be achieved for the patients,” says Professor Magnus Ingelman-Sundberg at Karolinska Institutet’s Department of Physiology and Pharmacology who led the study together with Professor Espen Molden. “Because CYP2C19 is involved in the metabolism of many different SSRIs, the finding is also applicable to other types of antidepressants.” The study was financed with grants from the Swedish Brain Fund, the Swedish Research Council and Horizon 2020 (the EU framework programme for research and innovation). Co-author Espen Molden has declared a fee from the company Lundbeck for running psychopharmacology courses for doctors; the other authors have reported no commercial interests. Publication “Impact of CYP2C19 Genotype on Escitalopram Exposure and Therapeutic Failure: A Retrospective Study Based on 2,087 Patients” Marin M. Jukic, Tore Haslemo, Espen Molden, Magnus Ingelman-Sundberg The American Journal of Psychiatry, online 12 January 2018, doi: 10.1176/appi.ajp.2017.17050550

One of the most intriguing properties of the brain is its means to undergo synaptic plasticity which represents the basis for learning and memory, abilities that severely decline in the case of a dementia. New research, published on 9 January in the scientific journal Brain, suggests that particular proteins important in the communication between neurons could be targets for early interventions in patients with different types of dementias. In the nervous system, a synapse is the place where signals are passed from neuron to neuron. The recently published paper focuses on synaptic dysfunction and its impact on dementia severity and cognition in the elderly with various dementia diagnoses. In addition to Alzheimer`s disease, the Lewy body dementias are the most common forms of neurodegenerative dementias with a very severe prognosis.  “Our findings suggest that particular pre- and postsynaptic proteins have an important predictive and discriminative molecular fingerprint in neurodegenerative diseases and represent potential targets for early disease intervention, such as synaptic regeneration,” Erika Bereczki says, first author of the publication and researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet. A new and broad perspective across dementias Synaptic loss, a prominent feature in Alzheimer`s disease is strongly correlated with dementia severity. Much less is known regarding synaptic loss in Lewy body dementias.  The study is the first in-depth quantitative proteome studies on pre-frontal post-mortem brain tissues where beside the whole proteome comparison, the researchers also profiled the entire synaptic proteome of Alzheimer`s disease, Parkinson`s disease with dementia and dementia with Lewy bodies patients and compared them to control cases. Taking benefit of the technological advance of proteomics analyses (a technique for large-scale studies of proteins) Erika Bereczki and her colleagues have identified key synaptic proteins underlying synaptic dysfunction which were associated with the degree of cognitive decline across dementias.  “Our results suggest shared mechanisms, with major implications for prognostic and diagnostic marker development as well as advancing future therapeutic interventions for improving the disease course. This places synaptic dysfunction and repair approaches in the spotlight of attention, especially since the therapeutic intervention window for synaptic repair and regeneration is longer than the recent toxin-clearance approaches”, Erika Bereczki says. Funding The study involved collaborators from Sweden, Norway, Hungary and the UK and was supported by grants from Alzheimerfonden, Parkinsonfonden, Demensfonden, Karolinska Institutet geriatric funds and UK Brains for Dementia Research among others. Publication Synaptic markers of cognitive decline in neurodegenerative diseases: a proteomic approach Brain, Published: 09 January 2018. Erika Bereczki, Rui M Branca, Paul T Francis, Joana B Pereira, Jean-Ha Baek, Tibor Hortobágyi, Bengt Winblad, Clive Ballard, Janne Lehtiö, Dag Aarsland

An international team of researchers led from Karolinska Institutet have, in experiments on mice, pinpointed a mechanism for the conversion of energy-storing white fat into energy-expending brown fat. The study is published in the Journal of Experimental Medicine. Obesity is a major global health issue, affecting all age groups. Obesity increases the risk of several serious human diseases, including cardiovascular disease, type 2 diabetes and cancer. Despite this knowledge, effective drugs for the treatment of obesity and related metabolic disease are lacking. ​Scientists differentiate between white adipose tissue, which constitutes most human fat and which stores surplus energy, and brown adipose tissue, which generates heat by consuming energy. One possible way of tackling potential obesity, suggest researchers, is to stimulate the conversion of parts of the white fat into brown. Stimulating the formation of blood vessels in white adipose tissue In a new study conducted on obese mice, a research team led by Professor Yihai Cao Karolinska Institutet and their colleagues at the University of Connecticut and Qingdao University stimulated the formation of blood vessels in white adipose tissue by blocking the receptor molecule for a growth factor known as VEGFR1, an effect that was achieved in one group of mice by means of a drug, and on another through genetic modification. The result was an increase in the conversion of white fat to brown, as well as a reduction in obesity and improved sensitivity to insulin. “Our discoveries can hopefully help us to develop new drugs for the treatment of obesity and diabetes,” says Yihai Cao, professor in vascular biology at the Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet. Professor Cao´s research was financed by: The European Research Council, the Swedish Research Council, the Swedish Cancer Foundation, the Karolinska Institute Foundation, the Karolinska Institute distinguished professor award, the Torsten Soderberg Foundation, the Maud and Birger Gustavsson Foundation, the NOVO Nordisk Foundation and the Knut and Alice Wallenberg Foundation. Publication  Ablation of endothelial VEGFR1 improves metabolic dysfunction by inducing adipose tissue browning Seki T, Hosaka K, Fischer C, Lim S, Andersson P, Abe M, Iwamoto H, Gao Y, Wang X, Fong GH, Cao Y.  Journal of Experimental Medicine, online 5th of January 2018, doi:10.1084/jem.20171012.  

According to the previous plan, research groups from Karolinska Institutet and Karolinska University Hospital were due to move into the new Bioclinicum research building on the hospital site in Solna in mid-January 2018. The NKS Programme Office, together with hospital management, have now decided to postpone the move due to the risk of the network in the research building interfering with the network in the already commissioned buildings, and thereby negatively impacting patient safety. Approximately 900 researchers will be affected by the delay. “Yesterday, we informed heads of departments whose researchers are specifically affected. This delay will affect a great many projects and will naturally be a cause of disappointment to many members of staff. We are maintaining an ongoing dialogue and will be announcing a new timetable for occupancy as soon as possible,” says Ole Petter Ottersen, Vice-Chancellor at Karolinska Institutet. Programme management at NKS is now reviewing the various factors affecting the delay and will then set a new date for occupancy. This announcement will be made after the coming weekend at the earliest. “It is extremely unfortunate that we are unable to carry out the relocation of research groups in January. A great many people have worked hard to prepare for the commissioning of the building, the move and the various projects that will be started once the move is complete. That said, patient safety must always come first, and this is the criteria by which we are evaluating the planning of the move. If we are unable to guarantee patient safety, we will not be able to take occupancy. Our task now is to identify the necessary measures as soon as possible and put in place a revised timetable for researchers to move into the new building,” says Stanley Holsteiner, director of the Programme Office. Network interference experienced during November made the problem apparent and resulted in both a review of the network as a whole, and a decision by hospital management to revisit the timetable. This review is currently underway under the leadership of the IT directors of Stockholm County Council and Karolinska University Hospital.

Researchers at Karolinska Institutet have managed to sequence the giant genome of a salamander, the Iberian ribbed newt, which is a full six times greater than the human genome. Amongst the early findings is a family of genes that can provide clues to the unique ability of salamanders to rebuild complex tissue, even body parts. The study is published in Nature Communications. This is the first time that an entire newt genome has been sequenced, an achievement that can give rise to new discoveries on the amphibian’s ability to recreate brain neurons as well as entire body parts. Amongst the first findings are a multitude of copies of a certain microRNA group, which in mammals is mainly found in embryonic stem cells, but also in tumour cells. Resistant to tumour formation “It will be exciting to figure out how regeneration in the adult organism re-activates embryonic genes,” says study leader Professor András Simon at Karolinska Institutet’s Department of Cell and Molecular Biology. “What’s needed now are functional studies of these microRNA molecules to understand their function in regeneration. The link to cancer cells is also very interesting, especially bearing in mind newts’ marked resistance to tumour formation.” Even though the abundance of stem cell microRNA genes is quite surprising, it alone cannot explain how salamanders regenerate so well. Professor Simon predicts that the explanation lies in a combination of genes unique to salamanders and how other more common genes orchestrate and control the actual regeneration process. Technical and methodological challenge One of the reasons why salamander genomes have not been sequenced before is its sheer size – six times bigger than the human genome in the case of the Iberian newt, which has posed an enormous technical and methodological challenge. “It’s only now that the technology is available to handle such a large genome,” says Professor Simon. “The sequencing per se doesn’t take that long – it’s recreating the genome from the sequences that’s so time consuming.” “We all realised how challenging it was going to be,” recounts first author Ahmed Elewa, postdoctoral fellow at the same department. “But the very fact that it was such a challenge made it all the more exciting.” Can recreate cells that die in Parkinson’s disease The group at Karolinska Institutet is now engaging with other researchers to discover what can be learned from the newt genome and test new hypotheses through systematic comparisons with mammals. “We showed ten years ago that salamanders can recreate all the cells that die in Parkinson’s disease in the space of four weeks,” says Professor Simon. “We can now delve deeply into the molecular processes underlying this ability. Although we’re doing basic research, our findings can hopefully lead to the development of new regenerative strategies for humans.” The sequencing project was conducted in collaboration with SciLifeLab and Uppsala University and was largely financed with grants from the Swedish Research Council, the National Institutes of Health (USA), the European Research Council, the Swedish Cancer Society and the Wenner-Gren Foundation. Publication “Reading and editing the Pleurodeles waltl genome reveals novel features of tetrapod regeneration” Ahmed Elewa, Heng Wang, Carlos Talavera-López, Alberto Joven, Gonçalo Brito, Anoop Kumar, L Shahul Hameed, May Penrad-Mobayed, Zeyu Yao, Neda Zamani, Yamen Abbas, Ilgar Abdullayev, Rickard Sandberg, Manfred Grabherr, Björn Andersson, András Simon Nature Communications, online 22 December 2017, doi: 10.1038/s41467-017-01964-9

Karolinska Institutet is now taking the initiative to coordinate, develop and streamline support to researchers and students with regard to the utilisation and commercialisation of research results. This will take place through KI Innovations, in addition to its existing activities, taking on the task of running KI’s Innovation Office. Previously, KI Innovation’s organisation has focused on business consultancy, marketing and patent issues and commercial development. Agreement has now been reached to expand these activities to include the management of KI’s Innovation Office. This important assignment will require increased communication with KI’s organisation, focusing on inspiration, consultancy and guidance to researchers, students and other staff engaged in developing ideas and dealing with innovation issues. The purpose is to increase awareness of these opportunities, and to publicise the results among both staff and students at KI. In addition, this year KI Innovations qualified for Vinnova’s incubator excellence programme, making it possible to offer development support to startups in the life science sector. Together, these three roles will be integrated to contribute to a more efficient innovation programme, with the goal of achieving increased utility and commercialisation of both research results and other ideas generated by staff and students. In order to clarify the importance of an innovation system that is clearly integrated with KI’s organisation, as of 2018 these activities will be run from new premises at Berzelius väg 3, in the heart of the campus. About KI Innovations Karolinska Instsitutet Innovations AB is a wholly-owned subsidiary of Karolinska Institutet’s holding company. KI Innovations assists in the commercialisation of research results in the field of life science. Karolinska Institutet’s innovation support includes consultancy, training, guidance, professional networking, financing, expertise in entrepreneurship and business development and incubation opportunities for projects and companies in the life science sector.

Three researchers at Karolinska Institutet have been appointed Wallenberg Academy Fellows 2017. The three researchers are Emanuela Santini, Carmen Gerlach and Joanna Rorbach, all in the field of medicine. In total this year, 24 young researchers receive this prestigious award and funding by Knut and Alice Wallenberg Foundation. The purpose of the Wallenberg Academy Fellowship programme is to boost Sweden as a research nation by retaining the greatest talents in the country and by recruiting young international researchers to Swedish universities. Via an integral mentor program, they also have an opportunity to strengthen their scientific leadership and better utilize their research results. The program has been established in partnership with the royal academies and 16 Swedish universities. The investment provides the best young researchers with long-term resources so that they can concentrate on their research. “It is particularly pleasing that there are as many women as men among this year’s Academy Fellows. Those who are appointed to be Wallenberg Academy Fellows go through a thorough evaluation process. First, the university nominates candidates; they are then reviewed by evaluation panels in each subject, which are led by the five royal academies,” says Peter Wallenberg Jr, Chairman of the Knut and Alice Wallenberg Foundation in a press release. Emanuela Santini Repetitive behaviours in autism. Emanuela Santini is today working at Columbia University in New York, but as Wallenberg Academy Fellow she will move her research to Karolinska Institutet. With the long-term goal of finding a treatment that subdues repetitive behaviors shown by some people with autism spectrum diagnoses, Emanuela Santini will investigate how they arise at a molecular level. Some people with autism repeat specific sounds, words or sentences, others bite their nails or spin around – behaviors that have a negative effect on quality of life, both for the sufferer and their relatives. Previous studies indicate that mutations in the eIF4E gene may be responsible; when Emanuela Santini overexpressed the equivalent gene in mice, they developed behaviors that were reminiscent of the repetitive symptoms of autism spectrum disorders. Her hypothesis is therefore that the change in eIF4E affects the signals between the nerve cells in the striatum, an area of the brain that controls how we move, among other things. More about Emanuela Santini's research Carmen Gerlach More effective vaccines and therapies against cancer. Carmen Gerlach, moving her research from Harvard Medical School to Karolinska Institutet, studies how the body’s immune system protects us from infections and combats cancer cells. As Wallenberg Academy Fellow she will investigate specific groups of immune cells, CD8 T cells, to better understand how they work. Current vaccines primarily activate cells that produce antibodies, and Carmen Gerlach will try to develop knowledge that can be used to design vaccines that also make the right types of CD8 T cells. The hope is, among other things, that such vaccines could provide protection from diseases for which current vaccines do no work. More about Carmen Gerlach's research Joanna Rorbach Mitochondrial ribosomes to be mapped in atomic detail. Joanna Rorbach is a principl investigator at Karolinska Institutet’s Department of Medical Biochemistry and Biophysics. As Wallenberg Academy Fellow she will investigate the large molecular machinery in the mitochondria, the cell’s power plant that puts together the proteins used in cellular respiration. These molecular protein factories are called mitochondrial ribosomes and are central to our survival. However, despite their importance there is limited knowledge of how the mitochondrial ribosomes are built together and function. In her work, Joanna Rorbach will use the latest advancements in genetics and proteomics together with cryo-electron microscopy.  Beyond describing the workings of the cell nucleus in atomic detail, in-depth knowledge of mitochondrial ribosomes may contribute to further understanding of the mechanisms behind aging, cancer and many inherited and neurodegenerative diseases. More about Joanna Rorbach's research

People who have been treated for attempted suicide or suicidal behaviour have a much shorter life expectancy and usually die of non-suicide-related causes, a new study from Karolinska Institutet and Umeå University published in the scientific journal Acta Psychiatrica Scandinavica reports. “Suicide is, of course, very common in this vulnerable patient group, but a deeper analysis shows that the excess mortality is largely attributable to non-psychiatric diseases,” explains Jussi Jokinen, psychiatrist and professor at Umeå University and researcher at Karolinska Institutet’s Department of Clinical Neuroscience. “We also found significant gender differences in life expectancy, especially in the younger patients.” Up to 18 years shorter life expectancy The researchers studied over 185,000 individuals in care for self-harming behaviour between 1970 and 2010. Their results show that 20-year-old men, after their first attempted suicide, had a remaining life expectancy that was a full 18 years shorter than the rest of the population; the corresponding figure for women was 11 years. For 50-year-olds who had made their first suicide attempt, the reduction in life expectancy for men and women was 10 and 8 years respectively. If the first suicide attempt was not made until the individual’s 70s, the reduction in remaining life expectancy was about 4 years for both sexes. By way of comparison, in Sweden in 2016, newborns have a life expectancy of 80.6 years (boys) and 84.1 years (girls). 50-year-olds have a remaining life expectancy of 31.9 years (men) and 34.9 years (women). Reveal a lack of equal treatment  The study shows that actual suicide caused a smaller proportion of deaths in those who had been admitted into care for attempted suicide or self-harming behaviour. A more common cause of death was disease. “Our results reveal a lack of equal treatment whereby psychiatric patients don’t seem to receive the care they need,” says principal investigator Dr Rickard Ljung, docent at Karolinska Institutet’s Institute of Environmental Medicine. “Our previous research has shown that psychiatric patients receive poorer treatment for their non-psychiatric disorders and diseases.” The study was financed by the Swedish Society of Medicine’s Söderström-König Foundation. Publication “Life expectancy after the first suicide attempt” Jussi Jokinen, Mats Talbäck, Maria Feychting, Anders Ahlbom & Rickard Ljung Acta Psychiatrica Scandinavica, online 14 December 2017

A majority of new students at Karolinska Institutet has KI as their first choice. This was shown in a survey taken in in the autumn 2017. And the interest in studying at KI is consistently high compared with the average for universities and university colleges. “It is very gratifying to see that confidence in education at KI is still high,” says Annika Östman Wernerson, Dean of Education. What students are these, why do they choose to study at KI and what plans do they have for the future? These questions are answered in a student survey every other year at Karolinska Institutet, KI. This year's survey shows that 78 per cent of the students applied to KI as their first choice. In the last three years, the proportion doing this has increased by one per cent a year. As the reason for choosing KI, 70 per cent said that KI has the best education and 58 per cent said that KI has a good international reputation. “Confidence in education at KI has been increasing rather than decreasing,” says Annika Östman Wernerson, Dean of Education at KI. The survey has been taken since 1999, which means that trends over time can be seen, and according to Annika Östman Wernerson, this is important. “The survey is part of a total quality system. The idea is also that the results can be seen in relation to other evaluations, such as that which is made when students leave KI,” she says. KI adapts its information to students’ needs The results of the survey help KI to adapt its information to students’ needs, “We want to see where our students come from. Have they studied before, what is their socio-demographic background, were their parents born abroad? It is interesting to see how they found us, what their most important sources of information are,” Johanna Bäckström says, Head of the Student and Career Service Unit, Education Support Office. The survey shows that most of the students, 71 per cent, are women. The average age is 24.3, but there are great differences between programmes. The psychotherapists have the highest average age, 40.5, while the candidate programme in biomedicine has the youngest students, at 20.7. Just under a third, 29 per cent, were born abroad. This is the highest percentage since the survey began. “It is a very valuable thing that more foreign born students are applying for the programmes. Students from more varied backgrounds reflect society as a whole and can contribute to our work on diversity and internationalisation of education,” says Annika Östman Wernerson. Information from friends and family is important Many students come from an academic family: 66 per cent have one parent with an academic examination, while 36 per cent come from homes where both parents are academics. The website is the most important information channel for information about education at KI, but the survey shows that friends and family are also important.   “It is interesting that information from friends and family is so important. This may be because many of the students come from academic families. We can think about what information channels we can develop to broaden recruitment,” says Annika Östman Wernerson. Since the start of the 2000s it has become less common for students to take a summer job or gain some professional experience before studying. Around a third of this year’s students have done so. This sets some special demands on the education programmes and according to Annika Östman Wernerson it would be an advantage if more tried working in the area that they will be studying. “It is a general trend in all universities that we are seeing more drop-outs. Part of the reason for this may be that students did not really understand at the beginning what the education and work involves,” she says. Interest in research has declined In terms of the future, 45 per cent of the students were interested in studying abroad and 18 per cent were seriously considering working abroad. 23 per cent were planning a career in research. Interest in research has declined over the years the survey has been performed. Information from KI, the education and the students’ union scored well overall. But many pointed out in their comments that it was difficult to find KI’s website and the learning platform Ping Pong. “We will be replacing the learning platform. A new platform was procured just before the survey. We are also working on improving the websites that are aimed at students,” says Annika Östman Wernerson. The survey an invaluable resource according to the students' union It is valuable for the students’ union that there is a student survey. “We can find out who chose to study at KI and why they did so. That makes it easier to sell KI as a university and as a brand. The survey is also an invaluable resource for evaluating how new students are welcomed,” Pontus Dannberg says, Vice Chair of the Medical Students’ Union. The Medical Students’ Union helps to organise the introduction and get-together camp, popularly known as “kollot”, which was scored very highly by the students this year. As many as 89 per cent rated this as good or very good. Kollot was more appreciated than, for example, KI’s general welcome day, which also scored highly. But there are differences between the various programmes. For example, fewer speech therapists participated in kollot and those that did gave lower marks than the others. “This kind of thing is useful to know, so that we can improve how students are welcomed. Next time, we can see what we can do to attract more participants form the speech therapy programme,” Pontus Dannberg says. He also believes that KI needs to work on the one-sided gender distribution seen in the results. The medical programme had an even gender distribution, but the other programmes have a majority of women. “Those who study to become midwives, speech therapists and nurses are almost exclusively women. This may have its roots in an old world view and assessment of who does what kind of job. It is sad to see that KI has not succeeded in countering the uneven gender distribution in these programmes.” Text: Ann Patmalnieks About the student survey 2017 The student survey, also known as the beginners’ survey, has been performed since 1999. Questionnaires are given out during lessons. This year’s survey was completed by students who began in autumn 2017 and applied for educational programmes in Spring 2017, a total of 864 students on 17 programmes, including three continuation programmes. The results are based on the responses of the 802 students on beginners’ programmes. The survey has also been completed by students on seven master’s programmes. These responses are reported separately. Heavy demand for Karolinska Institutet Interest in studying on Karolinska Institutet’s educational programmes is consistently high compared with the average for universities and university colleges. This is shown by statistics from the Swedish Higher Education Authority (UKÄ). Application demand is measured in the number of first-choice applicants per place. For example there were 12.6 first-choice applicants for every place on the medical programme before autumn 2017*, compared with an average of 7.1 for all other educational institutions. One programme that stands out as having a lower application demand than others is the psychology programme. Application demand for some of KI’s educational programmes. The figure in brackets is for all universities. Occupational therapist 2.3 (2.1) Audiology 1.8 (1.4) Midwifery 4.7 (4.3) Biomedical analyst 1.6 (1.2) Physiotherapy 5.9 (6.4) Speech therapy 2.6 (1.9) Medicine (doctor) 12.6 (7.1) Psychology 7.1 (10) Psychotherapy 6.8 (3.9) Radiology nursing 2.3 (2.0) Nursing 3.9 (2.6) Dental hygienist 6.9 (4.0) Dentistry 5.0 (4.7) Comment: The application demand for the above courses is somewhat lower than the previous year, both at KI and nationally. The University and Higher Education Council, UKÄ states the good labor market situation as a reason why the number of applicants has decreased. By autumn 2017, the number of applicants in Sweden decreased by 2.2 per cent compared with the year before. The total number of applicants increased until autumn 2014. Thereafter, the number of applicants has decreased from year to year. *Statistics from the University and Higher Education Council for the spring 2018 are not yet complete, therefore statistics from HT2017 are reported above.

The government is proposing one year of “basic residential training” for medical students and that the medical programme be extended to six years. A licence to practise will be issued straight after graduation and the current system of “AT” residential training will be discontinued. “This will be a good opportunity to review and develop the medicine study programme at KI and also adapt it to the needs of healthcare in the future,” says Annika Östman Wernerson, Dean of Higher Education at KI. A completely new and extended medical programme after which a licence to practise will be issued straight after graduation and instead of intern employment [AT], basic residential training [bastjänstgöring] will be incorporated into the study programme. This can be reality for the students who start studying medicine as of around the year 2020. The proposal regarding basic residential training, which is intended to be an independent initial part of specialist training, was sent out by the Ministry of Health and Social Affairs for consultation on 22 November. The government's proposal was presented in more detail at the InFuturum conference on 23 November. The focus of basic residential training will be on primary care and emergency care. It has not been regulated exactly how long basic residential training will last; normally, it will take one year but it could also be done faster. It will be possible for a person with previous experience to be given credit for that. According to the proposal, knowledge of psychiatry will be “taken into particular account”. The ability to cooperate with others will be important and also to constantly strive to make improvements. In addition, students will practise taking decisions and medical science and professional training will be integrated throughout the study programme. All skills will be assessed, not only knowledge. Another way the medicine study programme will be changed is that there will be more clinical assessments and fewer written exams. “I can see many positive aspects in the proposal, for example, a strong emphasis on the importance of future doctors having different skills and the importance of collaboration with society, other professions and patients. Other important elements are the use of pedagogical methods that activate the student and a review of examination methods," says Annika Östman Wernerson, Dean of Higher Education at KI. Basic residential training will be introduced if the new, reformed six-year medicine study programme comes about. Medical training has previously focused on acute illness processes but now there will be a stronger emphasis on chronic illness processes. The medical students need to be where the patients are Next year, the new highly specialised intensive care emergency centre will open at Karolinska University Hospital where only the most seriously ill patients will be treated. This means that when patients with less serious diagnoses are treated at other hospitals, many diagnoses will no longer be represented at Karolinska University Hospital. Moreover, the number of patients at the highly specialised intensive care emergency centre is expected to be low. In order for medical students to get the right training, the study programme must now be organised differently. “This will be a good opportunity to review and develop the medicine study programme at KI and also adapt it to the needs of healthcare in the future. Our students need to be where the patients are. That is why primary care is an important arena and we hope that the academic specialist centres in Stockholm will play a prominent role in the study programmes at KI,” says Annika Östman Wernerson. The extension of the medical programme is also mentioned in the government’s autumn budget. SEK 9 million will be invested during 2018 which is the equivalent of 40 student places distributed among the universities that offer medical training. It is unclear how many places KI will be given but when the Board of Higher Education at KI met at the end of October, a plan for increasing the number of places by four was presented. Text: Maja Lundbäck New education places at KI with more funding The government’s autumn budget includes several major investments in education. In addition to an earmarked increase of the medical programme, KI will also be given substantially more funding with no restrictions regarding how the money is used. At a meeting on 25 October, the Board of Higher Education at KI presented a plan for how the funding will be distributed. The first step will be to increase, as of 2018, the number of places for new students on: The Occupational Therapy programme: 8 extra places The Biomedical Laboratory Science programme: 10 extra places The Physiotherapy programme: 10 extra places The Medical programme: 4 extra places The Optometry programme: 3 extra places

It was a packed Aula Medica that listened to Jeffrey C. Hall, Michael Rosbash and Michael W. Young as they delivered their Nobel lectures. After expressing gratitude at the attention their work has received, the trio took the audience on a scientific journey through time to role models known and unknown, fruit flies and night owls.  “I’m going to make some remarks having to do with gratitude,” said Jeffrey Hall, who, dressed in a suit and cap, held the first of the three Nobel lectures. Karolinska Institutet’s vice-chancellor, Ole Petter Ottersen, and Professor Juleen Zierath, member of the Nobel Committee for physiology or medicine, welcomed and described the three Nobel laureates’ discoveries about the workings of our internal clock. But Jeffrey Hall said little about his own achievements. Instead, he turned back the clock and took the audience on a journey through the family tree of scientific forebears that had made his research possible. One invited him in to speak, as a newly-fledged researcher, at a conference in the 1970s; another was a master at discovering interesting fruit-fly variants, whose genetic descendents still dart around the researchers’ laboratories to this day. A third predecessor researched for years without publishing a word, but whose articles, when he did eventually deliver, earned him a Nobel Prize. Jeffrey Hall also praised all unsung “AIs” (Actual Investigators), the hard-working colleagues who unlike PIs (Principal Investigators) rarely get any credit for the discoveries they help to make.   When Jeffrey Hall, Michael Rosbash and Michael Young started working together, it was a merging of personal chemistry and genetic knowledge. At last they were able to identify the genes and proteins that give our cells a circadian rhythm. “It came out better than we intended, at least from the beginning,” said Professor Emeritus Hall. After having raised his cap to his forerunners, he declared that this year’s Nobel Prize has two more recipients. “One of them should be the little flies, because they have created massive amounts of biological knowledge, going back more than a hundred years of time,” he said. He went on to claim that the phenomenon itself, biological rhythms, should also be awarded a prize, expressing his fascination at how biological systems contain tiny clocks that keep track of night and day. “I’m done… well I am really done in life as well. If there has been any attention, I thank you for it,” he said, drawing much laughter and applause. Circadian rhythms are found everywhere in nature Michael Rosbash said that he had been speechless since 2 October, when he was notified about the prize, but assured the audience that the condition would not affect him today. He then described how circadian rhythms are found everywhere in nature, the oldest known being found in cyanobacteria, which although they seem to have evolved independently of those in plants and animals, obey the same basic principles. Something that had long puzzled scientists was how the feedback loop that involves a protein called Period and that gives the clock its rhythms actually works. There were many possible explanations, but Michael Rosbash had a bet with Michael Young that the regulation occurred at a genetic level. After much research, it turned out that his hypothesis was right. “He paid his debt and we had a lovely dinner together with our wives,” he said. It eventually transpired that the inner clock works in the same way in mammals, even if some of the components differ. We also know today that the human body contains a wide variety of time-controlled molecules, most of which seem to derive their rhythm from the basic clock mechanism described by the laureates. “50 percent of our genes are under circadian control,” explained Professor Rosbash. That he happened to be the one who managed to make the Nobel-winning discoveries is, he said, down to tenacity, a little knowledge and a lot of luck. He then showed the audience a list of important “rhythm and fly people” and of “yeast people”, one of whom was his wife. "My view of science is that it is a very romantic profession - you never know what you will discover and each day is an adventure,” he said, and read a love ode to a fruit fly. All tissues in the body contain biological clocks Last up was Michael Young, who opened with a series of images illustrating circadian rhythms: a flower opening and closing, a hamster who is active at the same time every day, even in darkness, and a map of hundreds of time-controlled fruit fly genes. All tissues in the body contain biological clocks that are normally set by the light. But sometimes, such as when we travel, the clocks fall out of sync which each other and their environment. They generally become reset after a while, but a defective internal clock makes some people suffer from a kind of chronic jet lag. “We can think of these individuals as extreme night owls,” he said, and showed a graph of the fragmentary sleep pattern of an individual with delayed sleep phase disorder (DSPD). By mapping the genes of a person with DSPD and his/her family members, Professor Young has recently demonstrated that the condition is caused by a mutation of the CRY1 gene, which destroys the clock’s sensitivity to extraneous time signals in the form of light. His subsequent studies have shown that the mutation is common. Professor Young concluded by stating that knowledge of the internal clock gives scientists new openings into researching exactly how sleep and the circadian rhythm are connected to health. “A variety of metabolic and psychiatric disorders are often said to be associated with disordered sleep, but it has been difficult to establish causal relationships,” he explained. “We should now be able test whether particular sleep mutations extend to other medical problems.” Text: Ola Danielsson Watch the Nobel lectures The whole film with all the lectures 2017 Nobel Lectures in Physiology or Medicine   Jeffrey C. Hall Title: The Little Flies: Multifaceted Basic Research Coming Out Better than Intended Nobel Lecture: Jeffrey C. Hall, Nobel Prize in Physiology or Medicine 2017   Michael Rosbash Title: The Circadian Clock, Transcriptional Feedback and the Regulation of Gene Expression Nobel Lecture: Michael Rosbash, Nobel Prize in Physiology or Medicine, 2017   Michael W. Young Title: Time Travels: A 40 Year Journey from Drosophila's Clock Mutants to Human Circadian Disorders Nobel Lecture: Michael W. Young, Nobel Prize in Physiology or Medicine 2017

Once the final notes have rung out across the Golden Hall, it is time for the guests of the Nobel Banquet to experience a legendary event: Students' Nobel Nightcap. Top secret, as usual, but we can reveal one small detail... For over a year, 170 KI students have worked to invite royalty, Nobel laureates and a total of 1,200 guests to “the most magical night of the year”. It’s not for nothing that the Students’ Nobel NightCap after the Nobel Banquet has been referred to as the world’s coolest after party.  “I look forward to the guests’ arrival, when we open up the doors and everyone can see what we have worked so hard for and marvel at how well it turned out,” says Johan Wallin, who is active in the party planning group and on his tenth semester of medical studies.  A top secret theme permeates everything from food and drink to entertainment, and each room has its own sub-theme.  “Last time the party was held at KI, the theme was ‘around the world’ and all the rooms were different countries and parts of the world. One room was Japan. An entire wall had been painted with Tokyo’s underground map and sushi and saki were served on tap,” explains Johan. The planning group really goes all out. The students’ union building has been repainted inside and new walls have been put up. The event promises something bombastic, student-inspired and fanciful. Johan reveals just one detail: A gigantic wall consisting entirely of roses.   “We hope that people will go home feeling absolutely wowed. What happens at the party stays at the party. No cameras allowed. But there will be photo booths. Who would Johan most like to take a selfie with?  “Michael Young and his team. They have made such amazing discoveries!” Text: Ebba Arnborg Since 1978, the student unions at KTH Royal Institute of Technology, Stockholm University, Stockholm School of Economics and Karolinska Institutet have taken turns to organise the Students’ Nobel NightCap.

In families who carry certain inherited mutations that increase the risk for melanoma, members who do not carry the mutation also have an increased risk of melanoma, a study from Karolinska Institutet published in Genetics in Medicine reports. The phenomenon, which is called phenocopy, could result from other shared risk-enhancing genes or environmental factors within the families. Malignant melanoma of the skin is one of the fastest increasing cancer types in the West. The main risk factors for melanoma are UV light exposure and hereditary factors. It is therefore relatively common for the afflicted to have family members with the disease. Inherited mutations of the tumour suppressor gene CDKN2A are the strongest known risk factors for familial melanoma and mutations in this gene also increase the risk of other cancers. Children, siblings or parents of mutation carriers have a 50-50 chance of also having the mutation, which can be identified with a gene test. Swedish and American families The present study included Swedish and American families with inherited CDKN2A mutations. The researchers studied whether family members who have not inherited the mutation have any higher than normal risk of developing melanoma or other cancers. Melanoma, but no other cancers, was more common in the non-carriers in these families compared to the normal population. The phenomenon whereby non-carriers of a specific mutation copy the phenotype (in this case melanoma) from their mutation-carrying relatives is known as phenocopy. “Phenocopy can be caused by other risk-modifying genes or exposure patterns that increase the probability of the specific phenotype manifesting itself,” says the study’s first author Hildur Helgadottir, researcher at Karolinska Institutet’s Department of Oncology-Pathology. Certain pigmentation variants increase the risk Previous studies have shown that people with the mutation who also have certain pigmentation variants run an even higher risk of melanoma. Even though the CDKN2A mutation should be present in all populations, it has almost exclusively been identified in families with a Caucasian heritage. “This suggests that dark-skinned people with this mutation probably don’t develop melanoma as often and are therefore not tested for this specific mutation, presumably because they lack the risk-modifying pigmentation variants that increase the risk of melanoma,” says Dr Helgadottir. Should be informed about the risks The researchers believe that such pigmentation variants also contribute to a higher melanoma risk in the family members who do not carry the mutation. “Our results suggest that family members that test negatively for their family’s CDKN2A mutation should be informed that they still can have an increased risk of developing melanoma. They should be advised to avoid sunburn, be aware of any change in their moles, and some might even need to be monitored by a dermatologist,” says Dr Helgadottir. The study was conducted by researchers at Karolinska Institutet and colleagues at Lund University and the USA’s National Institutes of Health (NIH). It was financed from several sources, including the Swedish Cancer Society, the Cancer Research Funds of Radiumhemmet and the NIH. The researchers have declared no potential conflicts of interest. Publication “Phenocopies in melanoma-prone families with germline CDKN2A mutations” Hildur Helgadottir, Håkan Olsson, Margaret A. Tucker, Xiaohong R. Yang, Veronica Höiom, Alisa M. Goldstein Genetics in Medicine, online 7 December 2017, doi: 10.1038/GIM.2017.216

Five researchers at Karolinska Institutet have been approved Distinguished Professor Grant by the Swedish Research Council, each of approximately 3.5-5 million SEK annualy for ten years. In total almost half a billion SEK will be allocated to ten researchers in Sweden. The aim of the Distinguished Professors Grant programme is to create conditions for the most distinguished researchers to conduct long-term, innovative research with great potential to achieve scientific breakthroughs. The five Distinguished Professors from Karolinska Institutet Henrik Ehrsson, Professor of Cognitive Neuroscience at the Department of Neuroscience Project title: Ego experiences: Experimental studies and biopsychological processes [Jagupplevelse: experimentella studier och biopsykologiska processer]     Abdel El Manira, Professor of Neuroscience at the Department of Neuroscience Project title: The organization of neuronal networks that control motor movements [Organisationen av neuronala nätverk som styr motoriska rörelser]     Ulf Eriksson, Professor of Vascular Biology at the Department of Medical Biochemistry and Biophysics Project title: Studies of vascular diseases and underlying mechanisms [Studier av vaskulära sjukdomar och underliggande mekanismer]     Gunilla Karlsson Hedestam, Professor of Vaccine Research at the Department of Microbiology, Tumor and Cell Biology Project title: Genetic studies of antibody diversity [Genetiska studier av antikroppsdiversitet]     Rickard Sandberg, Professor of Molecular Geneticsprofessor at the Department of Cell and Molecular Biology Project title: Understanding gene regulation by massive parallel genomic analysis of individual cells [Förstå genreglering genom massiv parallell genomisk analys av enskilda celler]    

A new study in Nature by an international team including researchers from Karolinska Institutet, reports that the alcohol-abuse drug Antabuse is effective against cancer. The study also identifies a potential mechanism of action for the anti-tumour effect. As developing new cancer drugs is costly and time-consuming, repurposing drugs that are already approved to treat other diseases is a promising alternative. Disulfiram (Antabuse) is a cheap, safe and long-established alcohol-aversion drug that provokes symptoms like sickness, eczema, headache and tachycardia when combined with alcohol. In collaboration with an international research team in five countries, Jiri Bartek, professor of cancer biology at Karolinska Institutet and senior researchers at the Danish Cancer Society Research Center in Copenhagen, studied disulfiram’s potential as an anti-cancer drug. The researchers combined experimental studies of the mechanisms behind the anti-tumour effect with epidemiological analyses based on the records of cancer patients across Denmark. Lower risk of death from cancer “We discovered that patients who were prescribed disulfiram for alcohol dependency and continued taking the drug after they had received a cancer diagnosis had a lower risk of death from cancer than those who stopped taking the drug at their cancer diagnosis”, says Professor Jiri Bartek at the Department of Medical Biochemistry and Biophysics, Karolinska Institutet. The anti-cancer effect of Antabuse has been shown before, but it has remained unclear how the drug affects the cancer cells. Through laboratory experiments, the team found that in mice and in the human body, disulfiram becomes metabolised into a molecule that causes a naturally occurring protein called NPL4 to clump together with its partner, the body’s p97 enzyme. This process ‘freezes’ and thereby functionally disables the otherwise very mobile and tumour growth-supporting NPL4-p97 duo, resulting in cancer cell death. “Our study fills an important knowledge gap regarding the anti-cancer mechanism of disulfiram and paves the way for future clinical trials”, says Jiri Bartek. The study received funding from many different sources, including the Swedish Research Council and the Swedish Cancer Society. Publication “Alcohol-abuse drug disulfiram targets cancer via p97 segregase adaptor NPL4” Zdenek Skrott, Martin Mistrik, Klaus Kaae Andersen, Søren Friis, Dusana Majera, Jan Gursky, Tomas Ozdian, Jirina Bartkova, Zsofia Turi, Pavel Moudry, Marianne Kraus, Martina Michalova, Jana Vaclavkova, Petr Dzubak, Ivo Vrobel, Pavla Pouckova, Jindrich Sedlacek, Andrea Miklovicova, Anne Kutt, Jing Li, Jana Mattova, Christoph Driessen, Q. Ping Dou, Jørgen Olsen, Marian Hajduch, Boris Cvek, Raymond J. Deshaies & Jiri Bartek Nature, online 6 December 2017, doi: 10.1038/nature25016

Using genetic information, researchers at Karolinska Institutet provide new evidence that higher educational attainment is strongly associated with a lower risk of Alzheimer’s disease. The study is published in The BMJ. The causes of Alzheimer’s disease are largely unknown and treatment trials have been disappointing. This has led to increasing interest in the potential for reducing the disease by targeting modifiable risk factors. Many studies have found that education and vascular risk factors are associated with the risk of Alzheimer’s disease, but whether these factors actually cause Alzheimer’s has been difficult to disentangle. Mendelian randomisation is a method that uses genetic information to make causal inferences between potential risk factors and disease. If a gene with a specific impact on the risk factor is also associated with the disease, then this indicates that the risk factor is a cause of the disease. Analysed more than 900 genetic variants Susanna C. Larsson, associate professor at the Institute of Environmental Medicine at Karolinska Institutet, and colleagues in Cambridge and Munich, used the Mendelian randomisation approach to assess whether education and different lifestyle and vascular risk factors are associated with Alzheimer’s disease. The analysis included more than 900 genetic variants previously shown to be associated with the risk factors. Comparisons of these genetic variants among 17 000 patients with Alzheimer’s disease and 37 000 healthy controls revealed a strong association for genetic variants that predict education. “Our results provide the strongest evidence so far that higher educational attainment is associated with a lower risk of Alzheimer’s disease. Therefore, improving education may substantially decrease the number of people developing this devastating disease,” says Susanna C. Larsson. Cognitive reserve could be one explanation According to the researchers, one possible explanation for this link is ‘cognitive reserve’, which refers to the ability to recruit and use alternative brain networks or structures not normally used in order to compensate for brain ageing. “Evidence suggests that education helps improve brain networks and thus could increase this reserve,” says Susanna C. Larsson. The study was financed by the European Union's Horizon 2020 research and innovation programme and the Swedish Brain Foundation. Publication “Modifiable pathways in Alzheimer’s disease: Mendelian randomisation analysis” Susanna C Larsson, Matthew Traylor, Rainer Malik, Martin Dichgans, Stephen Burgess, Hugh S Markus; for the CoSTREAM Consortium, on behalf of the International Genomics of Alzheimer’s Project. The BMJ, online 7 December 2017

A few questions to Hedda Langeby, project coordinator of Karolinska Institutet’s alumni activities, who is currently organising a book fair in the Aula Medica building on 14 December. KI is organising its own book fair just in time for Christmas. Tell us, what’s the plan? “There are lots of researchers and teachers at KI who write popular science books in the field of health and medicine. Furthermore, we still have quite a large stock of books from our own now dormant publishing house Karolinska Institutet University Press. But there will also be other publishers at the book fair, so we’re hoping for quite a large selection of books.” Ideal for picking up Christmas gifts, then? “Yes, I really think so. We’ll be offering our own books at good prices and have asked the other publishers involved to be as generous as possible.  We’ll also be holding interviews on stage with some authors, and other authors will also be there to answer readers’ questions and sign books. So if you’re lucky, you can pick up a signed copy of your Christmas gift book.” You usually work with KI’s alumni activities, so is the book fair only open to former KI students? “No, not at all, everyone’s welcome. Students, employees, alumni and anyone else who happens to be passing the Aula Medica on 14 December. Apart from books and short interviews with authors, we’ll be holding a lottery and other activities on the subject of medicine and health. There is also a café in the foyer for anyone who feels like a coffee and a cake.” I assume you’ve already sneaked a look at the selection available at the book fair, is there a book you can recommend? “I’m curious about a book called ‘Hjärnan’, so I was thinking of buying that as a Christmas gift for myself. I’m also looking forward to hearing Emma Frans talk about how we are taking a more critical view of alleged facts in the media flow.” Text: Katarina Sternudd (in translation from Swedish) What: Book fair in the field of medicine and health When: Thursday 14 December 2017, 15:00-18:00. Where: The foyer, level 2, Aula Medica, Nobels väg 6, Campus Solna More about the programme in the KI calendar

Research projects are subject to ethical review to protect people who are involved in the research. The Swedish Government now wants to create uniformity in ethical review throughout the country and has proposed a new government agency for this purpose, which will be in place on 1 January 2019, writes Dagens Nyheter. The Ethical Review Board in Stockholm is one of six regional ethical review boards in Sweden, and is based at the Karolinska Institutet’s Solna Campus. In a bill to the Parliament, the Swedish Government now wants to replace these regional boards with a single new national authority. This national authority will still have six regional boards with equivalent routines who will make decisions on individual cases. But from 2019, the cases will be distributed from the central authority, which means that it no longer needs to be the closest ethical review board geographically that reviews the case. Minister for Higher Education and Research Helene Hellmark Knutsson has said to Dagens Nyheter that the advantage of the new organisation is that equivalent evaluations of ethical review applications can now be done throughout the country, and that disqualification situations can be avoided by assigning evaluations to an ethical review board without any personal connections between the researcher and persons on the board. The organisation will be in place on 1 January 2019.