Integrative Molecular Phenotyping

KI News

Updated: 1 hour 3 min ago

Seven researchers responsible for scientific misconduct in Macchiarini case

Mon, 25/06/2018 - 13:44
On 25 June, the President of Karolinska Institutet made the decision to find seven researchers responsible for scientific misconduct in research. The case concerns six articles published in the scientific journals The Lancet, Biomaterials, The Journal of Biomedical Materials Research and Thoracic Surgery Clinics. Paolo Macchiarini is one of the main authors of the articles. The research reported in the articles relates to the transplantation of synthetic tracheal prostheses and describes the clinical course of treatment of three patients who were transplanted at Karolinska University Hospital 2011–2013. According to the President's decision, an additional 31 authors are blameworthy for their contributions to the articles, however not responsible for scientific misconduct. Another five authors are cleared of blame and of responsibility for scientific misconduct. Karolinska Institutet is requesting that the six articles be retracted without undue delay. Today's decision was made following a new investigation of the six articles, and overturns the decision made on 28 August 2015 by the President at the time. The case was reopened in February 2016. The new investigation points to serious inaccuracies and misleading information in the reviewed articles. The articles contain fabricated and distorted descriptions of the patients’ conditions before and after the operations. Justification is lacking for treatment of the patients on the grounds of so-called vital indication (when a given treatment is the last resort for survival), and one misses reference to relevant animal experiments which must precede human studies that involve unproven methods. Furthermore, ethical approvals are lacking, as are appropriate informed consents. “This decision has been made after careful investigations in a case that has had major impact on Karolinska Institutet, on the scientific community at large, and on public confidence in medical research. In particular, the case has had tragic consequences for patients and their relatives, for which I am deeply sorry. Karolinska Institutet will now continue to implement the measures that are necessary to prevent something like this from happening again,” says Ole Petter Ottersen, President of Karolinska Institutet. One of the authors that was found responsible for misconduct was among those who blew the whistle on Macchiarini in 2014. “The investigation points to inaccuracies for which Paolo Macchiarini is ultimately responsible but for which several of the co-authors also bear responsibility. The four whistle blowers are to be commended for their action in this case that has contributed to the investigation. However, it is KI:s firm opinion that a whistle blower who has participated in a scientific study and also as author of a scientific article, despite reporting, cannot be freed from blame or absolved from responsibility”, says Ole Petter Ottersen. According to Chapter 1, § 16 of the Higher Education Ordinance, a university that becomes aware of suspected scientific misconduct at said institution is obliged to investigate. In the course of an ongoing investigation, the higher education institution may solicit the opinion of the Expert group for misconduct in research at the Central Ethical Review Board, CEPN. According to KI procedure, suspected scientific misconduct is to be reported to the president of the university, and the president shall initiate an investigation and make a decision in the case. The university where the research was conducted has an obligation to investigate suspected scientific misconduct even if all the involved researchers are not employed at or affiliated to that university. Today's decision differs from the report of the Expert group for misconduct in research at the Central Ethical Review Board, CEPN, who considers all authors responsible for scientific misconduct. Karolinska Institutet's investigation has examined the responsibility of each individual author (a total of 43 researchers). Only a few of the authors are currently employed at or affiliated to Karolinska Institutet. The decision made on 25 June 2018 relates to the following articles: - Tracheobronchial transplantation with a stem-cell-seeded bioartificial nanocomposite: a proof-of-concept study, Lancet 2011; 378(9808): 1997–2004, - Engineered whole organs and complex tissues, Lancet 2012; 379(9819): 943–952, - Verification of cell viability in bioengineered tissues and organs before clinical transplantation, Biomaterials 2013; 34(16): 4057–4067, - Are synthetic scaffolds suitable for the development of clinical tissue-engineered tubular organs? Journal of Biomedical Material Research 2014; 102(7): 2427–2447, - Airway transplantation, Thoracic Surgery Clinics 2014; 24(1): 97–106, - Biomechanical and biocompatibility characteristics of electrospun polymeric tracheal scaffolds, Biomaterials 2014; 35(20): 5307–5315.

KI launches global alumni chapter in Vietnam

Thu, 21/06/2018 - 11:18
Một hai ba uống! (One two three, cheers!) filled the room as joyful KI alumni raised glasses to sing a celebratory song in unison. Gathered in the idyllic village of Ninh Bình KI:s alumni in Vietnam united to celebrate the launch of the KI Alumni Vietnam global chapter on Saturday 16 June 2018. – The official launch of the KI Alumni chapter is important for everyone in Vietnam. The establishment of the chapter confirms that we are important to the university, and provides greater opportunity to maintain our connection with KI, says Nguyễn Thị Thanh Hương, ambassador of KI Alumni Vietnam Chapter. A short dinner program began with a video greeting sent by KI President Ole Petter Ottersen. – This is a major step forward for KI and for our profile in southeast Asia. You, our alumni, are our most important ambassadors. You contribute to our vision, which is to improve human health, not only in Sweden, but globally. Sida-funded sandwich model Ingeborg van der Ploeg, or ”Chị In” as she is affectionately known, has been a key facilitator between KI and Vietnam as a coordinator for the Sida-funded sandwich model PhD program. Ingeborg has followed the progress of more than twenty alumni including exchange students since 2000. KI has had collaborations with Vietnam for several decades, and today has several ongoing projects including the collaborative Stint-funded Trac (Teaching and Research Academic Collaboration) project, and Edushare, a capacity-building project led by Tartu University in Estonia. Professor Marianne Schultzberg, Dean of Doctoral Education, is the chair of the Trac owner group. – The establishment of the KI Alumni Vietnam global chapter will add great value to Trac and similar projects by facilitating a consistent network through which further collaboration can arise – both with KI and between our alumni, remarks Marianne Schultzberg. The KI alumni in Vietnam hope that the establishment of the chapter will foster the KI spirit in Vietnam, bring about better contact between KI and the alumni, and increase opportunities regarding teaching, and clinical and research exchange in both directions.

Lennart Nilsson Award 2018 is awarded to Thomas Deerinck

Wed, 20/06/2018 - 17:26
Bio-artist and scientist Thomas Deerinck wins the 2018 Lennart Nilsson Award. He gets the prize for developing novel microscopy techniques and methods to improve the ability to obtain information from biological specimens. Thomas Deerinck is a research scientist, technical specialist and bio-artist at the National Center for Microscopy and Imaging Reseach (NCMIR) and the Center for Research on Biological Systems at the University of California, San Diego. Over the past four decades he has developed novel techniques and methods to improve our ability to obtain information from biological specimens using many types of microscopes. He has made many important contributions to the field of bioimaging, including key work on developing chemical, molecular and genetic tagging methods for studying cells and tissues by both light and electron microscopy. Thomas Deerincks latest work is focused on improving serial block-face scanning electron microscopy; a method that is revolutionizing automated 3D imaging of cells and tissues at nanometer-scale resolution. He not only developed the now gold-standard protocol for preparing samples for this imaging technique, but also just recently co-developed a method to greatly extend the resolution and usefulness of this approach in the field of biomedical research. Thomas is married to the artist Karla Renshaw, who taught him to bring an artistic eye common to nature photography to scientific imaging with microscopes. The resulting images of even common everyday objects are turned from the invisible into beautiful works of art, and have appeared not only on the cover of numerous top tier scientific journals, but also in many non-scientific magazines, periodicals, documentaries as well as public art exhibitions.  

Mechanism controlling multiple sclerosis risk identified

Tue, 19/06/2018 - 11:01
While the DNA sequence remains the same throughout a person’s life, the expression of the encoded genes may change with time and contribute to disease development in genetically predisposed individuals. Researchers at Karolinska Institutet have now discovered a new mechanism of a major risk gene for multiple sclerosis (MS) that triggers disease through so-called epigenetic regulation. They also found a protective genetic variant that reduces the risk for MS through the same mechanism. The study is published in Nature Communications. Multiple sclerosis is a chronic inflammatory disease of the central nervous system, affecting people at a relatively young age. Most are between 20 and 40 years old when they get the first symptoms, in the form of, for example numbness in the arms and legs, visual impairment and dizziness, but also fatigue and depression. The symptoms are caused by an inflammation in the brain and the spinal cord that breaks down the myelin sheath protecting the nerves, thus damaging the axons. Currently there is no cure for MS, but the disease activity can often be halted through medication. Strongest risk factor Already over 40 years ago it was discovered that genetic variation in the so-called HLA region is the strongest risk factor for developing disease. HLA encodes molecules that are involved in the immune system. However, the specific genes and molecular mechanisms behind the emergence of the disease are not fully established. By using molecular analyses and combining several studies (so-called meta-analysis), including around 14,000 patients with MS and a control group of more than 170,000 healthy individuals, researchers at Karolinska Institutet found that people with the major risk variant HLA-DRB1*15:01 have an increased expression of the HLA-DRB1 gene, thus increasing the risk for the disease. The researchers further discovered a so-called epigenetic regulation of HLA expression as the mechanism mediating this effect. “We show for the first time that epigenetic mechanisms can cause the disease. In addition, we can connect this mechanism to the genetic variant with the strongest risk for developing MS,” says Maja Jagodic, researcher at the Department of Clinical Neuroscience at Karolinska Institutet and one of the authors of the article. Protective variant The researchers also discovered a new HLA gene variant, rs9267649, which reduces the risk of developing MS. This protective variant decreases the HLA-DRB1 gene expression – through the same epigenetic regulation mechanism – thus reducing the risk for MS. The results open new avenues for potential alternative treatments based on specific epigenetic modulation, i.e. to prevent gene expression artificially. This gives hope for people with MS, as well as other autoimmune diseases. “Almost all autoimmune diseases are associated with HLA,” says Lara Kular, co-author and researcher at the same department. The study was carried out through an international collaboration with researchers in the US, Germany, Norway, Denmark, and Iceland (the deCode company). Financing has been granted through funding from, among others, the Swedish Research Council, Neuro, the Swedish Brain Foundation, the European MS Foundation, Petrus and Augusta Hedlund Foundation, AFA Insurance, Knut and Alice Wallenberg Foundation, Stockholm County Council, and AstraZeneca. Several of the researchers are employed by deCode genetics/Amgen Inc. For more information, see the scientific article. Publication ”DNA methylation as a mediator of HLA-DRB1*15:01 and a protective variant in multiple sclerosis” Lara Kular, Yun Liu, Sabrina Ruhrmann, Galina Zheleznyakova, Francesco Marabita, David Gomez-Cabrero, Tojo James, Ewoud Ewing, Magdalena Lindén, Bartosz Górnikiewicz, Shahin Aeinehband, Pernilla Stridh, Jenny Link, Till F. M. Andlauer, Christiane Gasperi, Heinz Wiendl, Frauke Zipp, Ralf Gold, Björn Tackenberg, Frank Weber, Bernhard Hemmer, Konstantin Strauch, Stefanie Heilmann-Heimbach, Rajesh Rawal, Ulf Schminke, Carsten O. Schmidt, Tim Kacprowski, Andre Franke, Matthias Laudes, Alexander T. Dilthey, Elisabeth G. Celius, Helle B. Søndergaard, Jesper Tegnér, Hanne F. Harbo, Annette B. Oturai, Sigurgeir Olafsson, Hannes P. Eggertsson, Bjarni V. Halldorsson, Haukur Hjaltason, Elias Olafsson, Ingileif Jonsdottir, Kari Stefansson, Tomas Olsson, Fredrik Piehl, Tomas J. Ekström, Ingrid Kockum, Andrew P. Feinberg, and Maja Jagodic Nature Communications, online 19 June 2018, doi: 10.1038/s41467-018-04732-5

Russian research centre delegation visits KI

Sat, 16/06/2018 - 11:36
Thursday 14 June saw a visit to Karolinska Institutet by a Russian delegation from the Almazov National Medical Research Centre. The purpose of the visit was to discuss ongoing and strengthened collaboration. The Almazov National Medical Research Centre is a medical institute in St. Petersburg, primarily specialising in cardiology, cardiovascular surgery, haematology and endocrinology. A number of researchers at the Russian research centre have defended their theses at Karolinska Institutet under the supervision of Göran Hansson, Per Eriksson, Ulf Hedin, Thomas Sejersen, Olle Söder, Boris Zhivotovsky and Anna Kostareva, among others. The latter is an associate at Karolinska Institutet’s Department of Women's and Children's Health and is at the same time head of the Institute of Molecular Biology and Genetics at Almazov National Medical Research Centre in Russia. International challenges require collaboration The Russian research centre, which recently achieved the status of national centre, lists Karolinska Institutet as its foremost collaboration partner. “The challenges currently facing healthcare systems and the medical environments in various countries are not national, but international. This demands joint efforts on the part of research institutes and universities in different countries to identify new solutions and innovative methods. Our almost 20 years of collaboration with Karolinska Institutet has so far proved successful and I believe that the current stage of our relationship is the most important for both parties,” says Professor Evgeny Shlyakhto, Director General of the Almazov National Medical Research Centre and President of the Russian Society of Cardiology. Important collaboration for KI The delegation was received in Aula Medica in the presence of Karolinska Institutet’s President Ole Petter Ottersen, together with researchers who in various ways participate in the Russian collaboration. “Our collaboration with the Almazov Medical Centre is important to KI as it is Russia’s leading institute for cardiological research. Much of the research collaboration takes place with the Department of Women's and Children's Health here at KI, something that is well aligned with the goals of Agenda 2030, both with regard to good health and wellbeing, and gender equality,” says President Ole Petter Ottersen.

No link found between oral antifungal drug and stillbirth

Wed, 13/06/2018 - 09:56
New research led from Karolinska Institutet does not support a suggested link between treatment with the oral antifungal drug fluconazole during pregnancy and an increased risk of stillbirth. The study is published in the prestigious medical journal JAMA. Vaginal candidiasis is common in pregnancy. Intravaginal formulations of topical antifungal drugs are first-line treatment for the infection, but oral antifungal drugs – typically fluconazole – are used in cases with severe symptoms, recurrent candidiasis episodes, or when topical treatment has failed. Although use of oral fluconazole during pregnancy is generally discouraged, between 0.5 and 4 per cent of pregnant women use this drug anyway; with the lower numbers representative of the Nordic countries and the higher numbers reported from the United States. “In a study published in JAMA 2016, we reported that fluconazole use in pregnancy was linked to an increased risk of spontaneous abortion, and our results suggested that the drug might also be associated with stillbirth. There are concerns based on animal data that oral fluconazole use in pregnancy may lead to fetal death. Given this concern and the paucity of studies in humans, we wanted to investigate the issue further,” says Björn Pasternak, associate professor at Karolinska Institiutet’s Department of Medicine in Solna who led the new study. Swedish and Norwegian register data  The researchers at Karolinska Institutet have now conducted an independent study in collaboration with the Norwegian Institute of Public Health to investigate if fluconazole use in pregnancy is associated with stillbirth and neonatal death. More than 10 000 women using fluconazole during pregnancy were identified using nationwide Swedish and Norwegian register data and compared to 100 000 women who did not use the drug. The study, published in JAMA, shows that use of fluconazole was not associated with increased risk of stillbirth or neonatal death, and the results were similar for different drug doses. “The findings are reassuring but need to be interpreted considering other pregnancy safety issues with fluconazole, such as malformations, before recommendations to guide clinical decisions are made,” concludes Dr Pasternak. The study was supported by the Thrasher Research Fund, the Magnus Bergvall Foundation, and the Karolinska Institutet Research Foundation. Björn Pasternak and Olof Stephansson were also supported by the Strategic Research Area Epidemiology program at Karolinska Institutet. Publication “Oral fluconazole in pregnancy and risk of stillbirth and neonatal death” Björn Pasternak, Viktor Wintzell, Kari Furu, Anders Engeland, Martin Neovius, Olof Stephansson JAMA, online 12 June 2018, doi: 10.1001/jama.2018.6237

Genome-editing tool could increase cancer risk

Mon, 11/06/2018 - 17:01
Therapeutic use of gene editing with the so-called CRISPR-Cas9 technique may inadvertently increase the risk of cancer, according to a new study from Karolinska Institutet and the University of Helsinki published in Nature Medicine. Researchers say that more studies are required in order to guarantee the safety of these ‘molecular scissors’ for gene-editing therapies. CRISPR-Cas9 is a molecular machine first discovered in bacteria that can be programmed to go to an exact place in the genome, where it cuts the DNA. These precise ‘molecular scissors’ can be used to correct faulty pieces of DNA and are currently being used in clinical trials for cancer immunotherapy in the US and China. New trials are expected to be launched soon so as to treat inherited blood disorders such as sickle cell anaemia. Activates the p53 protein Two independent articles published in the journal Nature Medicine now report that therapeutic application of the genome-editing tool may, in fact, increase the risk of cancer. In one of the studies, scientists from Karolinska Institutet and the University of Helsinki report that use of CRISPR-Cas9 in human cells in a laboratory setting can activate a protein known as p53, which acts as a cell’s ‘first aid kit’ for DNA breaks. Once active, p53 reduces the efficiency of CRISPR-Cas9 gene editing. Thus, cells that do not have p53 or are unable to activate it show better gene editing. Unfortunately, however, lack of p53 is also known to contribute to making cells grow uncontrollably and become cancerous. “By picking cells that have successfully repaired the damaged gene we intended to fix, we might inadvertently also pick cells without functional p53”, says Dr Emma Haapaniemi, researcher at the Department of Medicine, Huddinge, Karolinska Institutet and co-first author of the study. “If transplanted into a patient, as in gene therapy for inherited diseases, such cells could give rise to cancer, raising concerns for the safety of CRISPR-based gene therapies.” A powerful tool “CRISPR-Cas9 is a powerful tool with staggering therapeutic potential”, adds Dr Bernhard Schmierer, researcher at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet, and Head of the High Throughput Genome Engineering Facility of Science for Life Laboratory (SciLifeLab), who co-supervised the study. “Like all medical treatments however, CRISPR-Cas9-based therapies might have side effects, which the patients and caregivers should be aware of. Our study suggests that future work on the mechanisms that trigger p53 in response to CRISPR-Cas9 will be critical in improving the safety of CRISPR-Cas9-based therapies.” Parts of the study were carried out at the Swedish National Genomics Infrastructure, funded by SciLifeLab. The Knut and Alice Wallenberg Foundation, the Swedish Cancer Society, the Swedish Childhood Cancer Fund and the Academy of Finland supported the research. Publication “CRISPR/Cas9-genome editing induces a p53-mediated DNA damage response” Emma Haapaniemi, Sandeep Botla, Jenna Persson, Bernhard Schmierer and Jussi Taipale Nature Medicine, online 11 June 2018, doi: 10.1038/s41591-018-0049-z

Immune system does not recover despite cured hepatitis C infection

Mon, 11/06/2018 - 11:01
Changes to the immune system remain many years after a hepatitis C infection heals, a new study by researchers at Karolinska Institutet and Hannover Medical School shows. The findings, presented in Nature Communications, increases understanding about chronic infection and the way it regulates and impacts composition of the immune system. Infection with hepatitis C virus (HCV) turns almost always chronic and poses a major health problem around the world. The infection can lead to cirrhosis and cancer of the liver when the immune system fails to fight the virus. Eventually the immune system becomes exhausted. Since a couple of years, however, most patients with HCV can now be cured in a matter of a few weeks with revolutionary new medications. New measurement method used The current study included 40 patients with chronic HCV infection whom researchers followed before, during and after treatment with these new medications to investigate impact on the composition and diversity of the immune system. Diversity is vital to the ability of the immune system to fight infections. Of particular importance are natural killer cells (NK), a type of white blood cells. The researchers used flow cytometry and a new measurement method to derive the composition of the immune system, as well as the appearance of NK cells and their function in the blood. “Researchers in the field previously focused on analysing individual components but were unable to draw any comprehensive conclusions,” says Niklas Björkström, physician and associate professor at the Department of Medicine, Huddinge, Karolinska Institutet, who led the study. “The immune system is extraordinarily complex, incorporating a large number of interacting parts. We adapted new methods in order to assess and analyse that complexity in a fresh manner.” The immune system was affected The results showed that the overall composition of the immune system was affected by the chronic infection, with significantly reduced diversity among the NK cells. Many of the changes remained long after the virus had been eliminated by means of medication. Researchers have not yet determined the long-term implications but are currently exploring whether patients have a harder time fighting future infection. “One strength of our study is that we monitored patients for more than two years following elimination of the virus,” Benedikt Strunz, physician and doctoral student at the same department. “To the best of our knowledge, nobody has ever monitored over such a long term like this before.” Nevertheless, a number of questions are outstanding. Researchers would like to investigate consequences for a good deal longer than two years, as well as identify strategies for rejuvenating the immune system and increasing its diversity. The study was financed by the Swedish Research Council, Swedish Cancer Society, Strategic Research Foundation, Swedish Foundation for Medical Research, Radiumhemmet Research Foundation, Knut and Alice Wallenberg Foundation, NovoNordisk Foundation, Åke Wiberg Foundation, Centre for Innovative Medicine at Karolinska Institutet, Stockholm County Council, Karolinska Institutet, International Research Training Group with support by the German Research Foundation, Centre Research Grants, 900 with support of DFG, German Centre for Infection Research and German Liver Foundation. Publication ”Chronic hepatitis C virus infection irreversibly impacts human NK cell repertoire diversity” Benedikt Strunz, Julia Hengst, Katja Deterding, Michael P. Manns, Markus Cornberg, Hans-Gustaf Ljunggren, Heiner Wedemeyer, and Niklas K. Björkström. Nature Communications, online 11 June, 2018, doi: 10.1038/s41467-018-04685-9

Makerere University and KI strengthen partnership

Fri, 08/06/2018 - 15:05
A delegation from Uganda’s Makerere University visited Karolinska Institutet on 7-8 June for talks on strengthening the collaborative partnership between the two universities.   The delegation, which was led by Makerere University’s vice-chancellor Professor Barnabas Nawangwe, met the Karolinska Institutet (KI) management to discuss the long-standing collaboration between the two institutions. The partnership, which began back in 2003  with the first memorandum of understanding, enables doctoral students to obtain a joint PhD from both universities. “The partnership with Makerere University is one of our most important and far-reaching international partnerships, including as it does student and teacher exchange, joint doctoral education and research collaboration,” says KI president Ole Petter Ottersen. Discussed research collaboration During the visit, which included a tour of KI’s new Neo and Biomedicum research facilities, discussions were held on common research interests surrounding non-communicable diseases, such as cardiovascular diseases, cancer, diabetes and chronic respiratory infections that can lead premature death. Apart for the human suffering they cause, they are also a major global economic burden and most countries are doing all they can to develop their healthcare systems to prevent and treat the diseases. KI and Makerere University are now working on strengthening their research and collaboration in the NCD field and will be launching a pilot study in August on conducting longitudinal studies of risk factors for cardiovascular disease in Uganda.   Locally targeted research project To date, some 40 doctoral students from Uganda have graduated through the partnership and joint degree scheme, and over 500 peer-reviewed scientific articles have been published. It is hoped that the enlarged pool of researchers and locally targeted research on health issues and healthcare systems will have an impact on the development of Ugandan civil society. In many cases, the outcome has been policy reforms and  changes in practice. More than 300 students and teachers from KI and Makerere University have been on exchange at a Bachelor’s and Master’s level at each university, and strong research capacity has been built in both countries over the years. There are now many alumni from the partnership, and both universities consider them a group worth taking better care of.

High-sensitivity troponin test reduces risk of future heart attack

Tue, 05/06/2018 - 09:48
The newer high-sensitivity troponin test discovers smaller amounts of heart-specific proteins, troponins, than the older troponin test and thus identifies more myocardial infarction patients than before. A new study from Karolinska Institutet published in The Journal of the American College of Cardiology now reports that the risk of a future heart attack is lower in patients diagnosed with the new test. A blood test that measures the presence of heart-specific proteins called troponins is used by emergency clinics to diagnose myocardial infarction in patients with chest pain. For the past few years a newer laboratory method has been used at most hospitals in Sweden that is ten times more sensitive than the conventional troponin test. The high-sensitivity troponin test can discover heart attacks earlier so that treatment can commence, which is thought to improve the patients’ prognosis. “But there is a lack of larger studies examining whether the high-sensitivity troponin test is of any significance for patients with newly diagnosed myocardial infarction in terms of survival or the risk of another heart attack,” says study leader Dr Martin Holzmann, associate professor of epidemiology at Karolinska Institutet’s Department of Medicine in Solna and physician at Karolinska University Hospital. Fewer new heart attacks The study included all patients in Sweden who had had their first heart attack between 2009 and 2013. This gave a study population of almost 88,000 patients, 40,000 of whom had been diagnosed using the high-sensitivity troponin test and just over 47,000 using the conventional troponin test. The researchers found that five per cent more myocardial infarctions were being diagnosed in hospitals that used the high-sensitivity troponin test. A year after the heart attack was registered there was no difference in mortality between the two groups, although the number of new heart attacks was lower in the group that had been diagnosed using the high-sensitivity troponin test. “This surprised us,” says Dr Holzmann. “We didn’t think that the more sensitive test would affect the risk of future heart attacks.” Better risk assessment The use of coronary angiography and balloon angioplasty was 16 and 13 per cent more common, respectively in the patients diagnosed with the high-sensitivity troponin test. In the USA, where the new test was not approved until 2017, there are fears that the more sensitive methods can entail a large increase in the number of examinations with no benefit to the patients. “The increase we observed in our study was less than expected, which means that the high-sensitivity troponin test has enabled doctors to single out the patients who benefit from such intervention. We found no differences in medication between the two groups, so the differences in prognosis with fewer new heart attacks could be attributed to the fact that more coronary angiography and balloon dilation procedures have been performed on the right patients,” says Dr Holzmann, who also believes that the study supports the idea that the handful of hospitals in Sweden that still do not use the high-sensitivity troponin test should start to do so. The study was conducted in association with the Sahlgrenska Academy and Uppsala University. Martin Holzmann receives a grant from the Swedish Heart and Lung Foundation. Per-Ola Andersson has received a lecture fee from pharmaceutical companies Roche, Gilead and Janssen and a consultancy fee from AbbVie, CTI Bipharma and Glaxo-Smith-Kline. Kai M. Eggers has received a consultancy fee from pharmaceutical company Abbott Laboratories, AstraZeneca and Fiomi Diagnostics. Martin Holzmann has received a consultancy fee from pharmaceutical companies Actelion and Pfizer. No other potential conflicts of interest have been reported. Text: Inna Sevelius Publication “High-Sensitivity Troponins and Outcomes After Myocardial Infarction” Maria Odqvist, Per-Ola Andersson, Hans Tygesen, Kai M. Eggers, Martin J. Holzmann Journal of the American College of Cardiology (JACC), online 4 June 2018, doi: 10.1016/j.jacc.2018.03.515

Lipid molecules can be used for cancer growth

Thu, 31/05/2018 - 17:01
Cancer cells can when the blood supply is low use lipid molecules as fuel instead of blood glucose. This has been shown in animal tumour models by researchers at Karolinska Institutet in Sweden in a study published in Cell Metabolism. The mechanism may help explain why tumours often develop resistance to cancer drugs that inhibit the formation of blood vessels. Tumour growth and spread rely on angiogenesis, a process of growing new blood vessels that supply the cancer cells with nutrients and hormones, including glucose (sugar). Treatment with antiangiogenic drugs reduces the number of blood vessels in the tumour as well as the blood glucose supply. Many such drugs have been developed and are now used in human patients for treating various cancer types. However, the clinical benefits of antiangiogenic drugs in cancer patients are generally low and the cancers treated often develop a resistance to drugs, especially cancer types that grow close to fat tissues such as breast cancer, pancreatic cancer, liver cancer and prostate cancers. A new mechanism discovered In collaboration with Japanese and Chinese scientists, a research group at Karolinska Institutet in Sweden has discovered a new mechanism by which cancers can evade antiangiogenic treatment and become resistant. The reduction of tumour blood vessels results in low oxygenation in tumour tissues – a process called hypoxia. In the current study, the researchers show that hypoxia acts as a trigger to tell fat cells surrounding or within tumour tissues to break down the stored excessive lipid energy molecules. These lipid energy molecules can when the blood supply is low be used for cancer tissue expansion. “Based on this mechanism, we propose that a combination therapy consisting of antiangiogenic drugs and drugs blocking lipid energy pathways would be more effective for treating cancers. In animal tumour models, we have validated this very important concept, showing that combination therapy is superior to monotherapy,” says Yihai Cao, Professor at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet, who led the study. Explore combination therapy effects Professor Cao’s group now plans to work with drug companies and clinical oncologists to explore whether such a new combination therapy would improve the quality of life and lifespan in human cancer patients. The study was financed by the Swedish Research Council, the Swedish Cancer Foundation, Karolinska Institutet, the Torsten Söderberg Foundation, the Tore Nilson Foundation, the Ruth and Richard Julin Foundation, the Ögonfonden Foundation, the Wera Ekström Foundation, the Lars Hierta Memorial Foundation, National Natural Science Foundation of China, the International Research Fund for Subsidy of Kyushu University School of Medicine Alumni, the Martin Rind Foundation, the Maud and Birger Foundation, the Alex and Eva Wallström Foundation, the Robert Lundberg Memorial Foundation, the Swedish Diabetes Foundation, the Swedish Childhood Cancer Fund, the European Research Council, the Knut and Alice Wallenberg Foundation, and the Novo Nordisk Foundation. Publication “Cancer lipid metabolism confers antiangiogenic drug resistance” Hideki Iwamoto, Mitsuhiko Abe, Yunlong Yang, Dongmei Cui, Takahiro Seki, Masaki Nakamura, Kayoko Hosaka, Sharon Lim, Jieyu Wu, Xingkang He, Xiaoting Sun, Yongtian Lu, Qingjun Zhou, Weiyun Shi, Takuji Torimura, Guohui Nie, Qi Li, and Yihai Cao. Cell Metabolism, online 31 May 2018, doi: 10.1016/j.cmet.2018.05.005

Inefficient fat metabolism a possible cause of overweight

Thu, 31/05/2018 - 17:01
Protracted weight gain can, in some cases, be attributed to a reduced ability to metabolise fat, a new study from Karolinska Institutet published in the esteemed journal Cell Metabolism shows. Sensitive individuals might need more intensive lifestyle changes if they are to avoid becoming overweight and developing type 2 diabetes, claim the researchers, who are now developing means of measuring the ability to break down fat. Scientists have long sought an explanation for variations in the tendency for people to develop overweight, obesity and type 2 diabetes. Apart from lifestyle factors, such as diet and physical activity, physiological differences in metabolism – which would eventually lead to differences in weight gain amongst people – is suspected to play a part.  “We’ve suspected the presence of physiological mechanisms in fatty tissue that cause some people to become overweight and others not, despite similarities in lifestyle, and now we’ve found one,” says Mikael Rydén, professor of clinical and experimental fat tissue research at Karolinska Institutet’s Department of Medicine in Huddinge.  Analysed tissue samples  In the present study, the researchers analysed tissue samples from subcutaneous fat taken from the stomachs of women before and after a follow-up period of about ten years. What they discovered was that the ability of the fat cells to free fatty acids, a process called lipolysis, in the first tissue sample could be used to predict which women would have developed type 2 diabetes by the end of the study. They also found that these women had reduced activity in a small number of specific genes involved in lipolysis. Lipolysis is the process whereby a fat cell frees fatty acids, which are then used as a source of energy by the muscles. Researchers differentiate between basal lipolysis, which is continual, and hormone-stimulated lipolysis, which is triggered in response to an increase in energy requirement. The fat cells from the women who later developed overweight showed high basal but low hormone-stimulated lipolysis, which gave a 3 to 6 times higher risk of weight gain and type 2 diabetes.  “It’s a bit like a car that’s at high revs but that’s lost its ability to get into gear when it needs to,” says Professor Rydén. “The end result is that the fat cells eventually take up more fat than they can get rid of.”  New method The teams first discovered the correlation in a group of 54 women, who gave the first tissue samples between 2001 and 2003 and who were followed up 13 years later. They then repeated the analysis on 28 other women who gave samples in 1998 and were followed up ten years later, with the same results.  One of the researchers’ aims is to find ways of identifying individuals who run the risk of developing overweight and type 2 diabetes. Analyses of fat tissue are, however, relatively resource-demanding and can only be performed by specially equipped laboratories. Consequently, the researchers have developed an algorithm based on simple clinical and biochemical parameters from hundreds of individuals in order to obtain an indirect estimation of the quantity of fatty acids freed by the fat cells and thus predict weight gain. “Our results now need to be corroborated in larger studies and for men as well, but we hope to develop a clinically expedient way of identifying individuals at risk of developing overweight and type 2 diabetes, who might need more intensive lifestyle intervention than others to stay healthy,” says Professor Rydén. The study was financed by the Swedish Research Council, the Novo Nordisk Foundation, the Swedish Diabetes Foundation, the European Foundation for the Study of Diabetes, Stockholm County Council and Karolinska Institutet. Genetic analyses were performed with grants from CLARINS, 92200 Neuilly sur Seine. Publication  “Weight gain and impaired glucose metabolism in women is predicted by inefficient subcutaneous fat cell lipolysis” Peter Arner, Daniel P. Andersson, Jesper Bäckdahl, Ingrid Dahlman and Mikael Rydén Cell Metabolism, online 31 May 2018, doi: 10.1016/j.cmet.2018.05.004

Hans Möller appointed new CEO of Karolinska Institutet Holding AB

Thu, 31/05/2018 - 11:23
Karolinska Institutet Holding AB has recruited Hans Möller as the new CEO for the KI Holding Group. Hans Möller will assume his new position as of July 16. He is presently holding the position as responsible for the Edinburgh BioQuarter at the University of Edinburgh.  Hans has extensive experience of working in the interface between academy and industry, including as CEO for Ideon Science Park in Lund and as a founder of Ideonfonden and the incubator Ideon Innovation. Hans acted until April 2018 as chairman of the board for KI Science Park AB. – Hans´ experience and knowledge of how to create good conditions and platforms to explore outcomes of research and education, are extremely valuable, says Karin Dahlman-Wright, Chairman of the Board for KI Holding. – I very much look forward to leading KI Holding into the future. The possibilities and challenges to create the right conditions, to support innovations within Life Science are many. Sweden in general and KI in particular, has a special position when it comes to world leading research in Life Science, says Hans Möller.

Anti-inflammatory strategy stops aggressive childhood cancer

Mon, 28/05/2018 - 16:09
Researchers at Karolinska Institutet and Karolinska University Hospital have discovered that an anti-inflammatory drug candidate inhibiting the prostaglandin E2 producing enzyme mPGES-1 in the tumour stroma reduces tumour growth in experimental neuroblastoma models. The findings are published in EBioMedicine and open for new treatment strategies for this aggressive childhood cancer. “High-risk neuroblastoma is the most common and deadly cancer in infants. Novel therapies are highly warranted, in particular if they improve survival without adding adverse side effects,” says Professor Per Kogner at Karolinska Institutet’s Department of Women’s and Children’s Health, who led the study together with Professor Per-Johan Jakobsson at Karolinska Institutet’s Department of Medicine, Solna. Neuroblastoma is an aggressive nerve cell tumour which is diagnosed early, often before two years of age, and is stratified into different risk categories: low-risk, intermediate-risk and high-risk. Children with high-risk neuroblastoma receive intensive multi-modal treatment that has increased survival over the years but survivors both have high risk of life-threatening relapse and severe life-long side effects. Targeting of the stromal compartment has been suggested as a new strategy to increase survival further and to increase the quality of life of children who survive the disease. Targeting benign cells “We found that the dominant cell type in the tumour stroma, benign cancer-associated fibroblasts, were the main producers of prostaglandin E2 in neuroblastoma,” says Anna Kock, PhD at the Department of Women’s and Children’s Health and first author of the study. “These normal cells support the growth of cancer cells and should be targeted since they are more genetically stable than the malignant cells, and therefore less prone to develop resistance.” Assistant professor Karin Larsson at the Department of Medicine, Solna, who has worked on the project for several years, explains: “Prostaglandin E2 not only mediates fever and pain, but also drives inflammation in the tumours, promoting tumour growth. Inhibition of the enzyme mPGES-1, that catalyses the production of prostaglandin E2, resulted in reduced tumour growth in experimental neuroblastoma models.” The researchers believe that the finding could lead to improved survival with fewer side effects for children with neuroblastoma. Begin to understand the mechanisms ”mPGES-1 is an emerging target for treatment of inflammation and pain with cardioprotective properties. NSAIDs, which result in reduced prostaglandin levels, have long been implicated as prophylaxis against certain cancers. Our present study pinpoints mPGES-1 in neuroblastoma and we now begin to understand the mechanisms behind its involvement in cancer growth,” says Professor Per-Johan Jakobsson, who discovered mPGES-1. The work was financed by the Swedish Childhood Cancer Foundation, the Swedish Cancer Society, the Swedish Research Council, The Cancer Research Funds of Radiumhemmet, the Swedish Foundation for Strategic Research, the Swedish Rheumatism Association and grants from the EU’s seventh framework program. Publication “Inhibition of Microsomal Prostaglandin E Synthase-1 in Cancer-Associated Fibroblasts Suppresses Neuroblastoma Tumor Growth” Anna Kock, Karin Larsson, Filip Bergqvist, Nina Eissler, Lotta H.M. Elfman, Joan Raouf, Marina Korotkova, John Inge Johnsen, Per-Johan Jakobsson, Per Kogner EBioMedicine, online 24 May 2018, doi: 10.1016/j.ebiom.2018.05.008

“Neo – a fine example of democracy”

Mon, 28/05/2018 - 10:41
Transparency is the word that best describes Neo, Karolinska Institutet’s new research facility in Flemingsberg, which saw its official opening on 25 May.  The ribbon was cut by Princess Christina, Mrs Magnuson. Neo is a vital part of the Life Science cluster that puts the Flemingsberg campus on the map of world-leading research. “This building is a fine example of democracy,” says Karolinska Institute president Ole Petter Ottersen. “What makes Neo unique is that it’s open access, creating fantastic opportunities and enabling unbeatable interactions. Neo symbolises transparency and collaboration. With so many people of different nationalities and backgrounds, something magical is bound to happen.” Professor Ottersen officially opened Neo in the company of Princess Christina, Mrs Magnuson, honorary doctor of medicine at Karolinska Institutet.  “Officiating at the opening of Neo means so many things to me,” she said. “I was involved in KI’s second-centenary celebrations and made sure that we raised superb proceeds for research. It was my way of saying thank you for the honorary doctorate.”  She went on to talk about the many illnesses she has had in the course of her life, and how grateful she feels to be healthy again.  “I’ve got a feeling that something amazing is happening here at Neo, it’s like a global microcosmos, with all the researchers from at least thirty countries bringing all sorts of experience. It’s a fantastic crucible of knowledge.”  Room for 400 researchers Neo covers an area of 15,000 square metres, with space for around 400 researchers on seven floors. Five thousand square metres consists of laboratory space. Here can be found four of KI’s departments represented:  The Department of Biosciences and Nutrition. The Department of Medicine, Huddinge. The Department of Neurobiology, Care Sciences and Society. The Department of Laboratory Medicine. During the opening ceremony, participants were able to attend a number of scientific mini-symposia on different themes, such as Alzheimer’s and diabetes research.  An atrium exploding with colour The ground floor of Neo boasts the brilliantly coloured atrium with its eye-catching spiral staircase shaped like DNA spirals. Next to the atrium are two spherical auditoriums built from translucent concrete (butong) modules. The surface is like bubble-wrap. “The new feels newer and more complete when juxtaposed with something broken,” says architect Laila Ifwer Sternhoff at Link Arkitektur. “This is why we’ve used translucent concrete to create a sense of weight and antithesis against the new.” The architects have designed the building along the motifs of “new”, “modern” and “germination”. The sound in the auditoriums is intended to facilitate group work, for example, and the rooms are everyone’s – the departments have access to all parts of the building. “In Neo, we’ve created a positive work environment with no distinct boundaries between departments and research groups,” says Karl Ekwall, head of the Department of Biosciences and Nutrition. According to Jan Bolinder, head of the Department of Medicine, there has always been an open mind here as regards interdisciplinary scientific collaboration. “I’m convinced that this spirit will flourish even more at Neo with its mix of research groups from different departments,” he says. Maria Eriksdotter, head of the Department of Neurobiology, Care Sciences and Society: “The combination of strong experimental and clinical research in these outstanding new premises, combined with the physical proximity to the hospital and other universities gives us every opportunity to strengthen our already successful research.”   

Aggression neurons identified

Fri, 25/05/2018 - 17:01
High activity in a relatively poorly studied group of brain cells can be linked to aggressive behaviour in mice, a new study from Karolinska Institutet shows. Using optogenetic techniques, the researchers were able to control aggression in mice by stimulating or inhibiting these cells. The results, which are published in the scientific journal Nature Neuroscience, contribute to a new understanding of the biological mechanisms behind aggressive behaviour. Aggression is a behaviour found throughout the animal kingdom and that shapes human lives from early schoolyard encounters to – in its most extreme expression – armed, global conflict. Like all behaviour, aggression originates in the brain. However, the identity of the neurons that are involved, and how their properties contribute to the stereotyped expression that interpersonal conflicts often manifest, remains largely a mystery. Researchers at Karolinska Institutet now show that a previously relatively unknown group of neurons in the ventral premammillary nucleus (PMv) of the hypothalamus, an evolutionarily well-preserved part of the brain that controls many of our fundamental drives, plays a key role in initiating and organising aggressive behaviour. Were able to control aggression in mice Studying male mice, the researchers found that the animals that displayed aggression when a new male was placed in their home cage also had more active PMv neurons. By activating the PMv through optogenetics, whereby neurons are controlled using light, they were able to initiate aggressive behaviour in situations where animals do not normally attack, and by inhibiting the PMv, interrupt an ongoing attack. The mapping of the PMv neurons also showed that they in turn can activate other brain regions, such as reward centres. “That could explain why mice naturally make their way to a place where they have experienced an aggressive situation,” says the study’s lead author Stefanos Stagkourakis, doctoral student at the Department of Neuroscience, Karolinska Institutet. “We also found that the brief activation of the PMv cells could trigger a protracted outburst, which may explain something we all recognise – how after a quarrel has ended, the feeling of antagonism can persist for a long time.” Aggression is often ritualised Aggression between male mice is often ritualised and focused less on causing harm than on establishing a group hierarchy by determining the strongest member. This can be studied experimentally in the so-called tube test, wherein two mice encounter each other in a narrow corridor, from which observations can be made about submission and dominance. By inhibiting the PMv cells in a dominant male and stimulating the same cells in a submissive male, the researchers were able to invert their mutual hierarchical status. “One of the most surprising findings in our study was that the role-switch we achieved by manipulating PMv activity during an encounter lasted up to two weeks,” says study leader Christian Broberger, associate professor at the Department of Neuroscience. The researchers hope that the results can contribute to new strategies for managing aggression. “Aggressive behaviour and violence cause injury and lasting mental trauma for many people, with costly structural and economic consequences for society,” says Dr Broberger. “Our study adds fundamental biological knowledge about its origins.” The study was financed by the European Research Council, the Swedish Research Council, the Swedish Brain Fund, the Novo Nordisk Foundation, and the Strategic Research Programme in Diabetes at Karolinska Institutet. Publication "A neural network for intermale aggression to establish social hierarchy” Stagkourakis S, Spigolon G, Williams P, Protzmann J, Fisone G, Broberger C Nature Neuroscience, online 25 May 2018, doi: 10.1038/s41593-018-0153-x

Strengthening and developing healthcare science

Tue, 22/05/2018 - 08:18
The future of healthcare science was the topic of discussion at a roundtable meeting held at Karolinska Institutet on 7 May, when deans, healthcare scientists, politicians, patient representatives and healthcare providers gathered to discuss what needs to be done to secure the quality of healthcare science. A Swedish Research Council report shows that healthcare science in Sweden maintains world-class standards, and according to a 2018 ranking, nursing research at Karolinska Institutet (KI) tops the list in Sweden, is third in Europe and is eleventh in the world. But the challenges facing healthcare science are many, hence the discussion, initiated by the management of the healthcare science Strategic Research Area, which is jointly run by KI and Umeå University. Journalist Marianne Rundström was moderator at the meeting, which produced some practical suggestions for improving the conditions of healthcare science. The group discussed the need to develop communication and implementation in healthcare research and to strengthen the academy-clinic partnership. PhDs are to be attracted back into healthcare by being offered more advanced responsibilities in keeping with their scientific competence, and clearer career paths must be created in both the healthcare and academic sectors. “KI will be advertising professorships in strategic areas, of which healthcare science is one,” said Anders Gustafsson, Dean of Research at KI. “Since a majority of healthcare scientists are women, this will also help us reach the 60 per cent target in terms of the proportion of women amongst newly appointed professors.” The discussion also addressed exposing status disparity between different research disciplines. Assessment criteria and processes commonly take a biomedical perspective, at the expense of healthcare science. Jan Hillert, R&D director at Karolinska University Hospital, held that both students and staff active in healthcare must become better at measuring and analysing results and quality in order to enhance the “value” of healthcare science and practice. “Joint appointments are the right way to go, and KI’s managers should take care to ensure that doctoral students and researchers do both clinical and academic work,” said Mikael Ohrling, hospital director for the Stockholm County healthcare area. Anna Starbrink (L), the county council’s Executive Member for Healthcare, said that the great potential for affecting the future of healthcare science lay in revising the council’s strategy along with KI. The benefits of healthcare science Two examples of high quality healthcare science at KI that have benefited patients are the MIMA model, which is used to reduce postnatal injury, and the DöBra-programme, a national research programme focussing on dying, death and grieving. Text: Anna-Maria Loimi and Sabina Bossi Photo: David Lagerlöf

Cell types underlying schizophrenia identified

Mon, 21/05/2018 - 17:00
Scientists at Karolinska Institutet in Sweden and University of North Carolina, USA, have identified the cell types underlying schizophrenia in a new study published in Nature Genetics. The findings offer a roadmap for the development of new therapies to target the condition. Schizophrenia is an often devastating disorder causing huge human suffering. Genetic studies have linked hundreds of genes to schizophrenia, each contributing a small part to the risk of developing the disease. The great abundance of identified genes have made it difficult to design experiments. Scientists have been struggling to understand what is linking the genes together and whether these genes affect the entire brain diffusely or certain components more. By combining new maps of all the genes used in different cell types in the brain with detailed lists of the genes associated with schizophrenia, scientists in the current study could identify the types of cells that underlie the disorder. The genetics point towards certain cell types being much more implicated than others. One finding was that there appears to be a few major cell types contributing to the disorder, each of which originates in distinct areas of the brain. “This marks a transition in how we can use large genetic studies to understand the biology of disease. With the results from this study, we are giving the scientific community a chance to focus their efforts where it will give maximum effect”, says Jens Hjerling-Leffler, research group leader at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet, one of the main authors. Possible treatment development The findings offer a roadmap for the development of new therapies. “One question now is whether these brain cell types are related to the clinical features of schizophrenia. For example, greater dysfunction in one cell type could make treatment response less likely. Dysfunction in a different cell type could increase the chances of long-term cognitive effects. This would have important implications for development of new treatments, as separate drugs may be required for each cell type involved,” says co-main author Patrick Sullivan, Professor at the Department of Medical Epidemiology and Biostatistics at Karolinska Institutet and Yeargan Distinguished Professor in the Department of Genetics and Psychiatry at the University of North Carolina. As a result of rapid progress in two separate fields of science; human genetics and single cell transcriptomics, it only recently has become possible to study diseases in this way. In coming years the researchers suggest that the approach should lead to breakthroughs in the biological understanding of other complex disorders such as autism, major depression, and eating disorders. “Understanding which cell types are affected in a disease is of critical importance for developing new medicines to improve their treatment. If we do not know what causes a disorder we cannot study how to treat it,” says Nathan Skene, Postdoc at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet and UCL Institute of Neurology, UK, one of the lead authors. The study was financed by the Swedish Research Council, StratNeuro, the Wellcome Trust, the Swedish Brain Foundation, the Swiss National Science Foundation, and the US National Institute of Mental Health. Schizophrenia genetic results were generated with support from the Medical Research Council Centre, Program Grant and Project Grant, and funding from the European Union’s Seventh Framework Programme for research, technological development and demonstration (CRESTAR Consortium). The authors report the following potentially competing financial interests. PF Sullivan: Lundbeck (advisory committee). J Hjerling-Leffler: Cartana (Scientific Adviser) and Roche (grant recipient). Publication ”Genetic identification of brain cell types underlying schizophrenia” Nathan G Skene, Julien Bryois, Trygve E Bakken, Gerome Breen, James J Crowley, Héléna A Gaspar, Paola Giusti-Rodriguez, Rebecca D Hodge, Jeremy A Miller, Ana B Muñoz-Manchado, Michael C O’Donovan, Michael J Owen, Antonio F Pardiñas, Jesper Ryge, James T R Walters, Sten Linnarsson, Ed S Lein, Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium, Patrick F Sullivan and Jens Hjerling-Leffler. Nature Genetics, online 21 May, 2018, doi: 10.1038/s41588-018-0129-5

Close check on footballing brains

Mon, 21/05/2018 - 13:59
The KI PhD student and psychologist Torbjörn Vestberg has attracted considerable attention for his new book “Hjärnboll” [Brainball] , which he co-authored with the KI researcher Predrag Petrovic and the journalist Thomas Lerner. The book presents reasoning and puts forward hypotheses and knowledge concerning which functions in the frontal lobe are essential in order to become a really successful football player – factors that are of particular interest in the weeks leading up to the World Cup tournament in Russia.  It was not a foregone conclusion that Torbjörn Vestberg would become a psychologist, having previously been a business developer and a Baptist pastor. He originally comes from Norrköping, but it was during his six years as a psychologist in China that he became interested in how the brain functions. In China, his work included developing requirements profiles for managers in the world of trade and industry, and it turned out that in China they conducted measurements differently to how it is done in Sweden.  – I started thinking about what it actually was that we were measuring – how relevant is it to look at how introverted or extroverted a person is when you’re looking for manager material? It actually says nothing about how successful a person can be as a manager, says Torbjörn.  He began his training in psychology after the age of 40. He has previously worked at a recording company that specialised in classical music, and before that he was a pastor in the Baptist church, having studied theology. – It might sound a bit exotic, but you have to remember that the free churches had a lot of followers in Sweden when I was growing up,” says Torbjörn. One of the driving forces for writing the book was actually to show that you can change track and do something sensible even as an old man. Decisions at very high speed The first impulse to investigate how people react to different stimuli came when Torbjörn Vestberg did his practical work as a psychology student at Karolinska University Hospital. He was struck by how people with diagnoses of psychosis, for example, were often worse at dealing with external stimuli rationally, if at all. He started thinking about what group of people could be considered the direct opposite and came up with top-class football players. They are forced to make decisions at very high speeds while being faced with very great demands to be able to adapt to an environment that is changing at breakneck speed – and they need to make the “right” decision in order to be successful. These are all abilities that are described as executive. – The more successful the player, the better his executive capacity, says Torbjörn. He has confirmed that there is a marked difference if you compare players in the Swedish premier league with players in Division one – in other words, two levels down in the series system. He has also tested the football players Andrés Iniesta and Xavi of Barcelona, and they scored even higher. But even the division one players had a higher executive capacity than the normal population. Torbjörn Vestberg is currently devoting his time to a study in which he, together with associate professor Predrag Petrovic, is testing a large group of elite players in order to see how executive functions interact with physical form, technique, mental fortitude, social skills and experience. The specific benefit of the research may be a better understanding of how the brain’s capacity in relation to executive functions drives behaviour in a number of different contexts and professions. It could be a matter of functional impairment as well as above-average ability. With regard to his academic career, Torbjörn Vestberg is in no rush: he intends to complete his doctorate before his sixtieth birthday next autumn – but until then it’s time for the football World Cup. What do you think are the chances for the Swedish team? – In general, I don’t have great hopes for Sweden – there’s usually too much focus on everyone doing well, and I don’t believe that’s a factor for success. I don’t actually like watching football on TV – I’m usually most interested in the players who don’t have the ball, and they’re not usually shown on TV,” says Torbjörn. Interview on TV 4 Interview on SR P1 How the tests work The tests are tried and tested from previous ADHD investigations and from the diagnosis of concussion. The tests are completed using both pen and paper and computers, and they indicate the capacity for, among other things, concentration, cognitive flexibility, general speed, impulse control, working memory and creativity. The tests measure both speed and accuracy, though speed is prioritised. The basis for the book’s research is based on twenty studies that have developed over the last seven years concerning executive functions and performance in sport and working life.  

New disease mechanism in chronic smokers discovered

Mon, 21/05/2018 - 12:53
A new study led by researchers from Karolinska Institutet shows that an immune signalling protein called IL-26 is increased among chronic smokers with lung disease. This involvement reveals disease mechanisms of interest for developing more effective therapy for these hard-to-treat patients. The study is published in the journal Clinical Science. Chronic tobacco smokers have an increased rate of chronic obstructive pulmonary disease (COPD), chronic bronchitis and bacterial lung infections and these disorders respond poorly to available therapies. Previous research has shown that smokers with lung disease have an accumulation of a type of white blood cell, called neutrophils, in their airways. Dr Karlhans Fru Che and Professor Anders Lindén at Karolinska Institutet led a team of researchers from universities in Sweden and Finland to investigate why this is the case. May represent a novel mechanism The researchers found that an immune signalling protein called IL-26 (interleukin-26) is present at high levels in the lungs of these patients. IL-26 levels were higher than normal in the chronic smokers, regardless of whether they had clinically stable COPD. Those who had chronic bronchitis or growth of bacteria had higher levels of IL-26 than those who did not. Moreover, the chronic smokers with exacerbations of COPD had higher levels of IL-26 than those with clinically stable COPD. Upregulation of IL-26 in the airways in response to tobacco smoke may represent a novel mechanism by which neutrophil recruitment to the lung is regulated, according to the researchers. “By showing that IL-26 is involved in the excessive mobilization of neutrophils in chronic smokers with or without COPD and chronic bronchitis, we strengthen the evidence that this cytokine bears potential as a target for monitoring of and therapeutic intervention in airway disorders characterised by neutrophilic inflammation,” says Dr Karlhans Fru Che at the Institute of Environmental Medicine, Karolinska Institutet, lead author on the study. More studies are needed The researchers acknowledge that more studies are needed to improve the understanding of the more precise mechanisms of action of IL-26 before this cytokine can be targeted in clinical trials. The study was carried out as a collaboration between Lund University, University of Gothenburg, University of Oulu, Karolinska University Hospital and Karolinska Institutet. The research was funded by the Swedish Heart-Lung Foundation, the Swedish Research Council, Karolinska Institutet, Region Skåne, Stockholms County Council and Region Västra Götaland, among others. This news article is based on a press release from The Biochemical Society, which owns the journal Clinical Science. Publication “The neutrophil-mobilizing cytokine interleukin-26 in the airways of long-term tobacco smokers” Karlhans Fru Che, Ellen Tufvesson, Sara Tengvall, Elisa Lappi-Blanco, Riitta Kaarteenaho, Bettina Levänen, Marie Ekberg, Annelie Brauner, Åsa M. Wheelock, Leif Bjermer, C. Magnus Sköld, Anders Lindén Clinical Science, online 21 May 2018, doi: 10.1042/CS20180057