BreakThrough Digest Medical News |
- Antibodies reverse type 1 diabetes in new immunotherapy study
- Novel nanotherapeutic delivers clot-busting drugs directly to obstructed blood vessels
- New study maps hotspots of human-animal infectious diseases and emerging disease outbreaks
- Discovery improves understanding of early onset inflammatory disease
- Rewiring DNA circuitry could help treat asthma
- Groundbreaking discovery of mechanism that controls obesity, atherosclerosis
| Antibodies reverse type 1 diabetes in new immunotherapy study Posted: 04 Jul 2012 09:00 PM PDT
Scientists at the University of North Carolina School of Medicine have used injections of antibodies to rapidly reverse the onset of Type I diabetes in mice genetically bred to develop the disease. Moreover, just two injections maintained disease remission indefinitely without harming the immune system.
The findings, published online ahead of print (June 29, 2012) in the journal Diabetes, suggest for the first time that using a short course of immunotherapy may someday be of value for reversing the onset of Type I diabetes in recently diagnosed people. This form of diabetes, formerly known as insulin-dependent diabetes mellitus, is an autoimmune disease in which the body’s own immune T cells target and destroy insulin-producing beta cells in the pancreas. The immune system consists of T cells that are required for maintaining immunity against different bacterial and viral pathogens. In people who develop Type 1 diabetes, “autoreactive” T cells that actively destroy beta cells are not kept in check as they are in healthy people. Senior study author Roland Tisch, PhD, professor of microbiology and immunology at UNC, said a need for effective immunotherapies also exists to treat Type 1 diabetes in people already living with the disease. “Clinically, there have been some promising results using so-called depleting antibodies in recently diagnosed Type 1 diabetic patients, but the disease process is blocked for only a short period of time,” Tisch said. “These antibodies don’t discriminate between T cells normally required for maintaining immunity to disease-causing pathogens and the autoreactive T cells. Therefore T cells involved in maintaining normal immune function are also going to be depleted. “You’re getting some efficacy from immunotherapy but its only transient, it doesn’t reverse the disease, and there are various complications associated with the use of these depleting antibodies.” Tisch said his UNC lab has been studying the use of certain “non-depleting antibodies.” These bind to particular proteins known as CD4 and CD8 expressed by all T cells. Just as the name implies, when these non-depleting antibodies selectively bind to CD4 and CD8 they don’t destroy the T cells; the overall numbers of T cells are unaffected. With this in mind Tisch wanted to determine whether these non-depleting antibodies could have a therapeutic effect in the non-obese diabetic, or NOD mouse, an excellent model for human Type 1 diabetes. The answer is yes. In some of the recently diagnosed NOD mice, blood sugar levels returned to normal within 48 hours of treatment. Within five days, about 80 percent of the animals had undergone diabetes remission, reversal of clinical diabetes. “The protective effect is very rapid, and once established, is long-term,” he said. “We followed the animals in excess of 400 days after the two antibody treatments, and the majority remained free of diabetes. And although the antibodies are cleared from within the animals in 2-3 weeks after treatment, the protective effect persists.” The study showed that beta cells in the NOD mice had been rescued from ongoing autoimmune destruction. In looking for the mechanism to explain how the therapy worked, the researchers found that the antibodies had a very selective effect on T cells that mediated beta cell destruction. After treatment, “all the T cells that we would normally see in the pancreas or in tissues associated with the pancreas had been purged,” said Tisch. This despite the fact that the numbers of T cells found in other tissues and blood were unaffected. The researchers also found an increase in the numbers of “immune regulatory” T cells. In the healthy individual, these regulatory T cells block autoimmunity, Tisch explained. “They protect us from the autoreactive cells that all of us have. And that’s why most of us don’t develop autoimmune diseases such as Type 1 diabetes.” “We’ve demonstrated that the use of non-depleting antibodies is very robust. We’re now generating and plan to test antibodies that are specific for the human version of the CD4 and CD8 molecules.” ### UNC study coauthors with Tisch are first-author, Zuoan Li, (now at the University of Iowa); Ramiro Diz, Aaron Martin, Yves Maurice Morillon, Douglas E. Kline, (now at the University of Chicago); Li Li (now at Harvard Medical School); and Bo Wang. Support for research came from the National Institute of Diabetes and Digestive and Kidney Diseases, part of the National Institutes of Health; and from the Juvenile Diabetes Research Foundation. Contact: Les Lang |
| Novel nanotherapeutic delivers clot-busting drugs directly to obstructed blood vessels Posted: 04 Jul 2012 09:00 PM PDT
Researchers at the Wyss Institute for Biologically Inspired Engineering at Harvard University have developed a novel biomimetic strategy that delivers life-saving nanotherapeutics directly to obstructed blood vessels, dissolving blood clots before they cause serious damage or even death. This new approach enables thrombus dissolution while using only a fraction of the drug dose normally required, thereby minimizing bleeding side effects that currently limit widespread use of clot-busting drugs.
The research findings, which were published online today in the journal Science, have significant implications for treating major causes of death, such as heart attack, stroke, and pulmonary embolism, that are caused by acute vascular blockage by blood thrombi. The inspiration for the targeted vascular nanotherapeutic approach came from the way in which normal blood platelets rapidly adhere to the lining of narrowed vessels, contributing to the development of atherosclerotic plaques. When vessels narrow, high shear stresses provide a physical cue for circulating platelets to stick to the vessel wall selectively in these regions. The vascular nanotherapeutic is similarly about the size of a platelet, but it is an aggregate of biodegradable nanoparticles that have been coated with the clot-busting drug, tissue plasminogen activator (tPA). Much like when a wet ball of sand breaks up into individual grains when it is sheared between two hands, the aggregates selectively dissociate and release tPA-coated nanoparticles that bind to clots and degrade them when they sense high shear stress in regions of vascular narrowing, such as caused by blood clot formation. Disruption of normal blood flow to the heart, lung, and brain due to thrombosis is one of the leading causes of death and long-term adult disability in the developing world. Today, patients with pulmonary embolism, strokes, heart attacks, and other types of acute thrombosis leading to near-complete vascular occlusion, are most frequently treated in an acute care hospital setting using systemic dosages of powerful clot-dissolving drugs. Because these drugs can cause severe and often fatal bleeding as they circulate freely throughout the body, the size of the dosage given to any patient is limited because efficacy must be balanced against risk. The new shear-activated nanotherapeutic has the potential to overcome these efficacy limitations. By targeting and concentrating drug at the precise site of the blood vessel obstruction, the Wyss team has been able to achieve improved survival in mice with occluded lung vessels with less than 1/50th of the normal therapeutic dose, which should translate into fewer side effects and greater safety. This raises the possibility that, in the future, an emergency technician might be able immediately administer this nanotherapeutic to anyone suspected of having a life-threatening blood clot in a vital organ before the patient even reached the hospital. The inter-disciplinary and inter-institutional collaborative research team, which was led by Wyss Founding Director Donald Ingber M.D., Ph.D., and Wyss Technology Development Fellow Netanel Korin, Ph.D., also included Wyss postdoctoral Fellow Mathumai Kanapathipillai, Ph.D., as well as Benjamin D. Matthews, Marilena Crescente, Alexander Brill, Tadanori Mammoto, Kaustabh Ghosh, Samuel Jurek, Sidi A. Bencherif, Deen Bhatta, Ahmet U. Coskun, Charles L. Feldman, and Denisa D. Wagner from Brigham and Women’s Hospital, Children’s Hospital Boston, Harvard Medical School, the Harvard School of Engineering and Applied Sciences, and Northeastern University. Ingber is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Children’s Hospital Boston, and Professor of Bioengineering at Harvard’s School of Engineering and Applied Sciences. Commenting on the work, Ingber noted that “the vascular nanotherapeutic we developed that selectively becomes activated in regions of high shear stress, much like living platelets do, is a wonderful example of how we at the Wyss Institute take inspiration from biology, and how biomimetic strategies can lead to new and unexpected solutions to age-old problems that existing technologies can’t address.” ### About the Wyss Institute for Biologically Inspired Engineering at Harvard University
The Wyss Institute for Biologically Inspired Engineering at Harvard University uses Nature’s design principles to develop bioinspired materials and devices that will transform medicine and create a more sustainable world. Working as an alliance among Harvard’s Schools of Medicine, Engineering, and Arts & Sciences, and in partnership with Beth Israel Deaconess Medical Center, Brigham and Women’s Hospital, Children’s Hospital Boston, Dana Farber Cancer Institute, Massachusetts General Hospital, the University of Massachusetts Medical School, Spaulding Rehabilitation Hospital, and Boston University, the Institute crosses disciplinary and institutional barriers to engage in high-risk research that leads to transformative technological breakthroughs. By emulating Nature’s principles for self-organizing and self-regulating, Wyss researchers are developing innovative new engineering solutions for healthcare, energy, architecture, robotics, and manufacturing. These technologies are translated into commercial products and therapies through collaborations with clinical investigators, corporate alliances, and new start-ups. Contact: Twig Mowatt |
| New study maps hotspots of human-animal infectious diseases and emerging disease outbreaks Posted: 03 Jul 2012 09:00 PM PDT
A new global study mapping human-animal diseases like tuberculosis (TB) and Rift Valley fever finds that an “unlucky” 13 zoonoses are responsible for 2.4 billion cases of human illness and 2.2 million deaths per year. The vast majority occur in low- and middle-income countries.
The report, which was conducted by the International Livestock Research Institute (ILRI), the Institute of Zoology (UK) and the Hanoi School of Public Health in Vietnam, maps poverty, livestock-keeping and the diseases humans get from animals, and presents a “top 20″ list of geographical hotspots. “From cyst-causing tapeworms to avian flu, zoonoses present a major threat to human and animal health,” said Delia Grace, a veterinary epidemiologist and food safety expert with ILRI in Kenya and lead author of the study. “Targeting the diseases in the hardest hit countries is crucial to protecting global health as well as to reducing severe levels of poverty and illness among the world’s one billion poor livestock keepers.” “Exploding global demand for livestock products is likely to fuel the spread of a wide range of human-animal infectious diseases,” Grace added. According to the study, Ethiopia, Nigeria, and Tanzania in Africa, as well as India in Asia, have the highest zoonotic disease burdens, with widespread illness and death. Meanwhile, the northeastern United States, Western Europe (especially the United Kingdom), Brazil and parts of Southeast Asia may be hotspots of “emerging zoonoses”?those that are newly infecting humans, are newly virulent, or have newly become drug resistant. The study examined the likely impacts of livestock intensification and climate change on the 13 zoonotic diseases currently causing the greatest harm to the world’s poor. The report, Mapping of Poverty and Likely Zoonoses Hotspots, was developed with support from the United Kingdom’s Department for International Development (DFID). The goal of the research was to identify areas where better control of zoonotic diseases would most benefit poor people. It also updates a map of emerging disease events published in the science journal Nature in 2008 by Jones et al.i Remarkably, some 60 percent of all human diseases and 75 percent of all emerging infectious diseases are zoonotic. Among the high-priority zoonoses studied here are “endemic zoonoses,” such as brucellosis, which cause the vast majority of illness and death in poor countries; “epidemic zoonoses,” which typically occur as outbreaks, such as anthrax and Rift Valley fever; and the relatively rare “emerging zoonoses,” such as bird flu, a few of which, like HIV/AIDS, spread to cause global cataclysms. While zoonoses can be transmitted to people by either wild or domesticated animals, most human infections are acquired from the world’s 24 billion livestock, including pigs, poultry, cattle, goats, sheep and camels. Poverty, zoonoses and markets
Today, 2.5 billion people live on less than US$2.00 per day. Nearly three-quarters of the rural poor and some one-third of the urban poor depend on livestock for their food, income, traction, manure or other services. Livestock provide poor households with up to half their income and between 6 and 35 percent of their protein consumption. The loss of a single milking animal can be devastating to such households. Worse, of course, is the loss of a family member to zoonotic disease. Despite the danger of zoonoses, the growing global demand for meat and milk products is a big opportunity for poor livestock keepers. “Increased demand will continue over the coming decades, driven by rising populations and incomes, urbanization and changing diets in emerging economies,” noted Steve Staal, deputy director general-research at ILRI. “Greater access to global and regional meat markets could move millions of poor livestock keepers out of poverty if they can effectively participate in meeting that rising demand.” But zoonoses present a major obstacle to their efforts. The study estimates, for example, that about one in eight livestock in poor countries are affected by brucellosis; this reduces milk and meat production in cattle by around 8 percent. Thus, while the developing world’s booming livestock markets represent a pathway out of poverty for many, the presence of zoonotic diseases can perpetuate rather than reduce poverty and hunger in livestock-keeping communities. The study found a 99 percent correlation between country levels of protein-energy malnutrition and the burden of zoonoses. “Many poor livestock keepers are not even meeting their own protein and energy needs,” said Staal. “Too often, animal diseases, including zoonotic diseases, confound their greatest efforts to escape poverty and hunger.” Assessing the burden of zoonoses
The researchers initially reviewed 56 zoonoses that together are responsible for around 2.5 billion cases of human illness and 2.7 million human deaths per year. A more detailed study was made of the 13 zoonoses identified as most important, based on analysis of 1,000 surveys covering more than 10 million people, 6 million animals and 6,000 food or environment samples. The analysis found high levels of infection with these zoonoses among livestock in poor countries. For example, 27 percent of livestock in developing countries showed signs of current or past infection with bacterial food-borne disease?a source of food contamination and widespread illness. The researchers attribute at least one-third of global diarrheal disease to zoonotic causes, and find this disease to be the biggest zoonotic threat to public health. In the booming livestock sector of developing countries, by far the fastest growing sectors are poultry and pigs. “As production, processing and retail food chains intensify, there are greater risks of food-borne illnesses, especially in poorly managed systems,” said John McDermott, director of the CGIAR Research Program on Agriculture for Nutrition and Health, led by the International Food Policy Research Institute (IFPRI). “Historically, high-density pig and poultry populations have been important in maintaining and mixing influenza populations. A major concern is that as new livestock systems intensify, particularly small- and medium-sized pig production, that more intensive systems will allow the maintenance and transmission of pathogens. A number of new zoonoses, such as Nipah virus infections, have emerged in that way.” Intensification and disease spread
The most rapid changes in pig and poultry farming are expected in Burkina Faso and Ghana in Africa and India, Myanmar and Pakistan in Asia. Pig and poultry farming is also intensifying more rapidly than other farm commodity sectors, with more animals being raised in more concentrated spaces, which raises the risk of disease spread. Assessing the likely impacts of livestock intensification on the high-priority zoonoses, the study found that livestock density is associated more with disease “event emergence” than with overall disease burdens. Both the northeastern United States and Western Europe have high densities of livestock and high levels of disease emergence (e.g., BSE, or “mad cow” disease, and Lyme disease), but low numbers of people falling sick and dying from zoonotic diseases. The latter is almost certainly due to the relatively good disease reporting and health care available in these rich countries. Bovine tuberculosis is a good example of a zoonotic disease that is now rare in both livestock and human populations in rich countries but continues to plague poor countries, where it infects about 7 percent of cattle, reducing their production by 6 percent. Most infected cattle have the bovine form of TB, but both the human and bovine forms of TB can infect cows and people. Results of this study suggest that the burden of zoonotic forms of TB may be underestimated, with bovine TB causing up to 10 percent of human TB cases. Human TB remains one of the most important and common human diseases in poor countries; in 2010, 12 million people suffered from active disease, with 80 percent of all new cases occurring in 22 developing countries. Massive underreporting
“We found massive underreporting of zoonoses and animal diseases in general in poor countries,” said Grace. “In sub-Saharan Africa, for example, 99.9 percent of livestock losses do not appear in official disease reports. Surveillance is not fulfilling its purpose.” The surveillance lacking today will be even more needed in the future, as the climate changes, she added. Previous research by ILRI and others indicates that areas with increased rainfall and flooding will have increased risk of zoonoses, particularly those diseases transmitted by insects or associated with stagnant water or flooding. The main finding of the study is that most of the burden of zoonoses and most of the opportunities for alleviating zoonoses lie in just a few countries, notably Ethiopia, Nigeria, and India. These three countries have the highest number of poor livestock keepers, the highest number of malnourished people, and are in the top five countries for both absolute numbers affected with zoonoses and relative intensity of zoonoses infection. “These findings allow us to focus on the hotspots of zoonoses and poverty, within which we should be able to make a difference,” said Grace. ### i Nature, Vol 451, 990-993, 21 February 2008, Global trends in emerging infectious diseases, Kate E. Jones, Nikkita G. Patel, Marc. Levy, Adam Storeygard, Deborah Balk, John L. Gittleman, & Peter Daszak. The International Livestock Research Institute (ILRI) works with partners worldwide to support the role livestock play in pathways out of poverty. ILRI research products help people in developing countries enhance their livestock-dependent livelihoods, health and environments through better livestock systems, health, productivity and marketing. ILRI is a member of the CGIAR Consortium of 15 research centres working for a food-secure future. ILRI has its headquarters in Nairobi, Kenya, a principal campus in Addis Ababa, Ethiopia, and other offices in southern and West Africa and South, Southeast and East Asia. Contact: Jeff Haskins Michelle Geis |
| Discovery improves understanding of early onset inflammatory disease Posted: 03 Jul 2012 09:00 PM PDT
Scientists at the University of East Anglia (UEA) have discovered a ‘constant cloud’ of potent inflammatory molecules surrounding the cells responsible for diseases such as thickening of the arteries and rheumatoid arthritis.
Published online today by The Journal of Cell Science, the findings could eventually lead to new treatments for chronic inflammatory diseases. Cardiovascular disease arising from atherosclerosis (thickening of the arteries) kills around 17 million people worldwide each year, including 120,000 people in England and Wales, while rheumatoid arthritis affects around 400,000 people in the UK. The UEA team studied a type of white blood cell called monocytes. Monocytes play an important role in the human immune system and help protect our bodies against infection. But they can also invade tissue, triggering the early stages of common inflammatory diseases. The researchers detected for the first time that monocytes were surrounded by a constant cloud. This cloud was found to be made up of potent inflammatory molecules called adenosine triphosphate, or ATP. Further study showed that the ATP molecules were being propelled through the cell wall by the actions of lysosomes. Lysosomes are sub-cellular compartments within blood cells which had previously been thought to only break down cell waste. “These unexpected findings shed light on the very early stages in the development of inflammatory diseases such as atherosclerosis and rheumatoid arthritis,” said lead author Dr Samuel Fountain of UEA’s School of Biological Sciences. “We found that lysosomes are actually highly dynamic and play a key role in the way inflammatory cells function. This is an exciting development that we hope will lead to the discovery of new targets for inflammatory drugs in around five years and potential new treatments beyond that.” Dr Fountain said further study was now needed to investigate how to control the release of ATP by lysosomes in monocytes and other white blood cells, and to understand how inflammation may be affected in patients with inherited diseases involving lysosomes. Dr Fountain is a Biotechnology and Biological Sciences Research Council (BBSRC) David Phillips Fellow and recently received £0.9m from the BBSRC to study how cells use ATP as a signalling molecule. ### ‘Constitutive lysosome exocytosis releases ATP and engages P2Y receptors in human monocytes’ by V Sivaramakrishnan (UEA), S Bidula (UEA), H Campwala (UEA), D Katikaneni (UEA) and S Fountain (UEA) is published online on July 5 by the Journal of Cell Science. The paper will be available here: http://jcs.biologists.org/content/early/recent Contact: Simon Dunford |
| Rewiring DNA circuitry could help treat asthma Posted: 03 Jul 2012 09:00 PM PDT
Reprogramming asthma-promoting immune cells in mice diminishes airway damage and inflammation, and could potentially lead to new treatments for people with asthma, researchers have found.
The researchers were able to reprogram the asthma-promoting cells (called Th2 (T-helper 2) cells) after identifying an enzyme that modifies the DNA of these cells. The enzyme could be a target for the development of new treatments for chronic inflammatory diseases, in particular allergic asthma, caused by an excess of Th2 cells. Walter and Eliza Hall Institute researcher Dr Rhys Allan led the research while working at Institut Curie, Paris. The research team from Institut Curie, National Centre for Scientific Research (CNRS), France, National Institute of Health and Medical Research (INSERM), France, and Montpellier Cancer Research Institute published the study today in the journal Nature. Dr Allan said the research team discovered that the enzyme Suv39h1 could switch off genes to control the function of Th2 cells, which are key to the allergic response. “Th2 cells have an important function in the immune response, but they also play a significant role in diseases such as allergic asthma,” Dr Allan said. “People with asthma have too many Th2 cells, which produce chemical signals that inflame and damage the upper airways. In this study, we discovered that the Suv39h1 enzyme plays a critical role in programming these asthma-promoting cells, making it a potential target for new therapies to treat asthma.” More than two million Australians have asthma ? approximately one in 10 people ? and the disease is even more common among Indigenous Australians. The prevalence of asthma in children in Australia is among the highest in the world. Dr Allan said the Suv39h1 enzyme was part of the ‘epigenetic circuitry’ of Th2 cells. “Epigenetics refers to changes or modifications in the DNA that alter how genes are switched on and off, without changing the fundamental DNA sequence. Suv39h1 effectively ‘tags’ the DNA to tell the cells which genes they need to switch on or off to promote an allergic response.” Using agents that inhibit Suv39h1 could destabilise Th2 cells in people who have an excess of these asthma-promoting cells so they no longer cause inflammation, Dr Allan said. “We had the idea that erasing these epigenetic tags could ‘short-circuit’ the asthma-promoting Th2 cells and diminish the inflammatory immune response. And, in fact, in mouse models of allergic asthma, blocking this pathway with an inhibitory compound did reduce allergy-related airway damage. Ultimately, our results have identified a potential target for therapeutic intervention in asthma and potentially other Th2-mediated inflammatory diseases, which could improve outcomes for patients,” Dr Allan said. Dr Allan is continuing to study the epigenetic circuitry of asthma-promoting immune cells in the institute’s Molecular Immunology division, with funding from the National Health and Medical Research Council of Australia (NHMRC). ### The research was supported by Institut Curie, CNRS and INSERM. Dr Allan was funded by an INSERM-NHMRC exchange fellowship. Contact: Liz Williams |
| Groundbreaking discovery of mechanism that controls obesity, atherosclerosis Posted: 03 Jul 2012 09:00 PM PDT
A*STAR scientists from the Institute of Molecular and Cell Biology (IMCB) and the Singapore Bioimaging Consortium (SBIC) have discovered a new signalling pathway that controls both obesity and atherosclerosis. The team demonstrated, for the first time, that mice deficient in the Wip1 gene were resistant to weight gain and atherosclerosis via regulation of the Ataxia telangiectasia mutated gene (ATM) and its downstream signalling molecule mTor. These groundbreaking findings were published in the journal Cell Metabolism on 3rd July and may provide significant new avenues for therapeutic interventions for obesity and atherosclerosis.
Obesity and atherosclerosis-related diseases account for over one-third of deaths in the Western world. Controlling these conditions remains a major challenge due to an incomplete understanding of the molecular pathways involved. Atherosclerosis, a progressive disease of the large arteries, is an underlying cause of many cardiovascular diseases. In Singapore, 10.8% of our population is obese and cardiovascular disease accounted for 31.9% of all deaths in 2010. Obesity and atherosclerosis are accompanied by the accumulation of lipid droplets in adipocytes (fat cells) and in foam cells respectively. Foam cells can subsequently rupture, damaging blood vessels, and contributing to further progression of atherosclerosis. The scientists discovered that Wip1 deficient mice, even when fed a high-fat diet, were resistant to obesity and atherosclerosis by preventing the accumulation of lipid droplets. This appeared to be through increased autophagy, the normal process by which the body degrades its own cellular components. They showed that the Wip1 deficient mice exhibited increased activity of ATM which decreased mTor signalling, resulting in increased autophagy. This degraded the lipid droplets and suppressed obesity and atherosclerosis. “This is the first time that Wip1-dependent regulation of ATM-mTor pathway has been linked to authophagy and cholesterol efflux thus providing an entirely new avenue for treatment of obesity and atherosclerosis,” said Dr Dmitry Bulavin, Senior Principal Investigator at IMCB and lead author of this paper. Mapping the mechanism to cancer
The scientists are hopeful that this ATM-mTor pathway could similarly map onto cancer to suppress tumour progression. Similar to suppression of obesity and atherosclerosis, activation of autophagy in cancer cells could result in degradation of cellular content that is essential for cancer cells to sustain rapid proliferation. This, in turn, will result in suppression of cancer growth. Said Dr Dmitry Bulavin, “We are building on this research to investigate if the same mechanism could also control tumour progression and hence potentially unlock new therapeutic treatments targeting Wip1, ATM and mTor in cancer as well and the preliminary results are promising.” This discovery also adds to the growing significance of ATM as an important gene with a key role in protecting us from major pathological conditions. Previous work has established Wip1-dependent regulation of ATM as a potent regulator of tumorigenesis via activation of tumour-suppressor p53. Together, these three pathological conditions – obesity, atherosclerosis and cancer – account for more than 70% of mortality worldwide, making ATM-related pathways very attractive therapeutic targets. 8Prof Hong Wanjin, Executive Director of IMCB, said, “This is the first time that these important molecules have been integrated into a linear pathway that plays a prominent role in controlling obesity and atherosclerosis. It is a fine example of how fundamental research can shed light on biological and medical questions to potentially open new avenues of formulating therapeutic strategies for the benefit of patients.” ### Notes for Editor:
The research findings described in this news release can be found in the July 3rd print issue of Cell Metabolism under the title “Wip1-dependent regulation of autophagy, obesity and atherosclerosis” by Xavier Le Guezennec1, Anna Brichkina1, Yi-Fu Huang1, Elena Kostromina2, Weiping Han2, Dmitry V Bulavin*1. 1 Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos 138673, Singapore 2 Laboratory of Metabolic Medicine, Singapore Bioimaging Consortium, Biomedical Sciences Institutes, 11 Biopolis Way, Helios 138667, Singapore AGENCY FOR SCIENCE, TECHNOLOGY AND RESEARCH (A*STAR) Enclosed: Annex A ? Two aortas stained for atherosclerosis For media queries and clarifications, please contact: Ong Siok Ming (Ms) About Institute of Molecular and Cell Biology (IMCB)
The Institute of Molecular and Cell Biology (IMCB) is a member of Singapore’s Agency for Science, Technology and Research (A*STAR) and is funded through A*STAR’s Biomedical Research Council (BMRC). It is a world-class research institute that focuses its activities on six major fields: Cell Biology, Developmental Biology, Genomics, Structural Biology, Infectious Diseases, Cancer Biology and Translational Research, with core strengths in cell cycling, cell signalling, cell death, cell motility and protein trafficking. Its achievements include leading an international consortium that successfully sequenced the entire pufferfish (fugu) genome. The IMCB was awarded the Nikkei Prize 2000 for Technological Innovation in recognition of its growth into a leading international research centre and its collaboration with industry and research institutes worldwide. Established in 1987, the Institute currently has 26 independent research groups, eight core facilities and 300 researchers. For more information about IMCB, please visit www.imcb.a-star.edu.sg About the Singapore Bioimaging Consortium (SBIC)
The Singapore Bioimaging Consortium (SBIC) is a research consortium of the Agency for Science, Technology and Research (A*STAR) in Singapore. SBIC aims to build a coordinated national programme for imaging research, bringing together substantial strengths in the physical sciences and engineering and those in the biomedical sciences. It seeks to identify and consolidate the various bioimaging capabilities across local research institutes, universities and hospitals, in order to speed the development of biomedical research discoveries. SBIC has built up an extensive network of partners, through collaborations and joint appointments with research institutes, university and clinical departments, and the industry. Its partners include the Singapore Institute for Clinical Sciences, the NUS Chemistry Department, the National Cancer Centre, Duke-NUS, Agilent, Bruker, Bayer, GlaxoSmithKline, Takeda, and Merck. For more information about SBIC, please visit www.sbic.a-star.edu.sg. About the Agency for Science, Technology and Research (A*STAR)
The Agency for Science, Technology and Research (A*STAR) is the lead agency for fostering world-class scientific research and talent for a vibrant knowledge-based and innovation-driven Singapore. A*STAR oversees 14 biomedical sciences and physical sciences and engineering research institutes, and six consortia & centres, located in Biopolis and Fusionopolis as well as their immediate vicinity. A*STAR supports Singapore’s key economic clusters by providing intellectual, human and industrial capital to its partners in industry. It also supports extramural research in the universities, and with other local and international partners. For more information about A*STAR, please visit www.a-star.edu.sg. Contact: Ong Siok Ming |
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