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Aug. 31, 2010 - U of T part of international effort identifying gene linked to child epilep
U of T part of international effort identifying gene linked to child epilepsy Mutations are often associated with Mabry Syndrome Tuesday, August 31, 2010 Researchers from the University of Toronto are part of an international team which has identified the gene causing the childhood form of epilepsy known as Mabry Syndrome. In an article published Aug. 30 in the journal Nature Genetics, an international team including Dr.Miles Thompson, a post-doctoral fellow, and Professor David Cole of laboratory medicine and pathobiology detail how they identified that mutations in the PIGV gene are often associated with Mabry Syndrome -- a rare genetic disorder which results in developmental delay and seizures. “Identifying the gene responsible is a key element in diagnosing Mabry Syndrome. While we are looking for other genes involved, it remains an important step toward improving treatments,” said Thompson, of the Department of Laboratory Medicine and Pathobiology and Banting Institute. Along with Cole of Sunnybrook Health Sciences Centre, Dr. Marjan Nezarati at North York General Hospital in Toronto and researchers in Germany, the Netherlands and France, Thompson co-ordinated the Canadian portion of the project - which used homozygosity mapping, exome sequencing and a candidate gene approach to identify the role of the PIGV gene in cases of Mabry syndrome. The discovery of the gene builds on research published in the July 2010 edition of the American Journal of Medical Genetics by Thompson, Nezarati, Cole and colleagues, which defined the syndrome for the first time and allowed the identification of the gene for the disorder, which will now allow better diagnosis of the condition -- and ultimately better treatment for patients and their families. Thompson's work has been supported by Epilepsy Canada. For more information, please contact mabry.syndrome@gmail.com Thompson’s contribution to the discovery reported in Nature Genetics is the result of four years of research work made possible by financial support from Epilepsy Canada, and he will be a recipient of a special award from the organization’s president on Aug. 31 at a public Epilepsy Canada meeting. For more information on the event, see http://www.epilepsy.ca/. http://www.news.utoronto.ca/health-and-medicine/u-of-t-part-of-international-effort-identifying-gene-linked-to-child-epilep.html … read more>>

Other News

Aug. 25, 2010 - New and improved Research & Innovation website launched
New and improved Research & Innovation website launched Refreshed site easier for researchers and staff to navigate Wednesday, August 25, 2010 Where do you find information on the upcoming Canada Foundation for Innovation proposal deadline? How about changes to research ethics policies? Or whom to contact regarding invention disclosures? The office of the vice-president (research) has redesigned the award-winning Research & Innovation (previously known as Experience Research) website to make it easier for the university’s research community to access the information they need to conduct their work. “We realized that while we had done good work in creating a site that promoted U of T’s research strengths and achievements to the world outside the university, it was still difficult and confusing for our researchers and their staff members to find the information they need,” said Professor Paul Young, vice president (research). “So our communications team worked with professionals throughout our portfolio over the past year reinventing the site so it would be easier to get this information. I think this is a huge improvement.” The refreshed site is now divided into two:• The right-hand side is now called For Researchers and Administrators and enables U of T faculty and staff to find essential information directly about Funding, Awards and Honours, Research Management & Accountability, Ethics, and Commercialization and Partnerships.• The left-hand side still features popular sections such as Behind the Headlines, video about U of T research, the “sliders” that profile research across the disciplines and connect to listings of centres and institutes, the portfolio’s Strategic Initiatives project, links to coverage of research in the external press and easier-to-find links to publications such as Edge Magazine and the Ideas That Could Change the World annual report. Another new feature of the Researchers and Administrators site is a section on Project RAISE (Research Administration Improvement & System Enhancement) - a joint project between the research office and the Enterprise Applications and Solutions Integration (EASI) team of the chief information officer portfolio. RAISE will strengthen business processes and create web-based tools for the administration of research by faculty and staff, saving time and facilitating accountability. The team is also designing a new service where faculty and staff can receive alerts about important research-related news - such as funding program changes and deadlines. “We are entering into a new era of improved service to the U of T research community,” said Judith Chadwick, assistant vice-president (research services). “A big part of this initiative is making sure our research community gets the information they need as quickly and easily as possible. That is a key part of this new version of our website and the alerts service we are developing.” Chadwick expects the alerts to be up and running early in 2011. The Research & Innovation website can be found at: http://www.research.utoronto.ca/. … read more>>

Aug. 23, 2010 - Neurology: Brain Communication Circuits
Neurology: Brain Communication Circuits Aug 23, 2010 Gaining greater insight into the structure of, or wiring behind, how the brain orchestrates body movements could have important implications for future treatment strategies for patients with Parkinson's disease or other neurological or psychiatric disorders. Findings from TWRI researchers are providing important new information on how the brain controls signals between its two hemispheres and what this could mean for patients. Dr. Robert Chen and collaborators stimulated different motor control regions of the brain to better understand short- (SIHI) and long-latency interhemispheric inhibition (LIHI)--periods of message delay between hemispheres--and short- (SICI) and long-interval intracortical inhibition (LICI)--periods of message delay within one hemisphere. Findings show that the organization of brain circuitry in the hemisphere where the message starts and where the message is targeted to differs, depending on the type of inhibition that is taking place. Also, the ability of specific types of inhibitory signals to work together may be important in the control of precise movements. "Our findings show that communication between brain hemispheres, and within a hemisphere, likely share some common circuitry and we are going to further investigate one pathway in particular," explains Dr. Chen. "If we can determine how the brain organizes and coordinates signals regarding movement, we may one day understand how this communication malfunctions in Parkinson's disease, schizophrenia and other movement disorders in order to help accelerate the development of new, targeted treatments." Find this story on the web at: www@uhnresearch.ca … read more>>

Aug. 20, 2010 - U of T researcher discovers key protein involved in DNA repair
U of T researcher discovers key protein involved in DNA repair Discovery gives insight into the way cells protect their own genetic material Friday, August 20, 2010 In a groundbreaking study, U of T researchers including Professors Daniel Durocher, Anne©\Claude Gingras and Frank Sicheri have uncovered a protein called OTUB1 that blocks DNA damage in the cell¡ªa discovery that may lead to the development of strategies to improve some cancer therapies. Lead author Durocher, a senior investigator at Mount Sinai Hospital¡¯s Samuel Lunenfeld Research Institute and the Thomas Kierans Research Chair in Mechanisms of Cancer Development, as well as colleagues at U of T, Mount Sinai Hospital and the Keio University in Japan, have revealed pivotal new information on how cells regulate their genetic material. In addition, the discovery improves understanding of familial breast and ovarian cancer, as the research shows that OTUB1 inhibits the action of BRCA1, a DNA repair protein often mutated in these cancers. ¡°In recent years, we have been very good at finding proteins necessary for DNA repair,¡± said Durocher. ¡°What we did not appreciate was that gatekeepers existed to inhibit the capacity of the cell to repair DNA. The obvious question now is: Can we enhance the ability of the cell to repair DNA by blocking OTUB1?¡± The findings were reported in the August 19 issue of the prestigious international journal Nature, in which only one or two high©\impact papers are published weekly. The researchers identified OTUB1 using RNA interference (or RNAi), an approach that helps scientists determine the functions of proteins and genes. After exposing cells to radiation, Durocher and his team used RNAi to discover that OTUB1 inhibits a cell¡¯s DNA repair mechanisms, through its role in a process known as ubiquination. Ubiquitins are small regulatory proteins in cells. The addition of many ubiquitins onto a targetprotein can act as a ¡®mayday¡¯ signal at the site of DNA damage, attracting repair mechanisms to fix the damage. Durocher¡¯s team found that OTUB1 mutes the mayday signal by preventing the addition of ubiquitin units. ¡°Perhaps the biggest surprise was that OTUB1 works by an entirely new and elegant mechanism,¡± said Durocher. ¡°Mutations in genes that repair our DNA can lead to cancer,infertility and immune deficiency. Therefore, inhibiting the proteins that block DNA repair couldlead to new types of therapeutics for these diseases.¡± For example, Durocher explained that by inhibiting OTUB1, healthy cells may be better able to withstand cancer treatment with radiation and certain chemotherapy medications such as doxorubicin. As well, inhibiting OTUB1 may lead to treatments for genetic immunodeficiency disorders such as RIDDLE syndrome, in which cells lose their ability to repair DNA damage. The study was supported by the Canadian Institutes of Health Research. http://www.news.utoronto.ca/lead-stories/u-of-t-researcher-discovers-key-protein-involved-in-dna-repair.html … read more>>

Aug. 13, 2010 - U of T launches Innovations and Partnerships Office
U of T launches Innovations and Partnerships Office New name reflects new mission Friday, August 13, 2010 The Innovations Group (TIG) at U of T has changed its name to the Innovations and Partnerships Office (IPO) to fully describe the function of the part of the vice-president (research) portfolio that helps faculty members develop partnerships and assists them in disclosing their innovations. “IPO recognizes and realizes the potential of innovations developed here at U of T by building meaningful relationships with members from the private, public and government sectors. Our new identity better reflects this mandate,” said Professor Peter Lewis, IPO’s acting executive director and U of T’s associate vice-president (research). TIG’s primary function was to focus on commercialization. In this role, the office received and assessed disclosures, sought financial resources, helped translate ideas into potential products and services and dealt with the legalities of marketing innovations. All that activity, however, didn’t allow for sufficient resources to direct towards seeking partnerships, specifically business development opportunities for researchers. The creation of MaRS Innovation (MI), a member-driven commercialization engine, redefined the entire playing field. IPO, as an MI member, has streamlined its commercialization efforts. It now receives disclosures and passes them on to MI for evaluation and, if accepted, for creation of an agency agreement by a ‘deal team’ composed of MI and IPO staff. “As a result, some IPO employees now ‘walk the halls’ and in time will visit every U of T faculty, department and lab to inform and assist professors with the disclosure process,” said Lewis. “More important, from the process of ‘walking the halls’ we will expand our own awareness about the diverse research being done at U of T and will be better able to appropriately match professors to relevant partnership opportunities - the partnership piece of IPO.” By disclosing their inventions to IPO, professors can bring benefits to both global society and businesses, and potentially reap financial gains through revenue generation. http://www.news.utoronto.ca/campus-news/u-of-t-launches-innovations-and-partnerships-office.html … read more>>

Aug. 13, 2010 - Parkinson's Disease: Understanding the Anatomy of Movement
Parkinson's Disease: Understanding the Anatomy of Movement  Announced on Aug 13, 2010 Over a prolonged period of time, patients undergoing treatment for Parkinson's disease (PD) with the drug commonly known as L-DOPA--a chemical related to dopamine used to increase levels of dopamine in the brain--commonly experience motor complications such as dyskinesia, or involuntary or uncontrolled body movements. However, recent findings out of TWRI are helping scientists better understand the mechanics behind dyskinesia and where future treatments could be targeted to prevent it. Dr. Jonathan Brotchie and his colleagues used a large animal model of PD and a series of in-depth molecular and physiological investigations to show that two areas in the brain intimately involved in motor control (the striatum and motor cortex middle layers) have increased levels of 5-HT2A receptors--brain proteins responsible for passing important information between cells. Moreover, the study provides evidence showing the pathway that information travels to promote L-DOPA induced dyskinsia. Comments Dr. Brotchie, "Our findings are adding important new knowledge of how prolonged L-DOPA use could promote dyskinesia in patients with PD. Building on these anatomical findings, future studies are necessary to see if, and how, chemicals blocking 5-HT2A from working could help prevent dyskinesia." Find this story on the web at: www@uhnresearch.ca   … read more>>

Aug. 06, 2010 - Lupus: Closely Monitoring Heart Disease Risk in Patients
Lupus: Closely Monitoring Heart Disease Risk in Patients Announced on Aug 06, 2010 Dr. Murray Urowitz, a Senior Scientist at the Toronto Western Research Institute and member of AARC, with TWRI/AARC collaborator Dr. Dafna Glaman and their fellow currently in Australia, have discovered important new findings highlighting the variability of cholesterol and blood pressure (BP) in patients with systemic lupus erythmatosus (lupus or SLE)--an autoimmune disease affecting the bodys connective tissue, resulting in damage to internal organs, joints and skin. "This study bears significant clinical importance because patients with SLE are at an increased risk of coronary artery disease (CAD), and understanding how the levels of total cholesterol (TC) and BP change over time will greatly assist medical teams to better understand risk factors and improve patient care," explains Dr. Urowitz. Sampling over 26,000 measurements of TC, and systolic and diastolic BP (SBP and DBP) from greater than 1,200 patients over a nine-year follow-up period, the study determined that over time, 64.7% of patients varied between having normal and elevated cholesterol levels, while 46.4% of patients varied between having normal or abnormally high BP, emphasizing the need for vigilant monitoring of lipid levels during active disease and treatment with corticosteroids. Also of note, patients using antimalarials had lower TC, SBP and DBP levels. "Other independent factors related to TC and BP were smoking and hormone replacement therapy," says Dr. Urowitz. "We have provided strong evidence showing the important concept of TC and BP variability over time, which makes a strong case for finding summary measures that better capture cumulative exposure to these risk factors over time. Future studies will work towards an even greater in-depth understanding of the complex relationship between various CAD risk factors in SLE." Find this story on the web at: www@uhnresearch.ca  … read more>>

Jul. 30, 2010 - U of T researchers identify trio of genes that help Salmonella cause diseas
U of T researchers identify trio of genes that help Salmonella cause disease Finding clues to battling antibiotic resistance, treating infections Friday, July 30, 2010 University of Toronto researchers have uncovered three genes in the Salmonella bacteria critical for it to cause disease and withstand antibiotic treatment and may hold the key to improved disease treatment. The study was published today in the journal Molecular Cell and conducted in partnership with laboratories headed by Dr. Michael Ibba at Ohio State University and Dr. Ferric Fang at the University of Washington in Seattle. The team found that three bacterial genes called poxA, yjeK andefp work together to protect the bacterial cell from stresses it encounters during infection and antibiotic treatment. Mice infected with Salmonella strains lacking any one of these genes do not get sick. Even more crucial is the discovery that these Salmonella strains are also highly sensitive to treatment with a variety of antibiotics and disinfectants. “Salmonella continues to be a major source of food poisoning in North America. In the past few years we have seen numerous recalls of food products including a major recall of peanut products just two years ago and a current outbreak in Canada resulting in the recall of headcheese.” said Professor William Navarre of U of T Faculty of Medicine’s Department of Molecular Genetics and lead author of the study. “We now aim to develop drugs that can inactivate poxA, yjeK or efp. By preventing these bacteria from responding appropriately to stress, we predict we will be able to prevent bacterial disease and decrease their resistance to antibiotics. We’re excited by the fact these genes exist in other bacteria that cause disease including E. coli so our strategy may work in cases beyond Salmonella.” The three genes are critical for bacterial resistance to chemical stress. “Despite their small size bacteria are actually quite sophisticated” said Navarre, “Salmonella and E. coli bacteria grown in a mild amount of disinfectant or antibiotics are able to make adjustments so that they can survive without too much of a problem. In order to do this they must be able to detect that they are in trouble and activate the genes necessary to make the appropriate changes to their metabolism and cell structure. “We are finding that Salmonella lacking poxA, yjeK or efp are unable to cause disease because they cannot withstand attack from the various immunity factors present in the mouse. Many of those factors attack the membrane of the bacterial cell and we believe that without poxA, yjeK or efp that the Salmonella becomes easy prey because it can’t respond to the damage.” The research team screened thousands of Salmonella bacteria for variants with altered resistance to certain antimicrobial compounds. Several of the identified variants had defects in either the poxA or yjeK genes. Using genetic engineering the researchers removed the poxA and yjeK genes from normal Salmonella cells. These newly constructed variants were also unable to cause disease in mice and were sensitive to a wide number of antibiotics. It was subsequently found that these two genes were working with the third gene, efp. The efp gene codes for a protein called “elongation factor P” or EF-P that allows other genes necessary for stress resistance to work properly. EF-P carries out its function by mimicking another molecule called tRNA, that plays a role in the synthesis of bacterial proteins. The researchers, in collaboration with the University of Toronto Structural Genomics Group headed by Professor Aled Edwards and Professor Alexei Savchenko, also determined the molecular structure of the PoxA protein and found that it was strikingly similar to a “tRNA synthetase,” an enzyme that modifies tRNA. “It’s a beautiful case of molecular mimicry where a molecule that usually modifies a tRNA evolved to instead modify a protein that looks like a tRNA.” http://www.news.utoronto.ca/health-and-medicine/u-of-t-researchers-identify-trio-of-genes-that-help-salmonella-cause-diseas.html … read more>>

Jul. 26, 2010 - Immunity and Disease: Cell Therapy to Combat Infectious Disease
Immunity and Disease: Cell Therapy to Combat Infectious Disease July 26, 2010 Sepsis--frequently called 'blood poisoning'--is the number one cause of death in critically ill patients and is caused by overwhelming infection. Currently, sepsis remains without an effective specific treatment strategy; however, new findings out of UHN, St. Michael's Hospital and the University of Ottawa harness the immune-regulating power of stem cells to improve clinical outcome in this devastating disease. Co-led by TGRI's Dr. W. Conrad Liles and the University of Ottawa's Dr. Duncan Stewart, a series of molecular investigations found that administering mesenchymal stem (stromal) cells (MSCs)--stem cells from the bone marrow--to mice with sepsis (and receiving appropriate antimicrobial therapy) significantly reduced mortality in comparison to mice who did not receive MSC treatment. Studies also went on to show that MSCs significantly reduced the level of proteins that are responsible for promoting inflammation, which is a critical component of sepsis. "MSCs were able to up-regulate or 'turn on' genes involved in positive immune action, specifically killing invading bacteria," explains Dr. Liles. "Our studies show that, by reducing inflammation and promoting the eradication of bacteria, MSC therapy may be an effective tool, in partnership with current therapies, to reduce sepsis-related morbidity and death. This study demonstrates the potential for therapeutic use of MSCs for sepsis and provides the basis for launching a clinical trial in patients with sepsis." Find this story on the web at: www@uhnresearch.ca    … read more>>

Jul. 23, 2010 - Influenza A: Identifying New Cell Population to Battle Infection
Influenza A: Identifying New Cell Population to Battle Infection  July 23, 2010 Recent findings out of the Arthritis and Autoimmunity Research Centre (AARC) and TGRI uncover a new population of immune cells--late-activator antigen presenting cells (LAPC)--that may play a pivotal role in regulating resistance against pulmonary influenza A virus infections. The influenza A virus primarily affects organs and tissues responsible for breathing; and once infected, these viruses grow rapidly in number (within hours of first exposure) sending the immune system into a tail spin. As explained by study lead and AARC Director Dr. Eleanor Fish, "For influenza virus infections, our bodies are equipped with two very distinct responses, known as T1 and T2 immunity. Our study specifically looked at T2 immunity within the context of disease cause and progression. We chose this route of study primarily because our understanding of the mechanics behind this T2 response is still in its infancy." Using an animal model of influenza A infection, Dr. Fish and her team conducted an in-depth investigation, revealing the novel LAPC cell population, as well as showing how these cells differ and are unique from other well-known immune cells. Importantly, the study also explained how LAPCs modulate influenza A infection to coax our T2 immune response into action. "Collectively, our findings here show that LAPCs have wide-spread involvement in different virus infections and they appear to have distinct roles in the immune response to virus infections. For flu infection, LAPCs leave the lungs much later than other virus fighting cells and trigger different responses," says Dr. Fish. "Future studies looking at the function of LAPCs in different virus infections and how they respond to different pathogens may provide us with new therapeutic targets for the treatment for a host of infections, including influenza A virus."   Find this story on the web at: www@uhnresearch.ca    … read more>>

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