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News Article | April 17, 2017
Site: www.eurekalert.org

Less than a year after publishing research identifying a single genetic mutation that caused multiple sclerosis (MS) in two Canadian families, scientists at the University of British Columbia have found a combination of two other mutations in another family that made them highly susceptible to the disease. The "double gene" mutation was identified in a large Canadian family with five members diagnosed with MS - all of whom had the DNA abnormality. Two other family members had the same mutation but didn't develop MS, indicating that some other genetic or environmental conditions are still necessary to trigger the disease process. The discovery of this mutation, on top of last year's findings, should help erase doubts that at least some forms of MS are inherited. The prevailing view has been that a combination of many genetic variations causes a slight increase in susceptibility. In this family, individuals with the double gene mutation have about a 7-in-10 chance of developing MS, compared to a 1-in-1,000 risk in the general population. These mutations, described in the journal Human Mutation, impair both immune function and phagocytosis, the process by which cells eliminate debris and pathogens. "This is the first time that problems with phagocytosis have been linked to MS, and provides scientists with a better understanding the disease's origins and targets for developing new treatments," said lead author Carles Vilarino-Guell, an Assistant Professor of Medical Genetics who collaborated with colleagues at Australia's Florey Institute of Neuroscience and Mental Health. The findings also could be used to screen people with a family history of the disease; an individual who was found to have this mutation could be a candidate for early diagnostic imaging long before symptoms appear, or could opt to reduce environmental risks by taking Vitamin D supplements or quitting smoking. MS results from the body's immune system attacking myelin, the fatty material that insulates neurons and enables rapid transmission of electrical signals. When myelin is damaged, communication between the brain and other parts of the body is disrupted, leading to vision problems, muscle weakness, difficulty with balance and coordination, and cognitive impairments. Canada has one of the highest rate of MS in the world, for reasons that elude scientists. The double mutation, unlike the single mutation described last year, leads to the more typical "relapsing-remitting" form of MS, in which the symptoms come and go. These differences in clinical symptoms suggests that different biological processes are responsible for each type of MS, which could explain why treatments for relapsing-remitting patients are ineffective for people with more debilitating, progressive form of the disease. The family with this mutation had donated to a Canadian-wide collection of blood samples from people with MS, begun in 1993 by co-author A. Dessa Sadovnick, a UBC Professor of Medical Genetics and Neurology. The 20-year project, funded by the MS Society of Canada and the Multiple Sclerosis Scientific Research Foundation, has samples from 4,400 people with MS, plus 8,600 blood relatives - one of the largest such biobanks in the world, stored at UBC and Vancouver Coastal Health's Djavad Mowafaghian Centre for Brain Health.


BOSTON--(BUSINESS WIRE)--MetaStat, Inc. (OTCQB:MTST), a pre-commercial biotechnology company focused on the development and commercialization of companion diagnostics and anti-metastatic therapeutics in the novel cancer treatments in drugs, today announced the promotion of Jerome B. Zeldis, M.D., Ph.D. from Vice Chairman to Chairman and the appointment of Douglas A. Hamilton, MetaStat’s President and Chief Executive Officer, to its board of directors in connection with a restructuring of MetaStat’s board. Dr. Zeldis stated, “MetaStat has an exciting technology platform based on the novel mechanisms that drive cancer metastasis and overcome tumor resistance to certain therapeutics, creating the potential to discover novel cancer drugs. I look forward to working with Doug and the MetaStat team in solidifying our mission to discover and develop truly novel approaches for treating a variety of cancers.” Mr. Hamilton said, “I am delighted Jerry is leading MetaStat’s Board of Directors and honored to serve on the board with him. We have a shared vision for the future of the Company, seeing multiple opportunities to make significant advances in treating cancer.” Mr. Hamilton continued, “Our driver-based diagnostic biomarkers are also therapeutic targets for the development of anti-metastatic drugs and combination therapies to overcome drug resistance. We plan to leverage our driver-based biomarkers and expand strategic partnerships to unlock opportunities in oncology.” Please see the company’s current report on Form 8-K filed with the Securities and Exchange Commission on May 8, 2017 for full details on the board restructuring, including the resignations of Messrs. Berman, Goodeve and Bronsther. Dr. Zeldis is the Chief Medical Officer of Sorrento Therapeutics, Inc., and previously served as Chief Medical Officer of Celgene Corporation and Chief Executive Officer of Celgene Global Health until June 2016. Prior to joining Celgene in 1997, Dr. Zeldis held positions at Sandoz Research Institute and Janssen Research Institute in both clinical research and medical affairs. He currently serves as Chairman of the board of Alliqua and Trek Therapeutics, in addition to board positions at PTC Therapeutics and Soligenix. He was Assistant Professor of Medicine at Harvard Medical School, Associate Professor of Medicine at University of California, Davis, Clinical Associate Professor of Medicine at Cornell Medical School, and Professor of Clinical Medicine at the Robert Wood Johnson Medical School. Dr. Zeldis received BA and MS degrees from Brown University, and M Phil, MD, and PhD degrees from Yale University. Dr. Zeldis has published 122 peer-reviewed articles and is a named inventor on 43 U.S. patents. Mr. Hamilton has been President and CEO of MetaStat since June 2015. Previously, Mr. Hamilton served as CFO for SEA Medical Systems and since 2007, Partner at New Biology Ventures, a life-sciences incubator accelerator and consulting firm. From 1999 to 2006, Mr. Hamilton served as CFO and COO for Javelin Pharmaceuticals, purchased by Hospira, where he led the company to commercialization and through its successful national markets up-listing. Prior to Javelin, Mr. Hamilton was the CFO and Director of Business Development for PolaRx Biopharmaceuticals (now Teva Pharmaceuticals). Mr. Hamilton held positions at Amgen and Pfizer in clinical research and product development, sales and marketing at Pharmacia Biotechnology (now GE Healthcare Life Sciences), and research at Connaught Laboratories (now Sanofi-Pasteur). Mr. Hamilton earned his honors Bachelor of Science degree from the Department of Medical Genetics at the University of Toronto and his MBA from the Ivey Business School at Western University. MetaStat is a pre-commercial biotechnology company focused on the discovery, development and commercialization of diagnostics tests that are prognostic for risk of cancer metastasis, companion diagnostics to predict drug response and therapeutics to prevent aggressive cancer from spreading. MetaStat’s driver-based diagnostic and therapeutic discovery platform technology is based on the pivotal role of the Mena protein and its isoforms, a common pathway for the development of metastatic disease and drug resistance in all epithelial-based solid tumors. MetaStat is based in Boston, MA. This press release contains "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, and such forward-looking statements are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. You are cautioned that such statements are subject to a multitude of risks and uncertainties that could cause future circumstances, events or results to differ materially from those projected in the forward-looking statements as a result of various factors and other risks, including those set forth in the company's Form 10-K and its other filings filed with the Securities and Exchange Commission. You should consider these factors in evaluating the forward-looking statements included herein, and not place undue reliance on such statements. The forward-looking statements in this release are made as of the date hereof and the company undertakes no obligation to update such statements.


News Article | April 26, 2017
Site: www.businesswire.com

DELRAY BEACH, Fla.--(BUSINESS WIRE)--Progeny Genetics LLC (Progeny), a leading risk modeling pedigree software for clinicians, announced today that Jamie L’Heureux, MS, CGC has been appointed to the role of Chief Executive Officer. For 20 years, Progeny has assisted healthcare providers with patient screening, risk analysis, order processing, clinical review, and letter generation. Ms. L’Heureux brings over 12 years of experience in both research and clinical genetics as a Board Certified genetic counselor. She received her Master’s degree in Medical Genetics from the University of Cincinnati’s Genetic Counseling Training Program and began her career at the University of Iowa as a Research Coordinator for several international research projects. Ms. L’Heureux’s strong background in software development includes implementing new laboratory information management systems and designing patient-facing Family History Questionnaires. For the past three years, Ms. L’Heureux served as Software Product Manager at Progeny, and was integral to development of Progeny’s letter generation feature and integrated risk models. “I am excited to be able to use my past experience as a Progeny user, both in the research and clinical genetic counseling settings, to help build upon the strong foundation that Progeny already has established, and make it even more user-friendly for our healthcare provider customers and their patients,” said Ms. L’Heureux. “We have some exciting improvements coming up that are focused on saving clinicians’ time and simplifying their workflow.” As a prominent member of the Progeny leadership team, Ms. L’Heureux helps guide the future of the company by leveraging her extensive experience as a genetic counselor. In addition, her software development knowledge provides a solid foundation for Ms. L’Heureux to harness the needs of Progeny’s healthcare provider clientele. Progeny’s software is available in over 2,400 unique sites in 80 countries worldwide. Progeny has played a prominent role in advancing science by bringing family history to the forefront of genetic healthcare, with the intention that the information provided to healthcare providers will assist them with early detection and intervention to patients with genetic predispositions. Progeny became a subsidiary of Ambry Genetics (Ambry), a genetic testing company based in Aliso Viejo, California, in April 2015. Progeny’s software helps healthcare providers analyze hereditary family history data so clinicians can effectively identify genetic risk factors in patients and their families. For more information about Progeny’s services and support, visit here. Progeny is a subsidiary of Ambry Genetics, providing customizable family history, pedigree, sample, and genetic data management software solutions to healthcare providers worldwide. Using Progeny’s sophisticated technology, healthcare providers can collect family history from patients, review and edit pedigrees, run integrated risk models, order and review genetic testing, and integrate into the electronic medical record, allowing healthcare providers to embrace personalized healthcare like never before. For more information about Progeny, visit www.progenygenetics.com. Ambry Genetics is both College of American Pathologists (CAP)-accredited and Clinical Laboratory Improvement Amendments (CLIA)-certified. Ambry leads in clinical genetic diagnostics and genetics software solutions, combining both to offer the most comprehensive testing menu in the industry. Ambry has established a reputation for sharing data while safeguarding patient privacy, unparalleled service, and responsibly applying new technologies to the clinical molecular diagnostics market. For more information about Ambry Genetics, visit www.ambrygen.com.


News Article | February 15, 2017
Site: www.eurekalert.org

WASHINGTON - Clinical trials for genome editing of the human germline - adding, removing, or replacing DNA base pairs in gametes or early embryos - could be permitted in the future, but only for serious conditions under stringent oversight, says a new report from the National Academy of Sciences and the National Academy of Medicine. The report outlines several criteria that should be met before allowing germline editing clinical trials to go forward. Genome editing has already entered clinical trials for non-heritable applications, but should be allowed only for treating or preventing diseases or disabilities at this time. Genome editing is not new. But new powerful, precise, and less costly genome editing tools, such as CRISPR/Cas9, have led to an explosion of new research opportunities and potential clinical applications, both heritable and non-heritable, to address a wide range of human health issues. Recognizing the promise and the concerns related to this technology, NAS and NAM appointed a study committee of international experts to examine the scientific, ethical, and governance issues surrounding human genome editing. Human genome editing is already widely used in basic research and is in the early stages of development and trials for clinical applications that involve non-heritable (somatic) cells. These therapies affect only the patient, not any offspring, and should continue for treatment and prevention of disease and disability, using the existing ethical norms and regulatory framework for development of gene therapy. Oversight authorities should evaluate safety and efficacy of proposed somatic applications in the context of the risks and benefits of intended use. However, there is significant public concern about the prospect of using these same techniques for so-called "enhancement" of human traits and capacities such as physical strength, or even for uses that are not possible, such as improving intelligence. The report recommends that genome editing for enhancement should not be allowed at this time, and that broad public input and discussion should be solicited before allowing clinical trials for somatic genome editing for any purpose other than treating or preventing disease or disability. "Human genome editing holds tremendous promise for understanding, treating, or preventing many devastating genetic diseases, and for improving treatment of many other illnesses," said Alta Charo, co-chair of the study committee and Sheldon B. Lubar Distinguished Chair and Warren P. Knowles Professor of Law and Bioethics, University of Wisconsin-Madison. "However, genome editing to enhance traits or abilities beyond ordinary health raises concerns about whether the benefits can outweigh the risks, and about fairness if available only to some people." Germline genome editing, in contrast, is contentious because genetic changes would be inherited by the next generation. Many view germline editing as crossing an "ethically inviolable" line, the report says. Concerns raised include spiritual objections to interfering with human reproduction to speculation about effects on social attitudes toward people with disabilities to possible risks to the health and safety of future children. But germline genome editing could provide some parents who are carriers of genetic diseases with their best or most acceptable option for having genetically related children who are born free of these diseases. Heritable germline editing is not ready to be tried in humans. Much more research is needed before it could meet the appropriate risk and benefit standards for clinical trials. The technology is advancing very rapidly, though, making heritable genome editing of early embryos, eggs, sperm, or precursor cells in the foreseeable future "a realistic possibility that deserves serious consideration," the report says. Although heritable germline genome editing trials must be approached with caution, the committee said, caution does not mean prohibition. At present, heritable germline editing is not permissible in the United States, due to an ongoing prohibition on the U.S. Food and Drug Administration's ability to use federal funds to review "research in which a human embryo is intentionally created or modified to include a heritable genetic modification." A number of other countries have signed an international convention that prohibits germline modification. If current restrictions are removed, and for countries where germline editing would already be permitted, the committee recommended stringent criteria that would need to be met before going forward with clinical trials. They include: (1) absence of reasonable alternatives; (2) restriction to editing genes that have been convincingly demonstrated to cause or strongly predispose to a serious disease or condition; (3) credible pre-clinical and/or clinical data on risks and potential health benefits; (4) ongoing, rigorous oversight during clinical trials; (5) comprehensive plans for long-term multigenerational follow-up; and (6) continued reassessment of both health and societal benefits and risks, with wide-ranging, ongoing input from the public. Policymaking surrounding human genome editing applications should incorporate public participation, and funding of genome editing research should include support to study the socio-political, ethical, and legal aspects and evaluate efforts to build public communication and engagement on these issues. "Genome editing research is very much an international endeavor, and all nations should ensure that any potential clinical applications reflect societal values and be subject to appropriate oversight and regulation," said committee co-chair Richard Hynes, Howard Hughes Medical Institute Investigator and Daniel K. Ludwig Professor for Cancer Research, Massachusetts Institute of Technology. "These overarching principles and the responsibilities that flow from them should be reflected in each nation's scientific community and regulatory processes. Such international coordination would enhance consistency of regulation." The study was funded by the Defense Advanced Research Projects Agency, the Greenwall Foundation, the John D. and Catherine T. MacArthur Foundation, U.S. Department of Health and Human Services, U.S. Food and Drug Administration, and the Wellcome Trust, with additional support from the National Academies' Presidents' Circle Fund and the National Academy of Sciences W.K. Kellogg Foundation Fund. The National Academy of Sciences and the National Academy of Medicine are private, nonprofit institutions that, along with the National Academy of Engineering, provide independent, objective analysis and advice to the nation to solve complex problems and inform public policy decisions related to science, technology, and medicine. The Academies operate under an 1863 congressional charter to the National Academy of Sciences, signed by President Lincoln. For more information, visit http://www. . Copies of Human Genome Editing: Science, Ethics, and Governance are available at http://www. or by calling 202-334-3313 or 1-800-624-6242. Reporters may obtain a copy from the Office of News and Public Information (contacts listed above). R. Alta Charo1 (co-chair) Sheldon B. Lubar Distinguished Chair and Warren P. Knowles Professor of Law and Bioethics University of Wisconsin Madison Richard O. Hynes1,2 (co-chair) Investigator Howard Hughes Medical Institute, and Daniel K. Ludwig Professor for Cancer Research Massachusetts Institute of Technology Cambridge Ellen Wright Clayton1 Craig Weaver Professor of Pediatrics, and Professor of Law Vanderbilt University Nashville, Tenn. Barry S. Coller1,2 David Rockefeller Professor of Medicine, Physician in Chief, and Head Allen and Frances Adler Laboratory of Blood and Vascular Biology Rockefeller University New York City Ephrat Levy-Lahad Director Fuld Family Department of Medical Genetics Shaare Zedek Medical Center Faculty of Medicine Hebrew University of Jerusalem Jerusalem Luigi Naldini Professor of Cell and Tissue Biology and of Gene and Cell Therapy San Raffaele University, and Director San Raffaele Telethon Institute for Gene Therapy Milan Duanqing Pei Professor and Director General Guangzhou Institute of Biomedicine and Health Chinese Academy of Sciences Guangzhou, China Janet Rossant2 Senior Scientist and Chief of Research Emeritus Hospital for Sick Children University of Toronto Toronto Dietram A. Scheufele John E. Ross Professor in Science Communication and Vilas Distinguished Achievement Professor University of Wisconsin Madison Jonathan Weissman2 Professor Department of Cellular and Molecular Pharmacology University of California San Francisco Keith R. Yamamoto1,2 Vice Chancellor for Science Policy and Strategy University of California San Francisco


News Article | February 15, 2017
Site: www.eurekalert.org

PHILADELPHIA (February 14, 2017) - Just before Rare Disease Day 2017, a study from the Monell Center and collaborating institutions provides new insight into the causes of trimethylaminura (TMAU), a genetically-transmitted metabolic disorder that leads to accumulation of a chemical that smells like rotting fish. Although TMAU has been attributed solely to mutations in a single gene called FMO3, the new study combined sensory and genetic approaches to identify additional genes that may contribute to TMAU. The findings indicate that genetic testing to identify mutations in the FMO3 gene may not be sufficient to identify the underlying cause of all cases of TMAU. TMAU is classified as a "rare disease," meaning that it affects less than 200,000 people in the United States. However, its actual incidence remains uncertain, due in part to inconclusive diagnostic techniques. "Our findings may bring some reassurance to people who report fish-like odor symptoms but do not have mutations in the FMO3 gene," said Monell behavioral geneticist Danielle R. Reed, PhD, a senior author on the study. The socially and psychologically distressing symptoms of TMAU result from the buildup of trimethylamine (TMA), a chemical compound produced naturally from many foods rich in the dietary constituent, choline. Such foods include eggs, certain legumes, wheat germ, saltwater fish and organ meats. TMA, which has a foul, fishy odor, normally is metabolized by the liver enzyme flavin-containing monooxygenase 3 (FMO3) into an odorless metabolite. People with TMAU are unable to metabolize TMA, presumably due to defects in the underlying FMO3 gene that result in faulty instructions for making functional FMO3 enzymes. The TMA, along with its associated unpleasant odor, then accumulates and is excreted from the body in urine, sweat, saliva, and breath. However, some people who report having the fish odor symptoms of TMAU do not have severely disruptive mutations in the FMO3 gene. This led the researchers to suspect that other genes may also contribute to the disorder. In the new study, reported in the open access journal BMC Medical Genetics, the research team combined a gene sequencing technique known as exome analysis with sophisticated computer modeling to probe for additional TMAU-related genes. The study compared sensory, metabolic and genetic data from ten individuals randomly selected from 130 subjects previously evaluated for TMAU at the Monell Center. Each subject's body odor was evaluated in the laboratory by a trained sensory panel before and after a metabolic test to measure production of TMA over 24 hours following ingestion of a set amount of choline. Although the choline challenge test confirmed a diagnosis of TMAU by revealing a high level of urinary TMA in all 10 subjects, genetic analyses revealed that the FMO3 gene appeared to be normal in four of the 10. Additional analyses revealed defects in several other genes that could contribute to the inability to metabolize the odorous TMA. "We now know that genes other than FMO3 may contribute to TMAU. These new genes may help us better understand the underlying biology of the disorder and perhaps even identify treatments," said Reed. TMAU's odor symptoms may occur in irregular and seemingly unpredictable intervals. This makes the disease difficult to diagnose, as patients can appear to be odor-free when they consult a health professional. This was evidenced in the current study. Although all of the subjects reported frequent fish-odor symptoms, none was judged by the sensory panel to have a fish-like odor at the time of the choline challenge. Monell analytical organic chemist George Preti, PhD, also a senior author, commented on the diagnostic implications of the combined findings, "Regardless of either the current sensory presentation TMAU or the FMO3 genetics, the choline challenge test will confirm the accumulation of TMA that reveals the presence of the disorder." Moving forward, the researchers would like to repeat the genetic analyses in a larger cohort of TMAU patients without FMO3 mutations to confirm which other genes are involved in the disorder. "Such information may identify additional odorants produced by TMAU-positive patients, and inform the future development of gene-based therapies" said Preti. Also contributing to the research were co-lead author Liang-Dar Hwang, Jason Eades, Chung Wen Yu, Corrine Mansfield, Alexis Burdick-Will, and Fujiko Duke of Monell; co-lead author Yiran Guo, Xiao Chang, Brendan Keating, and Hakon Hakonarson of the Center for Applied Genomics at the Children's Hospital of Philadelphia; co-lead author Jiankang Li, Yulan Chen, and Jianguo Zhang of BGI-Shenzhen (China); Steven Fakharzadeh of the Perelman School of Medicine, University of Pennsylvania; Paul Fennessey of the University of Colorado Health Sciences Center; and Hui Jiang of BGI-Shenzhen, the Shenzhen Key Laboratory of Genomics, and the Guangdong Enterprise Key Laboratory of Human Disease Genomics. Funding for the research was provided by the National Organization of Rare Diseases; Institutional funds from the Monell Chemical Center and the Children's Hospital of Philadelphia Research Institute; National Institute on Deafness and Other Communication of the National Institutes of Health (P30DC011735); Shenzhen Municipal Government of China (CXZZ20130517144604091); Shenzhen Key Laboratory of Genomics (CXB200903110066A); and Guangdong Enterprise Key Laboratory of Human Disease Genomics (2011A060906007). Philanthropic funding was provided by the TMAU Foundation, Volatile Analysis, Inc., the family of Mr. and Mrs. Richard Hasselbusch with matching funds from Merck Easy Match, and the late Ms. Bonnie Hunt. The Monell Chemical Senses Center is an independent nonprofit basic research institute based in Philadelphia, Pennsylvania. Poised to celebrate its 50th anniversary in 2018, Monell advances scientific understanding of the mechanisms and functions of taste and smell to benefit human health and well-being. Using an interdisciplinary approach, scientists collaborate in the programmatic areas of sensation and perception; neuroscience and molecular biology; environmental and occupational health; nutrition and appetite; health and well-being; development, aging and regeneration; and chemical ecology and communication. For more information about Monell, visit http://www. .


News Article | February 16, 2017
Site: www.eurekalert.org

Scientists at Trinity College Dublin have discovered how certain cancers hijack the immune system for their benefit, tricking it into helping rather than harming them. While most of us are aware that our immune system protects us from infection, we may be less aware of the key role that cells of the immune system also play in coordinating the repair of damaged tissue. This 'wound-healing' aspect of the immune response stimulates growth of new cells within damaged tissue and brings extra nutrients and oxygen into the injured tissue. However, cancers frequently exploit the wound-healing side of the immune system for their own ends. Indeed, cancers have been described as 'wounds that do not heal' due to their ability to masquerade as damaged tissue in order to receive help from the immune system. But just how cancers switch on this wound-healing response is not well understood. However, scientists from the Smurfit Institute of Genetics at Trinity College Dublin, led by Smurfit Professor of Medical Genetics, Seamus Martin, have just found that a molecule called TRAIL -- which is frequently found in high concentrations on many cancers -- can become 're-wired' in certain tumours to send an inflammatory 'wound-healing' signal. Ironically, TRAIL normally delivers a signal for cells to die, but the Trinity scientists found that this molecule can also send a wound-healing message from tumour cells. The research, conducted by Research Fellow at Trinity, Dr Conor Henry, has just been published in the internationally renowned journal, Molecular Cell. Commenting on the findings, Professor Martin said: "Understanding how cancers turn on the wound-healing response has been mysterious, so we are very excited to find that certain cancers exploit TRAIL for that purpose." "This suggests ways in which we can turn off this reaction in cancers that use TRAIL to hoodwink the immune system into helping rather than harming them." Work in the Martin laboratory at Trinity College Dublin is supported by Science Foundation Ireland and Worldwide Cancer Research.


News Article | February 28, 2017
Site: www.businesswire.com

QUEBEC CITY--(BUSINESS WIRE)--ITR Laboratories Canada Inc., a global provider of preclinical services, is pleased to announce new scientific leadership with the arrival of Abbas Fotovati, Ph.D., D.V.M., as senior veterinary scientist. In this role, Fotovati will be responsible for the company’s experimental and developmental veterinary services. Fotovati joins ITR from the University of British Columbia where he served on the faculty of the Department of Oncology and the Department of Experimental Medicine and Medical Genetics. He has also held academic, veterinary and pharmaceutical research positions in Japan, North America and the Middle East. With more than 25 years of experience, Fotovati is an accomplished scientist and published researcher in animal models on cancer, osteoporosis, wound healing, rheumatoid arthritis, angiogenesis and lipid metabolism, as well as in translational medicine and molecular therapeutics of novel drugs. In addition to his expertise in animal modeling, which has granted him eligibility for the board of American College of Laboratory Animal Medicine (ACLAM), he is a molecular and development biologist with extensive knowledge of new areas in this field, including stem cell biology. “We are pleased that Abbas has chosen to contribute to our ongoing success,” said Ginette Bain, senior vice president at ITR. “His broad preclinical knowledge and combination of industry experience and academic research will enable ITR to provide innovative scientific service and specialized surgical expertise to our clients.” ITR Laboratories Canada Inc. provides preclinical testing services for pharmaceutical and biotechnology industries worldwide. As a CRO with extensive experience, ITR provides clients with valuable input and best practices, which ultimately help them maximize the value of their investment.


News Article | March 2, 2017
Site: www.24-7pressrelease.com

BIRMINGHAM, AL, March 02, 2017-- Dr. Wayne Finley has been included in Marquis Who's Who. As in all Marquis Who's Who biographical volumes, individuals profiled are selected on the basis of current reference value. Factors such as position, noteworthy accomplishments, visibility, and prominence in a field are all taken into account during the selection process.A medical educator with more than six decades of experience, Dr. Finley is highly regarded for mentoring, inspiring, and motivating emerging physicians and graduate students so that they are set up for success at the start of their careers. Retired since 1996, he concluded his career with the University of Alabama School of Medicine, where he dedicated more than 36 years in a variety of roles, serving as Professor; Epidemiology and Public Health; and Chairman of Faculty Council. Certified by the American Board of Medical Genetics and Genomics, Dr. Finley served on the genetic counseling committee of the Children's Bureau of the U.S. Department HEW and on the National Research Resources Council of the National Institute of Health. He was a senior scientist for the Comprehensive Cancer Center and the Cystic Fibrosis Research Center at the University of Alabama at Birmingham (UAB). In recognition of his professional excellence, Dr. Finley was recognized by the Distinguished Faculty Lecturer Award, endowment of the Sara C. and Wayne H. Finley Chair in Medical Genetics, and renaming the Reynolds-Finley Historical Library and Annual Lecture by the UAB. He received community awards including the Lifetime Achievement Award from the Birmingham Business Journal. Named to the Alabama Healthcare Hall of Fame and presented the President's Medal by UAB, Dr. Finley was also honorably selected for inclusion into Who's Who in America, Who's Who in American Education, Who's Who in Medicine and Healthcare, Who's Who in Science and Engineering, and Who's Who in the South and Southwest.Before establishing his career in medicine, Dr. Finley served his country as a member of the U.S. Army Infantry in Germany in 1946 and later in the Army Chemical Corps and ultimately achieved the rank of Lieutenant Colonel in the Reserves. After his service, he attended Jacksonville State University, where he earned a Bachelor of Science in 1948, and the University of Alabama, where he achieved a Master of Arts in 1950, a Master of Science in 1955, a Ph.D. in 1958, and an MD in 1960. A fellow of the American College of Medical Genetics and Genomics, Dr. Finley remained at the top of his field through his memberships in American Medical Association, American Association for the Advancement of Science, New York Academy of Sciences, Society for Experimental Biology and Medicine, American Institute of Chemists, American Federation for Clinical Research, American College of Medical Genetics and Genomics, American Society of Human Genetics, the Southern Medical Association, Medical Association of the State of Alabama, and Jefferson County Medical Society. As he looks to the future, Dr. Finley intends to enjoy his retirement while taking on select consulting projects as they arise.About Marquis Who's Who :Since 1899, when A. N. Marquis printed the First Edition of Who's Who in America , Marquis Who's Who has chronicled the lives of the most accomplished individuals and innovators from every significant field of endeavor, including politics, business, medicine, law, education, art, religion and entertainment. Today, Who's Who in America remains an essential biographical source for thousands of researchers, journalists, librarians and executive search firms around the world. Marquis publications may be visited at the official Marquis Who's Who website at www.marquiswhoswho.com


(Philadelphia, PA) - Mitochondria - the energy-generating powerhouses of cells - are also a site for oxidative stress and cellular calcium regulation. The latter two functions have long been suspected of being linked mechanistically, and now new research at the Lewis Katz School of Medicine at Temple University (LKSOM) shows precisely how, with the common connection centering on a protein complex known as the mitochondrial Ca2+ uniporter (MCU). "MCU had been known for its part in driving mitochondrial calcium uptake for cellular energy production, which protects cells from bioenergetic crisis, and for its role in eliciting calcium overload-induced cell death," explained senior investigator on the study, Muniswamy Madesh, PhD, Professor in the Department of Medical Genetics and Molecular Biochemistry and Center for Translational Medicine at LKSOM. "Now, we show that MCU has a functional role in both calcium regulation and the sensing of levels of reactive oxygen species (ROS) within mitochondria." The study, published online March 2 in the journal Molecular Cell, is the first to identify a direct role for MCU in mitochondrial ROS-sensing. In previous work, Dr. Madesh and colleagues were the first to show how the MCU protein complex comes together to effect mitochondrial calcium uptake. "We know from that work, and from existing work in the field, that as calcium accumulates in mitochondria, the organelles generate increasing amounts of ROS," Dr. Madesh said. "Mitochondria have a way of dealing with that ROS surge, and because of the relationship between mitochondrial calcium uptake and ROS production, we suspected ROS-targeting of MCU was involved in that process." In the new study, Dr. Madesh and colleagues employed advanced biochemical, cell biological, and superresolution imaging to examine MCU oxidation in the mitochondrion. Critically, they discovered that MCU contains several cysteine molecules in its amino acid structure, only one of which, Cys-97, is capable of undergoing an oxidation-induced reaction known as S-glutathionylation. Structural analyses showed that oxidation-induced S-glutathionylation of Cys-97 triggers conformational changes within MCU. Those changes in turn regulate MCU activity during inflammation, hypoxia, and cardiac stimulation. They also appear to be relevant to cell survival - elimination of ROS-sensing via Cys-97 mutation resulted in persistent MCU channel activity and an increased rate of calcium-uptake, with cells eventually dying from calcium overload. Importantly, Dr. Madesh and colleagues found that S-glutathionylation of Cys-97 is reversible. "Reversible oxidation is essential to the regulation of protein function," Dr. Madesh explained. When switched on by oxidation, Cys-97 augments MCU channel activity that perpetuates cell death. Oxidation reverses when the threat has subsided. The findings could have implications for the understanding of metabolic disorders and neurological and cardiovascular diseases. "Abnormalities in ion homeostasis are a central feature of metabolic disease," Dr. Madesh said. "We plan next to explore the functional significance of ROS and MCU activity in a mouse model using genome editing technology, which should help us answer fundamental questions about MCU's biological functions in mitochondrial ROS-sensing." Other researchers involved in the study include Zhiwei Dong, Santhanam Shanmughapriya, Dhanendra Tomar, Neeharika Nemani, Sarah L. Breves, Aparna Tripathi, Palaniappan Palaniappan, Massimo F. Riitano, Alison Worth, Ajay Seelam, Edmund Carvalho, Ramasamy Subbiah, Fabia?n Jan?a, and Sudarsan Rajan, Department of Medical Genetics and Molecular Biochemistry and the Center for Translational Medicine at LKSOM; Jonathan Soboloff, Department of Medical Genetics and Molecular Biochemistry at LKSOM; Xueqian Zhang and Joseph Y. Cheung, Center for Translational Medicine at LKSOM; Naveed Siddiqui and Peter B. Stathopulos, Department of Physiology and Pharmacology, Western University, London, Ontario, Canada; Solomon Lynch and Jeffrey Caplan, Department of Biological Sciences, Delaware Biotechnology Institute, University of Delaware; Suresh K. Joseph, MitoCare Center, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia; Yizhi Peng and Zhiwei Dong, Institute of Burn Research, Southwest Hospital, Third Military Medical University, Chongqing, People's Republic of China. The research was supported in part by National Institutes of Health grants R01GM109882, R01HL086699, R01HL119306, 1S10RR027327, P01 DA037830, and RO1DK103558. Temple University Health System (TUHS) is a $1.6 billion academic health system dedicated to providing access to quality patient care and supporting excellence in medical education and research. The Health System consists of Temple University Hospital (TUH), ranked among the "Best Hospitals" in the region by U.S. News & World Report; TUH-Episcopal Campus; TUH-Northeastern Campus; Fox Chase Cancer Center, an NCI-designated comprehensive cancer center; Jeanes Hospital, a community-based hospital offering medical, surgical and emergency services; Temple Transport Team, a ground and air-ambulance company; and Temple Physicians, Inc., a network of community-based specialty and primary-care physician practices. TUHS is affiliated with the Lewis Katz School of Medicine at Temple University. The Lewis Katz School of Medicine (LKSOM), established in 1901, is one of the nation's leading medical schools. Each year, the School of Medicine educates approximately 840 medical students and 140 graduate students. Based on its level of funding from the National Institutes of Health, the Katz School of Medicine is the second-highest ranked medical school in Philadelphia and the third-highest in the Commonwealth of Pennsylvania. According to U.S. News & World Report, LKSOM is among the top 10 most applied-to medical schools in the nation. Temple Health refers to the health, education and research activities carried out by the affiliates of Temple University Health System (TUHS) and by the Katz School of Medicine. TUHS neither provides nor controls the provision of health care. All health care is provided by its member organizations or independent health care providers affiliated with TUHS member organizations. Each TUHS member organization is owned and operated pursuant to its governing documents.


This is Muniswamy Madesh, Ph.D., Professor in the Department of Medical Genetics and Molecular Biochemistry and Center for Translational Medicine at the Lewis Katz School of Medicine at Temple University. Credit: The Lewis Katz School of Medicine at Temple University Mitochondria - the energy-generating powerhouses of cells - are also a site for oxidative stress and cellular calcium regulation. The latter two functions have long been suspected of being linked mechanistically, and now new research at the Lewis Katz School of Medicine at Temple University (LKSOM) shows precisely how, with the common connection centering on a protein complex known as the mitochondrial Ca2+ uniporter (MCU). "MCU had been known for its part in driving mitochondrial calcium uptake for cellular energy production, which protects cells from bioenergetic crisis, and for its role in eliciting calcium overload-induced cell death," explained senior investigator on the study, Muniswamy Madesh, PhD, Professor in the Department of Medical Genetics and Molecular Biochemistry and Center for Translational Medicine at LKSOM. "Now, we show that MCU has a functional role in both calcium regulation and the sensing of levels of reactive oxygen species (ROS) within mitochondria." The study, published online March 2 in the journal Molecular Cell, is the first to identify a direct role for MCU in mitochondrial ROS-sensing. In previous work, Dr. Madesh and colleagues were the first to show how the MCU protein complex comes together to effect mitochondrial calcium uptake. "We know from that work, and from existing work in the field, that as calcium accumulates in mitochondria, the organelles generate increasing amounts of ROS," Dr. Madesh said. "Mitochondria have a way of dealing with that ROS surge, and because of the relationship between mitochondrial calcium uptake and ROS production, we suspected ROS-targeting of MCU was involved in that process." In the new study, Dr. Madesh and colleagues employed advanced biochemical, cell biological, and superresolution imaging to examine MCU oxidation in the mitochondrion. Critically, they discovered that MCU contains several cysteine molecules in its amino acid structure, only one of which, Cys-97, is capable of undergoing an oxidation-induced reaction known as S-glutathionylation. Structural analyses showed that oxidation-induced S-glutathionylation of Cys-97 triggers conformational changes within MCU. Those changes in turn regulate MCU activity during inflammation, hypoxia, and cardiac stimulation. They also appear to be relevant to cell survival - elimination of ROS-sensing via Cys-97 mutation resulted in persistent MCU channel activity and an increased rate of calcium-uptake, with cells eventually dying from calcium overload. Importantly, Dr. Madesh and colleagues found that S-glutathionylation of Cys-97 is reversible. "Reversible oxidation is essential to the regulation of protein function," Dr. Madesh explained. When switched on by oxidation, Cys-97 augments MCU channel activity that perpetuates cell death. Oxidation reverses when the threat has subsided. The findings could have implications for the understanding of metabolic disorders and neurological and cardiovascular diseases. "Abnormalities in ion homeostasis are a central feature of metabolic disease," Dr. Madesh said. "We plan next to explore the functional significance of ROS and MCU activity in a mouse model using genome editing technology, which should help us answer fundamental questions about MCU's biological functions in mitochondrial ROS-sensing." Explore further: Scientists identify key factor in mitochondrial calcium uptake and bioenergetics

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