Baker Heart and Diabetes Institute

Melbourne, Australia

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Melbourne, Australia

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News Article | June 22, 2017
Site: www.eurekalert.org

Coronary artery disease may have persisted in human populations because the genes that cause this late-striking disease also contribute to greater numbers of children, reports Dr Sean Byars of The University of Melbourne and Associate Professor Michael Inouye of the Baker Heart and Diabetes Institute, Australia, in a study published June 22, 2017 in PLOS Genetics. Coronary artery disease, a condition where plaque builds up gradually in the arteries that feed the heart, is one of the leading causes of death worldwide, and may have plagued humans for thousands of years. One of the big questions surrounding the disease is why natural selection has not removed genes for this common and costly disease. In a new study, researchers used genetic information from the 1000 Genomes database and the International HapMap3 project, along with lifetime reproductive data from the Framingham Heart Study, to identify genetic variation linked to the disease that natural selection had also modified recently. They showed that these same genetic variations also contribute in multiple ways to greater male and female reproductive success, which appears to represent an evolutionary trade-off between early-life reproductive benefits that compensate for later-life disease costs. The findings offer an answer to the question of why natural selection cannot weed out genes associated with coronary artery disease - parents pass them on to their offspring before experiencing advanced symptoms and death. The study also provides a novel approach for detecting the influence of natural selection on traits caused by the cumulative effects of multiple genes, which in the past, has been far more difficult to uncover than for disorders linked to a single gene. In your coverage please use this URL to provide access to the freely available article in PLOS Genetics: http://journals. Citation: Byars SG, Huang QQ, Gray L-A, Bakshi A, Ripatti S, Abraham G, et al. (2017) Genetic loci associated with coronary artery disease harbor evidence of selection and antagonistic pleiotropy. PLoS Genet 13(6): e1006328. https:/ Funding: This study was supported by the National Health and Medical Research Council (NHMRC) of Australia (grant no. 1062227) and the National Heart Foundation of Australia. MI was supported by a Career Development Fellowship co-funded by the NHMRC and the National Heart Foundation of Australia (no. 1061435). GA was supported by an NHMRC Peter Doherty Early Career Fellowship (no.1090462). SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 213506 and 129680), Academy of Finland (Grant No 251217 and 285380), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, Biocentrum Helsinki and the European Union's Seventh Framework Programme (FP7/2007-2013) under grant agreement No 201413 (ENGAGE) and 261433 (BioSHaRE-EU), and Horizon 2020 Research and Innovation Programme under grant agreement No 692145 (ePerMed). The Framingham Heart Study is conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with Boston University (Contract No. N01-HC-25195 and HHSN268201500001I). This manuscript was not prepared in collaboration with investigators of the Framingham Heart Study and does not necessarily reflect the opinions or views of the Framingham Heart Study, Boston University, or NHLBI. Funding for SHARe Affymetrix genotyping was provided by NHLBI Contract N02-HL-64278. SHARe Illumina genotyping was provided under an agreement between Illumina and Boston University. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist.


News Article | June 22, 2017
Site: www.sciencedaily.com

Coronary artery disease may have persisted in human populations because the genes that cause this late-striking disease also contribute to greater numbers of children, reports Dr Sean Byars of The University of Melbourne and Associate Professor Michael Inouye of the Baker Heart and Diabetes Institute, Australia, in a study published June 22, 2017 in PLOS Genetics. Coronary artery disease, a condition where plaque builds up gradually in the arteries that feed the heart, is one of the leading causes of death worldwide, and may have plagued humans for thousands of years. One of the big questions surrounding the disease is why natural selection has not removed genes for this common and costly disease. In a new study, researchers used genetic information from the 1000 Genomes database and the International HapMap3 project, along with lifetime reproductive data from the Framingham Heart Study, to identify genetic variation linked to the disease that natural selection had also modified recently. They showed that these same genetic variations also contribute in multiple ways to greater male and female reproductive success, which appears to represent an evolutionary trade-off between early-life reproductive benefits that compensate for later-life disease costs. The findings offer an answer to the question of why natural selection cannot weed out genes associated with coronary artery disease -- parents pass them on to their offspring before experiencing advanced symptoms and death. The study also provides a novel approach for detecting the influence of natural selection on traits caused by the cumulative effects of multiple genes, which in the past, has been far more difficult to uncover than for disorders linked to a single gene.


News Article | June 23, 2017
Site: www.sciencedaily.com

Researchers have found that genes for coronary heart disease (CAD) also influence reproduction, so in order to reproduce successfully, the genes for heart disease will also be inherited. Coronary artery disease, a condition where plaque builds up gradually in the arteries that feed the heart, is one of the leading causes of death worldwide. New research has found that the genes that cause this late-striking disease were also found to contribute to greater numbers of children. An international team led by researchers from the University of Melbourne and including scientists from Finland and the US worked on the study, which has been published in PLOS Genetics. Lead author Dr Sean Byars from the University of Melbourne says the team wanted to understand more about how CAD has been inherited in our evolutionary past, in order to better understand why it is so common presently. "CAD is often thought of as modern disease, but actually atherosclerosis, or thickening of the artery walls, has been detected in Egyptian mummies, so we suspect it has been in our genes for thousands of years." CAD currently affects 110 million people and causes 8.9 million deaths annually, from 2015 figures. "According to the theory of natural selection, as proposed by Charles Darwin, genes for traits that improve individual survival or reproduction will increase or be maintained in populations, whereas those that reduce these will be selected against and gradually removed or reduced over time. "So it is unclear why CAD is so common in modern humans and this is important to understand given the global health burden it represents," explains Dr Byars. The team analysed 56 genetic regions for CAD in 12 worldwide populations originating mainly from Africa, Europe and East Asia, and used a statistical score to measure whether there had been recent selective changes to the DNA associated with CAD. Associate Professor Michael Inouye, who also led the study, said the findings showed that many genes associated with CAD have actually been positively selected for through evolution. "After further research, we found CAD genes are also important for reproduction and that these genes are involved in important functions in male and female fertility being expressed in the testes, ovaries and endometrium, for example," said Assoc Prof Inouye, based at the Baker Heart and Diabetes Institute. Dr Byars added, "Evolution it seems is involved in a trade-off where CAD only begins to appear at around 40-50 years of age when the potential beneficial effects of these genes on reproduction will have already occurred. That will tend to compensate for any negative effects these genes also have on CAD later in life. "This doesn't necessarily mean that women with many children are more likely to develop heart disease, it may simply mean that the disease is a by-product of humans being able to reproduce well." The results also provide insight on how selection for CAD genes differs between populations, and how these populations might respond differently to the same heart disease prevention strategies. Dr Inouye says that ultimately these results give us some idea how complicated the effects of genes can be. He adds that we need to be cautious with new gene-editing techniques like CRISPR, as unintended effects may be introduced which may not reveal themselves for decades or more. "It's a bit like a balloon, if you push on one side of it, the air will push out in other places and if you don't know what the balloon looks like then you won't be able to predict where. Our genomes are similarly complex and we need to learn more in order to read them, much less write them."


News Article | June 14, 2017
Site: www.eurekalert.org

Monash University's Biomedicine Discovery Institute (BDI) researchers have collaboratively developed a therapeutic approach that dramatically promotes the growth of muscle mass, which could potentially prevent muscle wasting in diseases including muscular dystrophy and cancer. The approach, jointly developed with Baker Heart and Diabetes Institute scientists, combines - for the first time - molecules that inhibit three proteins which in turn repress muscle growth. Published this week in the journal Proceedings of the National Academy of Sciences, the scientists found that inhibiting activin A, activin B and myostatin resulted in skeletal muscle mass increase by as much as 150 per cent in preclinical models. Myostatin has long been recognised as the body's major negative regulator of skeletal muscle mass, helping to maintain muscle homeostasis in the body, but creating molecules to target all three related proteins together was a novel approach. "As a result of the study we can now more precisely regulate - and increase - muscle mass in the setting of disease," co-lead author from Monash BDI, Dr Craig Harrison, said. Dr Harrison said the study, the culmination of many years of research with the Baker Institute's Dr Paul Gregorevic, was aimed mostly at developing a way of preventing muscle loss in the wasting condition cachexia, in cancer. Dr Harrison said cachexia, observed in the end stages of cancer, was thought to contribute or directly cause 20 to 30 per cent of all cancer-related deaths. Palliative care is currently the only treatment for cancer cachexia. The condition is also seen in other diseases including diabetes, AIDS, and in heart and kidney failure. The paper showed that the combination treatment could prevent muscle wasting in a cancer cachexia model as well as in muscular dystrophy. It could also potentially be used after clinical development in healthy and in ageing individuals undergoing a slow wasting of muscles, Dr Harrison said. Activins and myostatin belong to the transforming growth factor-β (TGF-β) family of proteins, which both researchers have been investigating for a number of years. The findings were recently corroborated by a similar study by US scientists, although those experiments did not target activin B and did not demonstrate as great an effect, Dr Harrison said. The research was supported by the Australian National Health and Medical Research Council. Committed to making the discoveries that will relieve the future burden of disease, the newly established Monash Biomedicine Discovery Institute at Monash University brings together more than 120 internationally-renowned research teams. Our researchers are supported by world-class technology and infrastructure, and partner with industry, clinicians and researchers internationally to enhance lives through discovery.


News Article | June 23, 2017
Site: www.futurity.org

The genes that lead to coronary artery disease (CAD) also influence reproduction, research shows. In order to reproduce successfully, researchers say, the genes for heart disease will also be inherited. “Evolution, it seems, is involved in a trade-off where CAD only begins to appear at around 40-50 years of age when the potential beneficial effects of these genes on reproduction have already occurred,” explains lead author Sean Byars from the School of BioSciences at the University of Melbourne. He says the team wanted to understand more about how CAD has been inherited in our evolutionary past, to better understand why it is so prevalent now. “CAD is often thought of as modern disease, but actually atherosclerosis, or thickening of the artery walls, has been detected in Egyptian mummies, so we suspect it has been in our genes for thousands of years.” CAD currently affects 110 million people and causes 8.9 million deaths annually, according to 2015 figures. “According to the theory of natural selection, as proposed by Charles Darwin, genes for traits that improve individual survival or reproduction will increase or be maintained in populations, whereas those that reduce our chances of survival will be selected against and gradually removed or reduced over time. “So it was unclear why CAD remains so common in modern humans and this is important to understand given the global health burden it represents,” explains Byars. The team analyzed 56 genetic regions for CAD in 12 worldwide populations originating mainly from Africa, Europe, and East Asia, and used a statistical score to measure whether there had been recent selective changes to DNA associated with the disease. Associate Professor Michael Inouye, who also led the study, says the findings show that many genes associated with CAD have actually been positively selected through evolution. “So we suspected there must have been be some unknown benefit to retaining these genes for the disease,” says Inouye, based at the Baker Heart and Diabetes Institute. “After further research, we found CAD genes are also important for reproduction and involved in important functions in male and female fertility being expressed in the testes, ovaries, and endometrium, for example. “This represents direct evidence that genes that have been under selection are also beneficial for reproduction and, yet, are associated with occurrence of a common disease later in life,” Inouye says. “This doesn’t necessarily mean that women with many children are more likely to develop heart disease, it may simply mean that the disease is a by-product of humans being able to reproduce well,” adds Byars. The results also provide insights on how selection for CAD genes differs between populations, and how these populations might respond differently to the same heart disease prevention strategies. Inouye says that ultimately these results give us some idea how complicated the effects of genes can be. He adds that we need to be cautious with new gene-editing techniques like CRISPR, as unintended effects may be introduced which may not reveal themselves for decades or more. “It’s a bit like a balloon, if you push on one side of it, the air will push out in other places and if you don’t know what the balloon looks like then you won’t be able to predict where. “Our genomes are similarly complex and we need to learn more in order to read them, much less write them.” The study appears in the journal PLOS Genetics.


News Article | June 14, 2017
Site: www.sciencedaily.com

Monash University's Biomedicine Discovery Institute (BDI) researchers have collaboratively developed a therapeutic approach that dramatically promotes the growth of muscle mass, which could potentially prevent muscle wasting in diseases including muscular dystrophy and cancer. The approach, jointly developed with Baker Heart and Diabetes Institute scientists, combines -- for the first time -- molecules that inhibit three proteins which in turn repress muscle growth. Published this week in the journal Proceedings of the National Academy of Sciences, the scientists found that inhibiting activin A, activin B and myostatin resulted in skeletal muscle mass increase by as much as 150 per cent in preclinical models. Myostatin has long been recognised as the body's major negative regulator of skeletal muscle mass, helping to maintain muscle homeostasis in the body, but creating molecules to target all three related proteins together was a novel approach. "As a result of the study we can now more precisely regulate -- and increase -- muscle mass in the setting of disease," co-lead author from Monash BDI, Dr Craig Harrison, said. Dr Harrison said the study, the culmination of many years of research with the Baker Institute's Dr Paul Gregorevic, was aimed mostly at developing a way of preventing muscle loss in the wasting condition cachexia, in cancer. Dr Harrison said cachexia, observed in the end stages of cancer, was thought to contribute or directly cause 20 to 30 per cent of all cancer-related deaths. Palliative care is currently the only treatment for cancer cachexia. The condition is also seen in other diseases including diabetes, AIDS, and in heart and kidney failure. The paper showed that the combination treatment could prevent muscle wasting in a cancer cachexia model as well as in muscular dystrophy. It could also potentially be used after clinical development in healthy and in ageing individuals undergoing a slow wasting of muscles, Dr Harrison said. Activins and myostatin belong to the transforming growth factor-β (TGF-β) family of proteins, which both researchers have been investigating for a number of years. The findings were recently corroborated by a similar study by US scientists, although those experiments did not target activin B and did not demonstrate as great an effect, Dr Harrison said. The research was supported by the Australian National Health and Medical Research Council.


Researchers have found that genes for coronary heart disease (CAD) also influence reproduction, so in order to reproduce successfully, the genes for heart disease will also be inherited. Coronary artery disease, a condition where plaque builds up gradually in the arteries that feed the heart, is one of the leading causes of death worldwide. New research has found that the genes that cause this late-striking disease were also found to contribute to greater numbers of children. An international team led by researchers from the University of Melbourne and including scientists from Finland and the US worked on the study, which has been published [embargo 0400 Friday 23 June AEST] in PLOS Genetics. Lead author Dr Sean Byars from the University of Melbourne says the team wanted to understand more about how CAD has been inherited in our evolutionary past, in order to better understand why it is so common presently. "CAD is often thought of as modern disease, but actually atherosclerosis, or thickening of the artery walls, has been detected in Egyptian mummies, so we suspect it has been in our genes for thousands of years". CAD currently affects 110 million people and causes 8.9 million deaths annually, from 2015 figures. "According to the theory of natural selection, as proposed by Charles Darwin, genes for traits that improve individual survival or reproduction will increase or be maintained in populations, whereas those that reduce these will be selected against and gradually removed or reduced over time. "So it is unclear why CAD is so common in modern humans and this is important to understand given the global health burden it represents", explains Dr Byars. The team analysed 56 genetic regions for CAD in 12 worldwide populations originating mainly from Africa, Europe and East Asia, and used a statistical score to measure whether there had been recent selective changes to the DNA associated with CAD. Associate Professor Michael Inouye, who also led the study, said the findings showed that many genes associated with CAD have actually been positively selected for through evolution. "After further research, we found CAD genes are also important for reproduction and that these genes are involved in important functions in male and female fertility being expressed in the testes, ovaries and endometrium, for example," said Assoc Prof Inouye, based at the Baker Heart and Diabetes Institute. Dr Byars added, "Evolution it seems is involved in a trade-off where CAD only begins to appear at around 40-50 years of age when the potential beneficial effects of these genes on reproduction will have already occurred. That will tend to compensate for any negative effects these genes also have on CAD later in life. "This doesn't necessarily mean that women with many children are more likely to develop heart disease, it may simply mean that the disease is a by-product of humans being able to reproduce well." The results also provide insight on how selection for CAD genes differs between populations, and how these populations might respond differently to the same heart disease prevention strategies. Dr Inouye says that ultimately these results give us some idea how complicated the effects of genes can be. He adds that we need to be cautious with new gene-editing techniques like CRISPR, as unintended effects may be introduced which may not reveal themselves for decades or more. "It's a bit like a balloon, if you push on one side of it, the air will push out in other places and if you don't know what the balloon looks like then you won't be able to predict where. Our genomes are similarly complex and we need to learn more in order to read them, much less write them."


Genkyotex (Paris:GKTX) (Brussels:GKTX) (Euronext Paris & Brussels: FR00011790542 – GKTX), a biopharmaceutical company and the leader in NOX therapies, announced today that world-renowned diabetes experts Professor Mark Cooper, Head of the Department of Diabetes at Monash University, and Professor Jonathan Shaw, Deputy Director (Clinical and Population Health) at the Baker Heart and Diabetes Institute in Melbourne, Australia, will lead the conduct of a phase 2 clinical trial to evaluate the efficacy and safety of the Company’s lead product candidate, GKT831, in patients with type 1 diabetes and kidney disease (diabetic kidney disease). This investigator-initiated study will be based at the Baker Institute and will include multiple study sites across Australia. This research is financially supported by JDRF Australia, the recipient of the Australian Research Council Special Research Initiative in Type 1 Juvenile Diabetes funding, with additional financial support by the Baker Institute. Genkyotex shall provide GKT831 Good Manufacturing Practice (GMP) material for the trial. The trial is expected to begin patient enrollment during the second half of 2017. Diabetic kidney disease is a fibrotic disorder where progressive glomerulosclerosis and interstitial fibrosis leads to end stage renal disease. GKT831 is a NOX 1 and 4 enzyme inhibitor that has shown potent anti-fibrotic activity in a broad range of preclinical models including several DKD models [1-4]. In a previous, short-term phase 2 trial in patients with type 2 diabetes and kidney disease, GKT831 demonstrated an excellent safety profile and achieved statistically significant reductions in several secondary efficacy endpoints. However, improvements in albuminuria, the study’s primary efficacy endpoint, was not achieved after 12 weeks of treatment. The Baker Institute study will be a placebo-controlled, double blind, randomized, parallel group phase 2 trial to evaluate the effect of oral GKT831 on the urine albumin-to-creatinine ratio (UACR) in patients with type 1 diabetes and persistent albuminuria despite treatment with optimal standard of care. The primary endpoint of the study will be UACR difference between means at the end of treatment period of 48 weeks, adjusted for baseline. A key secondary endpoint of the study will be the effect of GKT831 on renal function, as defined by changes in estimated glomerular filtration rate. Patients will receive 200mg of oral GKT831 or placebo twice a day for 48 weeks. A total of 142 patients are planned to be enrolled into the study at up to 15 investigational centers in Australia. Professor Cooper has stated that “We are very excited to be commencing this study which arises in part from original research performed in our laboratories and which was initially supported by JDRF. This work is a classic example of bench to bedside clinical translation. We appreciate JDRF greatly assisting us in providing us with an opportunity to bring this new treatment forward for what is a major burden of T1D kidney disease.” “We are delighted to be working with Professor Cooper and his team to pursue the clinical evaluation of GKT831 in this severe diabetic complication,” said Dr. Philippe Wiesel, chief medical officer of Genkyotex. “The design of this phase 2 trial was informed by previous phase 2 results in patients with type 2 diabetes and kidney disease performed by Genkyotex, in particular the extended 48-week treatment duration, a more homogenous and earlier stage patient population, and a higher dose throughout the dosing period. We also wish to thank JDRF for supporting this study, as well as previous preclinical studies, which has enabled a number of investigators to evaluate GKT831’s impact on ophthalmic, vascular, and renal complications caused by type 1 diabetes.” 1. Gorin Y et al. Targeting NADPH oxidase with a novel dual Nox1/Nox4 inhibitor attenuates renal pathology in type 1 diabetes. Am J Physiol Renal Physiol. 2015 Jun 1;308(11):F1276-87. doi: 10.1152/ajprenal.00396.2014. 2. Gray SP et al. Combined NOX1/4 inhibition with GKT137831 in mice provides dose-dependent reno- and atheroprotection even in established micro- and macrovascular disease. Diabetologia. 2017 May;60(5):927-937. doi: 10.1007/s00125-017-4215-5. 3. Jha JC et al. Genetic targeting or pharmacologic inhibition of NADPH oxidase nox4 provides renoprotection in long-term diabetic nephropathy. J Am Soc Nephrol. 2014 Jun;25(6):1237-54. doi: 10.1681/ASN.2013070810. Epub 2014 Feb 7. 4. You YH. Metabolomics Reveals a Key Role for Fumarate in Mediating the Effects of NADPH Oxidase 4 in Diabetic Kidney Disease. J Am Soc Nephrol. 2016 Feb;27(2):466-81. doi: 10.1681/ASN.2015030302. Genkyotex is the leading biopharmaceutical company in NOX therapies. Listed on the Euronext Paris and Euronext Brussels markets, Genkyotex is established in France and, via its GenKyoTex Suisse SA subsidiary, in Switzerland. A leader in NOX therapies, its unique therapeutic approach is based on a selective inhibition of NOX enzymes that amplify multiple disease processes such as fibrosis, inflammation, pain processing, cancer development, and neurodegeneration. Genkyotex’s platform enables the identification of orally available small-molecules that selectively inhibit specific NOX enzymes. Genkyotex is developing a pipeline of first-in-class product candidates targeting one or multiple NOX enzymes. The lead product candidate, GKT831, a NOX1 and NOX4 inhibitor is expected to enter a phase II clinical trial in primary biliary cholangitis (PBC, a fibrotic orphan disease) during the first half of 2017. This product candidate may also be active in other fibrotic indications. Its second product candidate, GKT771, is a NOX1 inhibitor targeting multiple pathways in angiogenesis, pain processing, and inflammation, and should enter a phase I clinical study at the end of the second half of 2017. Genkyotex also has a versatile platform, Vaxiclase, that is particularly well-suited to the development of various immunotherapies. A partnership covering the use of Vaxiclase as an antigen per se (GTL003) has been established with Serum Institute of India Ltd (Serum Institute), the world’s largest producer of vaccine doses. This agreement covers territories outside the United States and Europe, and could generate up to $57 million in revenues for Genkyotex, before royalties on sales. It will enable Serum Institute to develop acellular multivalent combination vaccines against a variety of infectious diseases, including whooping cough. The last preclinical milestone foreseen in the agreement was reached in November 2016, opening the path to formal preclinical testing prior to potential clinical development and subsequent commercialization. For further information, please go to www.genkyotex.com. JDRF is the leading global organisation funding type 1 diabetes (T1D) research. JDRF Australia is built on a grassroots model of people connecting in their local communities, collaborating regionally for efficiency and broader fundraising impact, and uniting on an international stage to pool resources, passion and energy. Our mission is to accelerate life-changing breakthroughs to cure, prevent and treat T1D and its complications. To accomplish this, JDRF has invested nearly $2 billion since our inception. We collaborate with academic institutions, policymakers, and corporate and industry partners to develop and deliver a pipeline of innovative therapies to people living with T1D. Our staff and volunteers in seven countries are dedicated to advocacy, community engagement and our vision of a world without T1D. For more information, please visit jdrf.org.au. The Type 1 Diabetes Clinical Research Network (T1DCRN) is an innovative clinical research program led by JDRF Australia and funded by the Australian Government through the Australian Research Council (ARC) Special Research Initiatives scheme. The T1DCRN’s goal is to accelerate patient benefit through supporting the most promising research projects, promoting and retaining outstanding scientists and attracting new researchers to the field of type 1 diabetes research. For more information, please visit t1dcrn.org.au. This press release and the information it contains does not constitute an offer or solicitation to buy, sell or hold Genkyotex shares in any country, in particular any jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration, exemption from registration or other qualification under the securities laws of any such jurisdiction. This press release may contain forward-looking statements by the company with respect to its objectives. Such statements are based upon the current beliefs, estimates and expectations of Genkyotex’s management and are subject to risks and uncertainties such as the company's ability to implement its chosen strategy, customer market trends, changes in technologies and in the company's competitive environment, changes in regulations, clinical or industrial risks and all risks linked to the company's growth. These factors as well as other risks and uncertainties may prevent the company from achieving the objectives outlined in the press release and actual results may differ from those set forth in the forward-looking statements, due to various factors. Without being exhaustive, such factors include uncertainties involved in the development of Genkyotex’s products, which may not succeed, or in the delivery of Genkyotex’s products marketing authorizations by the relevant regulatory authorities and, in general, any factor that could affects Genkyotex’s capacity to commercialize the products it develops. No guarantee is given on forward-looking statements which are subject to a number of risks, notably those described in the registration document filed with the French Markets Authority (the AMF) on 1 April 2015 under number R.15-015, as updated in the Document E filed with the AMF on 31 January 2017 under number E.17-004 and in the Annual Financial Report of the company on 27 February 2017, and those linked to changes in economic conditions, the financial markets, or the markets on which Genkyotex is present. Genkyotex products are currently used for clinical trials only and are not otherwise available for distribution or sale.


News Article | August 2, 2017
Site: www.reuters.com

Reuters Health - The amount of salt a typical American adult consumes each day may be enough to damage the heart muscle and make it harder to pump blood, a U.S. study suggests. A high-salt diet has long been linked to higher odds of developing high blood pressure and heart disease as well as an increased risk of heart attack, stroke and heart failure. But determining the ideal amount of dietary salt is controversial because some research has also found an elevated risk of heart disease, high blood pressure and heart attacks in otherwise healthy people who consume too little salt. In the current study, half of the people consumed at least 3.73 grams a day of sodium, the equivalent of about two teaspoons of table salt. Compared with adults who ate less sodium, people who consumed more than 3.7 grams of sodium a day were more likely to have enlargement in the left chambers of the heart that are responsible for pumping oxygen-rich blood into the body. They were also more likely to have signs of muscle strain in the heart that can precede structural damage. “This study enhances our understanding of the adverse effects of salt intake on heart function,” said lead study author Dr. Senthil Selvaraj, a researcher at the Hospital of the University of Pennsylvania in Philadelphia. While the results don’t settle the debate over the optimal amount of salt, the findings should still encourage people who eat a lot of salt to cut back, Selvaraj said by email. That’s because reducing sodium intake can help reverse high blood pressure, a major risk factor for heart failure, stroke and heart attacks. “There is still a healthy debate ongoing,” Selvaraj added. “It is still worth the effort to reduce your sodium intake.” Cardiovascular diseases are the leading cause of death worldwide, killing almost one in every three people. Sodium is found not only in table salt, but also in a variety of foods such as bread, milk, eggs, meat, and shellfish as well as processed items like soup, pretzels, popcorn, soy sauce and bouillon or stock cubes. To lower the risk of heart disease, adults should reduce sodium intake to less than 2 grams a day, or the equivalent of about one teaspoon of salt, according to the World Health Organization (WHO). For the current study, researchers examined data from lab tests of sodium intake, heart structure and heart function for almost 3,000 adults. Participants were 49 years old on average, 54 percent had high blood pressure and half were African-American. They were typically overweight or obese. To assess how sodium intake influenced the heart, researchers accounted for age, sex, smoking status, alcohol use, activity levels, and certain medications. The study wasn’t a controlled experiment designed to prove how or if salt damages the heart or impairs heart function. One limitation of the study is that researchers tested sodium intake using overnight urine samples, which may not be as accurate as the gold standard, 24-hour urine collection, the authors note in the Journal of the American College of Cardiology. Researchers also didn’t have enough data on people who consumed very little sodium to assess how low salt intake influences the heart. “We know less than we should about salt,” said Thomas Marwick, author of an accompanying editorial and director of the Baker Heart and Diabetes Institute in Melbourne, Australia. “In general, most of the population take far more salt than is good for them and this is a reminder to reduce intake,” Marwick said by email. “It’s ubiquitous and hard to reduce to very low levels,” Marwick added. “While some zealots want to reduce intake to zero, I’m not sure that drastic reduction is necessarily beneficial.” SOURCE: bit.ly/2wlZgK5 Journal of the American College of Cardiology, online July 31, 2017.


Nestel P.,Baker Heart and Diabetes Institute
Clinical Therapeutics | Year: 2014

Objective The goal of this article was to review the causal link between trans fatty acids (TFA) produced from partially hydrogenated vegetable oil (PHVO) and cardiovascular disease (CVD) risk and its likely mechanisms. The potential risk of TFA from ruminant dairy and meats, which are currently the major sources of dietary TFA, is also discussed. Methods Evidence was derived from observational studies of large cohorts followed up prospectively; from randomized controlled trials of clinical interventions; and from specific case-control studies that investigated biomarkers in tissues. Searches included PubMed and Medline from 1990 to 2013. Results Despite TFA from PHVO being associated more strongly with CVD risk than even saturated fats, it may prove difficult to totally eliminate PHVO from all foods. This raises the issue of the lower limit of TFA consumption below which CVD risk is not increased. Limits of <1% of total energy have been suggested. The major mechanism underlying the increased CVD risk from TFA is an increase in LDL-C and Lp(a) lipoproteins and a decrease in HDL-C; increased inflammation and adverse effects on vascular function have also been shown. Both PHVO and ruminant TFA comprise a range of isomers, some specific to each source but including a substantial commonality that supports findings of similar adverse effects at equivalent intakes of TFA. However, the amount of TFA in ruminant fat is relatively small; this limits the CVD risk from eating ruminant products, an inference supported by analysis of prospective cohort studies. Conclusions Two key challenges to the health industry arise from this evidence. They must first determine whether a small intake of TFA from PHVO is safe and what constitutes a safe amount. They must also determine whether TFA from ruminant fat in currently consumed amounts represent limited cardiovascular risk that is balanced by the nutritional benefits of dairy products. © 2014 Elsevier HS Journals, Inc.

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