News Article | April 27, 2017
I am writing to express my concern for the addition of Bret Stephens to the NYT team as a columnist. I don’t expect a columnist who seemingly writes about everything to be wrong about nothing. But the Gray Lady should, at the very least, expect a columnist to know something about something. Stephens doesn’t simply express opinions that are not popular in certain, many, circles. He attempts to support his opinions with what we now seem to be calling alt-facts. For example, his opinion about the importance of climate change is that we don’t know what climate change will really do, if it will really do anything, or when. He supports this idea by asserting that there is too much uncertainty in the science for us to know. Elizabeth, you must know that science is nothing if it is not the study of variation in nature and its causes and properties. While the public face of many scientific findings is often the trend line showing the relationship between two variables, much of the science itself is about the uncertainty around that trend line; measuring, understanding the limits and extent of, and grappling with uncertainty is what scientists do. As a scientist (not a climate scientist, though I’ve published in that area) and a science communicator, I can tell you that when Mr. Stephens makes the claim that there is too much uncertainty about anthropogenic climate change to say much about it, he is simply wrong. He does not know the science, he has made up this thing that looks like a fact, and he has used it to buttress absurd arguments, and you, the New York Times, is now set to be a vehicle for passing this misinformation on to the general public. Many of my friends and colleagues have unsubscribed to the New York Times over this. I have not. Rather, I was just about to subscribe, as part of my overall effort to support good journalism in the Trump Era. In the past few weeks I’ve subscribed to my local paper, my regional paper, and one national paper (Washington Post) and I was just about to add the New York Times to that list. But now I can’t ethically do so, even though much of your other science coverage is pretty good, and even tough I grew up on the New York Times Science Section (remember that?). But this probable drop in subscription is nothing to you, because trends in the business side of the NYT operation are much larger and more complex than many, if not most, of the world’s climate scientists dropping off your list over the addition of Bret Stephens to your staff. The bigger problem is this: The New York Times editorial staff has lost our respect. I look forward to your prompt and decisive attention to this manner, and the quick repair of the mistake the NYT has made.
News Article | November 13, 2016
NEW ORLEANS, Nov. 13, 2016 -- Active marijuana use may double the risk of stress cardiomyopathy, an uncommon heart muscle malfunction that can mimic heart attack symptoms, according to research presented at the American Heart Association's Scientific Sessions 2016. The researchers found that marijuana users were almost twice as likely to develop stress cardiomyopathy compared to non-users, even after taking other cardiovascular risk factors into consideration. Active marijuana use was identified either by information provided by the patient in their medical history, or by a marker in the patient's urine. "The effects of marijuana, especially on the cardiovascular system, are not well known yet. With its increasing availability and legalization in some states, people need to know that marijuana may be harmful to the heart and blood vessels in some people," said Amitoj Singh, M.D. study co-author and chief cardiology fellow at St. Luke's University Health Network in Bethlehem, Pennsylvania. Stress cardiomyopathy is a sudden, usually temporary, weakening of the heart muscle that reduces the heart's ability to pump, leading to chest pain, shortness of breath, dizziness and sometimes fainting. Data from the Nationwide Inpatient Sample identified 33,343 people who were hospitalized with stress cardiomyopathy between 2003-2011 in the United States. Of those, 210 (less than one percent) were also identified as marijuana users. Compared with non-users, researchers found that marijuana users were more likely to be younger, male with fewer cardiovascular risk factors, including less high blood pressure, diabetes and high cholesterol. However, despite being younger and with fewer cardiovascular risk factors than non-users, during stress cardiomyopathy the marijuana users were significantly more likely to go into cardiac arrest (2.4 percent vs. 0.8 percent) and to require an implanted defibrillator to detect and correct dangerously abnormal heart rhythms (2.4 percent vs. 0.6 percent). "This development of stress cardiomyopathy in younger patients who used marijuana suggests a possible link that needs to be further investigated," said Sahil Agrawal, M.D., co-author of the paper and also a chief cardiology fellow at St. Luke's. Marijuana users were more likely than non-users to have a history of depression (32.9 percent vs. 14.5 percent), psychosis (11.9 percent vs. 3.8 percent), anxiety disorder (28.4 percent vs. 16.2 percent), alcoholism (13.3 percent vs. 2.8 percent), tobacco use (73.3 percent vs. 28.6 percent) and multiple substance abuse (11.4 percent vs. 0.3 percent). Because some of these can increase the risk of stress cardiomyopathy, the researchers adjusted for known risk factors to investigate the association between marijuana use and stress cardiomyopathy. "If you are using marijuana and develop symptoms such as chest pain and shortness of breath, you should be evaluated by a healthcare provider to make sure you aren't having stress cardiomyopathy or another heart problem," Singh said. The study has some limitations. Because this was a retrospective study, the researchers could not determine how frequently the marijuana users were using marijuana, or what the timeframe was between the use of marijuana and occurrence of stress cardiomyopathy. Observational studies are not designed to prove cause and effect; therefore, it cannot be said that marijuana is or is not a direct cause of stress cardiomyopathy. In addition, because the database the researchers used reports regional but not state-by-state statistics, the researchers could not analyze whether possibly marijuana-related heart problems are increasing where use is legal. Co-authors are Mark Fegley, M.D.; Yugandhar Manda, M.D.; Sudip Nanda, M.D.; and Jamshid Shirani, M.D. Author disclosures are on the abstract. This study did not receive outside funding. Note: Scientific presentation is at 2 p.m. CT, Sunday, Nov. 13 in the Science and Technology Hall, Clinical Science Section. Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www. .
News Article | November 7, 2016
SOUTH SAN FRANCISCO, Calif., Nov. 07, 2016 (GLOBE NEWSWIRE) -- Cytokinetics, (Nasdaq:CYTK) today announced that a new analysis of left atrial structure and function from COSMIC-HF (Chronic Oral Study of Myosin Activation to Increase Contractility in Heart Failure), a Phase 2 trial evaluating omecamtiv mecarbil in patients with chronic heart failure, will be presented on November 14 at the American Heart Association (AHA) Scientific Sessions in New Orleans, LA. Abstract Title: Cardiac Myosin Activator Omecamtiv Mecarbil Improves Left Atrial Structure and Function in Chronic Heart Failure (COSMIC-HF) Abstract Number: M 4180 Session Title: Impact of Novel Therapies on Cardiac Structure and Function Location: Science and Technology Hall, Clinical Science Section Date: Monday, November 14, 2016 Time: 2:00 – 3:15 PM Omecamtiv mecarbil is a novel cardiac myosin activator. Cardiac myosin is the cytoskeletal motor protein in the cardiac muscle cell that is directly responsible for converting chemical energy into the mechanical force resulting in cardiac contraction. Cardiac myosin activators are thought to accelerate the rate-limiting step of the myosin enzymatic cycle and shift the enzymatic cycle in favor of the force-producing state. Preclinical research has shown that cardiac myosin activators increase contractility in the absence of changes in intracellular calcium in cardiac myocytes. Omecamtiv mecarbil is being developed by Amgen in collaboration with Cytokinetics. Amgen holds an exclusive, worldwide license to omecamtiv mecarbil and related compounds, subject to Cytokinetics’ specified development and commercialization rights. Amgen has granted a sublicense to Servier to commercialize omecamtiv mecarbil in Europe, as well as the Commonwealth of Independent States, including Russia. Cytokinetics is a late-stage biopharmaceutical company focused on discovering, developing and commercializing first-in-class muscle activators as potential treatments for debilitating diseases in which muscle performance is compromised and/or declining. As a leader in muscle biology and the mechanics of muscle performance, the company is developing small molecule drug candidates specifically engineered to increase muscle function and contractility. Cytokinetics’ lead drug candidate is tirasemtiv, a fast skeletal muscle troponin activator, for the potential treatment of ALS. Tirasemtiv has been granted orphan drug designation and fast track status by the U.S. Food and Drug Administration and orphan medicinal product designation by the European Medicines Agency for the potential treatment of ALS. Cytokinetics retains the right to develop and commercialize tirasemtiv, subject to an option held by Astellas Pharma Inc. Cytokinetics is also collaborating with Astellas to develop CK-2127107, a fast skeletal muscle activator, for the potential treatment of spinal muscular atrophy, chronic obstructive pulmonary disease and ALS. Cytokinetics is collaborating with Amgen Inc. to develop omecamtiv mecarbil, a novel cardiac muscle activator, for the potential treatment of heart failure. Amgen holds an exclusive license worldwide to develop and commercialize omecamtiv mecarbil and Astellas holds an exclusive license worldwide to develop and commercialize CK-2127107. Both licenses are subject to Cytokinetics' specified development and commercialization participation rights. For additional information about Cytokinetics, visit http://www.cytokinetics.com/. This press release contains forward-looking statements for purposes of the Private Securities Litigation Reform Act of 1995 (the “Act”). Cytokinetics disclaims any intent or obligation to update these forward-looking statements, and claims the protection of the Act’s Safe Harbor for forward-looking statements. Examples of such statements include, but are not limited to, statements relating to Cytokinetics’ and its partners’ research and development activities, including the significance and utility of COSMIC-HF clinical trial results and the likelihood and timing for the progression of omecamtiv mecarbil to Phase 3 development; and the properties and potential benefits of Cytokinetics' drug candidates. Such statements are based on management's current expectations, but actual results may differ materially due to various risks and uncertainties, including, but not limited to Amgen's decisions with respect to the design, initiation, conduct, timing and continuation of development activities for omecamtiv mecarbil; potential difficulties or delays in the development, testing, regulatory approvals for trial commencement, progression or product sale or manufacturing, or production of Cytokinetics' drug candidates that could slow or prevent clinical development or product approval, including risks that patient enrollment for or conduct of clinical trials may be difficult or delayed, Cytokinetics' drug candidates may have adverse side effects or inadequate therapeutic efficacy, the U.S. Food and Drug Administration or foreign regulatory agencies may delay or limit Cytokinetics' or its partners' ability to conduct clinical trials, and Cytokinetics may be unable to obtain or maintain patent or trade secret protection for its intellectual property; Cytokinetics may incur unanticipated research and development and other costs or be unable to obtain additional financing necessary to conduct development of its products; standards of care may change, rendering Cytokinetics' drug candidates obsolete; and competitive products or alternative therapies may be developed by others for the treatment of indications Cytokinetics' drug candidates and potential drug candidates may target. For further information regarding these and other risks related to Cytokinetics' business, investors should consult Cytokinetics' filings with the Securities and Exchange Commission. Forward-looking statements are not guarantees of future performance, and Cytokinetics' actual results of operations, financial condition and liquidity, and the development of the industry in which it operates, may differ materially from the forward-looking statements contained in this press release. Any forward-looking statements that Cytokinetics makes in this press release speak only as of the date of this press release. Cytokinetics assumes no obligation to update its forward-looking statements whether as a result of new information, future events or otherwise, after the date of this press release.
News Article | November 4, 2016
Clinical Data from Phase 1 SAD Trials of MYK-461 in Hypertrophic Cardiomyopathy Patients and Healthy Volunteers SOUTH SAN FRANCISCO, Calif., Nov. 04, 2016 (GLOBE NEWSWIRE) -- MyoKardia, Inc. (Nasdaq:MYOK), a clinical stage biopharmaceutical company pioneering a precision medicine approach for the treatment of heritable cardiovascular diseases, today announced presentations at American Heart Association (AHA) Scientific Sessions 2016 highlighting the Company’s clinical and animal model research in hypertrophic cardiomyopathy (HCM), novel insights from its SHaRe registry and precision cardiovascular approach, as well as two of MyoKardia’s cofounders presenting research in understanding HCM causes and outcomes. AHA Scientific Sessions 2016 will be held Nov. 12-16 in New Orleans. Clinical Data from Phase 1 SAD Trials of MYK-461 in Hypertrophic Cardiomyopathy Data from MyoKardia’s two Phase 1 single ascending dose trials of MYK-461 in HCM patients and healthy volunteers will be presented by Martin S. Maron, M.D., Director of the Hypertrophic Cardiomyopathy Center at Tufts Medical Center in Boston. Topline data from the studies were released in July 2016. The studies were designed to establish the safety and tolerability of single oral doses of MYK-461. Secondary objectives included establishing the preliminary pharmacokinetic and pharmacodynamics profiles of MYK-461. Clinical proof of mechanism was observed overall as a dose-dependent reduction in cardiac contractility following single oral doses, in both healthy volunteers and HCM patients. MyoKardia is currently studying MYK-461 in PIONEER-HCM, a Phase 2 open-label single-arm pilot study to evaluate safety, tolerability and efficacy of MYK-461 in subjects with symptomatic, obstructive HCM (oHCM). The U.S. Food and Drug Administration has granted the company Orphan Drug Designation for MYK-461 for the treatment of symptomatic oHCM. The poster presentation, “Obstructive Hypertrophic Cardiomyopathy: Initial Single Ascending Dose Data in Healthy Volunteers and Patients,” is part of the “Hypertrophic Cardiomyopathy: New Insights” session. The presentation is on Nov. 15, 10:45 AM to 12:00 PM, in the Science and Technology Hall, Clinical Science Section. Previous MyoKardia research, including results published in a recent paper in the leading medical journal Science, has provided evidence of the ability of MYK-461 to prevent and reverse development of HCM in multiple animal models. A new study highlighted at AHA sheds further light on how mutations in sarcomere genes lead to the physiology of HCM. The findings of the MyoKardia study provide the first evidence integrating molecular, cellular and organ-level studies that hypercontractility, subclinical ischemia and fibrosis contribute to the early pathogenesis of HCM. Ferhaan Ahmad, M.D., Ph.D., Director of the Cardiovascular Genetics Program at the University of Iowa, will present “A Minipig Genetic Model of Hypertrophic Cardiomyopathy.” The presentation is part of the “Molecular Basis of Cardiac Hypertrophy” session on Nov. 15, from 1:30 to 2:45 PM, and is being held in the Science and Technology Hall, Clinical Science Section. The experiments highlighted by Dr. Ahmad were performed on proprietary genetic pig models of HCM, which were created by Exemplar Genetics, a wholly-owned subsidiary of Intrexon Corporation. MyoKardia and Exemplar Genetics have formed a multi-year collaboration, in which MyoKardia may direct the development of additional pig models of disease by Exemplar Genetics, each with distinct genetic defects known to cause heritable cardiomyopathies. Researchers anticipate this model, and future models created under the collaboration, will be valuable for advancing our understanding of disease pathophysiology and for the further development of novel therapeutics to treat heritable cardiomyopathies. MyoKardia Co-Founders Leslie Leinwand and Christine Seidman Present Research on Cardiomyopathy Causes and Outcomes MYK-461 is an orally administered small molecule designed to reduce left ventricular contractility by allosterically modulating the function of cardiac myosin, the motor protein that drives heart muscle contraction. MyoKardia has evaluated MYK-461 in three Phase 1 clinical trials, primarily designed to evaluate safety and tolerability of oral doses of MYK-461, as well as provide pharmacokinetic and pharmacodynamic data. In April 2016, the U.S. FDA granted the company Orphan Drug Designation for MYK-461 for the treatment of symptomatic oHCM, a subset of HCM. MyoKardia is currently studying MYK-461 in PIONEER-HCM, a Phase 2 open-label single-arm pilot study to evaluate safety, tolerability and efficacy of MYK-461 in patients with symptomatic oHCM. The primary endpoint of PIONEER-HCM is the level of reduction in post-exercise left ventricular outflow tract (LVOT) gradient over 12 weeks of drug treatment. PIONEER-HCM will also explore the relationship between reduction in contractility and LVOT gradient, endpoints measuring functional capacity (i.e., exercise) and clinical symptoms in addition to gathering safety and tolerability data on MYK-461 in an outpatient setting. It is estimated that one in every 500 people in the United States has HCM, the most prevalent form of heritable cardiomyopathy. HCM is defined as an otherwise unexplained thickening of the walls of the heart, known as hypertrophy. The consequences include reduced left ventricular volumes and cardiac output, reduced ability of the left ventricle to expand, and elevated filling pressures. These can all contribute to reduced effort tolerance and symptoms that include shortness of breath and chest pain. HCM is a chronic disease and for the majority of patients, the disease progresses slowly and can be extremely disabling. HCM substantially increases the risk of developing atrial fibrillation that can lead to stroke or malignant ventricular arrhythmias that can cause sudden cardiac death. There are currently no approved drug products indicated for the treatment of HCM. Patients are typically prescribed one or more drugs (including beta blockers, non-dihydropyridine calcium channel blockers and disopyramide) indicated for the treatment of hypertension, heart failure or other cardiovascular disorders more generally. oHCM is a physiological complication of HCM in which the thickened heart muscle obstructs the LVOT. Approximately two thirds of all HCM patients have obstruction, either at rest or with provocation like exercise. Measured most commonly by non-invasive imaging (echocardiography), oHCM is defined as ≥30 mm Hg pressure gradient across the LVOT. Symptoms of oHCM can include shortness of breath, chest pain, dizziness, fainting, and palpitations. The presence of obstruction in an HCM patient further increases risk of progression to severe symptoms, and risk of death from heart failure or stroke. The degree of LVOT obstruction in oHCM patients is a primary criterion for surgical and other invasive interventions (recommended for symptomatic patients with LVOT gradients measured at ≥50 mmHg). Relief of obstruction has been associated with improved symptoms, function and clinical outcomes. Surgical or other invasive interventions, including septal myectomy, an open heart procedure, may be appropriate. There are no approved drug products indicated for this condition. The primary endpoint of the Phase 2 PIONEER-HCM study is to assess level of reduction in LVOT gradient over 12 weeks of drug treatment. The trial is also exploring relationships among reductions in contractility, LVOT gradient and endpoints that include safety, tolerability, functional capacity and clinical symptoms. MyoKardia is a clinical stage biopharmaceutical company pioneering a precision medicine approach to discover, develop and commercialize targeted therapies for the treatment of serious and rare cardiovascular diseases. MyoKardia’s initial focus is on the treatment of heritable cardiomyopathies, a group of rare, genetically-driven forms of heart failure that result from biomechanical defects in cardiac muscle contraction. MyoKardia has used its precision medicine platform to generate a pipeline of therapeutic programs for the chronic treatment of the two most prevalent forms of heritable cardiomyopathy—hypertrophic cardiomyopathy, or HCM, and dilated cardiomyopathy, or DCM. MyoKardia’s most advanced product candidate, MYK-461, is an orally-administered small molecule designed to reduce excessive cardiac muscle contractility leading to HCM and has been evaluated in three Phase 1 clinical trials. MyoKardia is now studying MYK-461 in a Phase 2 PIONEER-HCM pilot study in symptomatic oHCM, for which the FDA has granted MYK-461 Orphan Drug Designation. A cornerstone of the MyoKardia platform is the Sarcomeric Human Cardiomyopathy Registry, or SHaRe, a multi-center, international repository of clinical and laboratory data on individuals and families with genetic heart disease, which MyoKardia helped form in 2014. MyoKardia believes that SHaRe, currently consisting of data from approximately 10,000 individuals, is the world’s largest registry of patients with heritable cardiomyopathies. MyoKardia’s mission is to change the world for patients with serious cardiovascular disease through bold and innovative science. For more information, please visit www.myokardia.com.
News Article | November 13, 2016
NEW ORLEANS, Nov. 13, 2016 -- After a multi-faceted campaign that included policy changes and community education efforts, residents of one Maryland county put fewer sugary drinks in their grocery carts, according to research presented at the American Heart Association's Scientific Sessions 2016. Drinks loaded with added sugars are one of the leading sources of empty calories in the diet of both children and adults, and overconsumption of sugar is associated with obesity and an increased risk of heart disease. In 2012, the Horizon Foundation and several community partners began a multi-year campaign to encourage people to reduce consumption of sugary sodas, sports drinks, energy drinks, fruit drinks and flavored water/teas in Howard County, Maryland. Comparing 2012, before the campaign, to 2015, researchers found: The researchers note that this is the first study to use objective retail sales data to measure the effectiveness of a community led campaign to reduce the consumption of sugary drinks. "This study shows that a public health campaign combining community-wide education, policy changes and culture-shifting efforts can significantly reduce sugary drink sales," said Marlene B. Schwartz, Ph.D., Director of the Rudd Center for Food Policy and Obesity at the University of Connecticut. "Through complementary strategies from advocating for changes to child care nutrition standards to creating TV ads, "Howard County Unsweetened" made a concerted effort to encourage families to switch their drinks." The campaign included policy measures such as: The campaign also educated the community through: To determine the impact of the overall campaign, researchers compared weekly beverage sales of top-selling brands from 15 supermarkets in Howard County with a matched set of 17 supermarkets in southeastern Pennsylvania, controlling for marketing influences such as product prices. The study did not have sales data from non-supermarket vendors, such as convenience stores, and only included the top selling brands sold rather than all brands sold. The American Heart Association recommends that children and adult women consume no more than 6 teaspoons of added sugars a day. Adult men should have no more than 9 teaspoons. One 12-ounce can of soda has more than 8 teaspoons of added sugar. Co-authors are Glenn E. Schneider, M.P.H.; Yoon-Young Choi, Ph.D.; Xun Li, Ph.D.; Jennifer Harris, Ph.D.; Tatiana Andreyeva, Ph.D.; Maia Hyary, M.P.A.; Nicolette Highsmith Vernick, M.P.A.; and Lawrence J. Appel, M.D., M.P.H. Author disclosures are on the abstract. The study is funded by the Horizon Foundation, the Robert Wood Johnson Foundation, and the Rudd Foundation. Note: Scientific presentation is 2:15 p.m. CT/3:15 p.m. ET, Sunday, Nov. 13, in the Science and Technology Hall, Population Science Section. Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www. .
News Article | November 14, 2016
NEW ORLEANS, Nov. 14, 2016 -- Bariatric surgery and other treatments that cause substantial weight loss can significantly reduce the risk of heart failure in obese patients, according to preliminary research presented at the American Heart Association's Scientific Sessions 2016. Researchers compared 25,804 bariatric surgery patients in a Scandinavian obesity surgery registry to 13,701 Swedish nationwide registry patients who used an intensive structured lifestyle-modification program. Both groups had no history of heart failure before starting treatment and body mass indices greater than 30 and weighed on average 119 kilograms/262.35 pounds before treatment. The lifestyle modification program participants consumed a very low-energy diet of 500 calories a day for 3 to 10 weeks followed by 2 to 8 weeks of gradual incorporation of food, and then 9 months of a weight-maintenance regimen that included regular exercise, dietary advice and behavioral therapy. Around 20 percent of patients in the lifestyle modification program dropped out by the first year. "Our study shows an association between obesity and heart failure and offers support for efforts to prevent and treat obesity aggressively, including the use of bariatric surgery," said Johan Sundstrom, M.D., Ph.D., senior author of the study and professor of epidemiology at Uppsala University in Sweden. "Bariatric surgery might affect the incidence of atrial fibrillation, diabetes and hypertension -- known risk factors of heart failure -- explaining the lower risk of heart failure we observed." While the findings report that heart failure risk is lower in patients who lose more weight, it does not prove that obesity causes heart failure, he said. But, patients in both treatment groups lost weight intentionally, supporting the idea. The study was done in a most likely white Scandinavian population. Whether the study's findings would relate to a U.S. population is unclear. In addition, because the study's participants did not have heart failure before the weight-loss treatment, "the study does not provide any advice on how to treat cardiovascular disease in obese patients," Sundstrom said. American Heart Association, American College of Cardiology and the Obesity Society Clinical Practice guidelines advise adults with a body mass index (BMI) of 40 or higher and patients with a BMI of 35 or higher, who have two other cardiovascular risk factors such as diabetes or high blood pressure, that bariatric surgery may provide significant health benefits. The guidelines do not recommend weight loss surgery for people with a BMI under 35 and do not recommend one surgical procedure over another. Co-authors are Gustaf Bruze, Ph.D.; Johan Ottosson, M.D., Ph.D.; Claude Marcus, M.D., Ph.D.; Ingmar Näslund, M.D., Ph.D.; and Martin Neovius, Ph.D. Author disclosures are on the abstract. The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases, Uppsala University, Karolinska Institute, and the Swedish Research Council. Note: Scientific presentation time is 10:45 a.m. CT on Monday, Nov. 14, in the Science and Technology Hall, Population Science Section. Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www. .
News Article | April 11, 2016
A five-member team of researchers from the U.S. Naval Research Laboratory (NRL) Center for Corrosion Science and Engineering received the Office of Naval Research (ONR) Prize for Affordability, Aug. 26, at an award ceremony held at ONR in Alexandria, Va. The award honors materials research engineers James Martin, head of the Marine Coatings Science Section, Jimmy Tagert, and John Wegand; research chemist, Dr. Erick Iezzi; and physical scientist technician, Paul Slebodnick for significant contributions to an overall reduction in the total ownership costs associated with corrosion control of Navy ships and submarines and achievements in the development and transition of nonskid and topside coatings to the fleet. The team formulated, synthesized, and commercialized topside and nonskid coatings having longer life, high durability, improved weathering resistance and color stability, to replace both legacy nonskid decking and topside coatings. The Navy installs nearly 3.7 million square feet of non-skid coatings per year that typically cost over $56 million annually. Conventional epoxy based nonskids have a 12 to 36 month lifecycle, while topside coatings have a 24 to 36 month life. The new NRL-developed polysiloxane system doubles or triples the life expectancy of this system. For topside coatings, not only are lifetimes increased, but also installation costs are reduced by up to 28 percent through the reduced number of coats over conventional systems. As a result, polysiloxane coatings systems have been qualified and approved for use by Naval Sea Systems Command (NAVSEA) and have been mandated for all topside depot level maintenance availabilities. The NRL polysiloxane nonskid decking system is planned for qualification in 2015. At present, the nonskid coatings system has exceeded the one-year flight deck requirement on-board the USS Theodore Roosevelt (CVN 71), has outperformed all previous nonskids on-board the USS Michigan (SSGN 727), and is still performing well on-board the USS Bulkeley (DDG 84). On Navy submarines, this system is the only system ever to pass the submarine nonskid requirements. The Center for Corrosion Science and Engineering (CCSE) conducts broad scientific and engineering programs to understand and reduce the effects of the marine environment on naval systems. Within the CCSE, the Marine Coatings Science Section conducts basic and applied research to synthesize and produce advanced, multi-functional marine coatings technology for all naval environments including immersion, alternate immersion and atmospheric exposures typical of Navy and Marine Corps platforms. About the U.S. Naval Research Laboratory The U.S. Naval Research Laboratory provides the advanced scientific capabilities required to bolster our country's position of global naval leadership. The Laboratory, with a total complement of approximately 2,500 personnel, is located in southwest Washington, D.C., with other major sites at the Stennis Space Center, Miss., and Monterey, Calif. NRL has served the Navy and the nation for over 90 years and continues to advance research further than you can imagine. For more information, visit the NRL website or join the conversation on Twitter, Facebook, and YouTube.
News Article | November 15, 2016
NEW ORLEANS, Nov. 15, 2016 -- Repeatedly losing and regaining weight, known as weight cycling or yo-yo dieting, may increase the risk of death from heart disease among postmenopausal women who were of normal weight at the start of the study, according to research presented at the American Heart Association's Scientific Sessions 2016. "Weight cycling is an emerging global health concern associated with attempts of weight loss, but there have been inconsistent results about the health hazards for those who experience weight cycling behavior," said Somwail Rasla, M.D., study lead author and internal medicine resident at Memorial Hospital of Rhode Island, Alpert Medical School, Brown University, in Providence, Rhode Island. Researchers classified self-reported weight history from 158,063 post-menopausal women into four categories: stable weight, steady gain, maintained weight loss, and weight cycling. During a follow-up of 11.4 years, they found: Evidence indicates that being overweight in midlife increases the risk of dying from two types of heart disease. In the first type, coronary heart disease, the blood vessels to the heart become blocked by fat and other substances, decreasing blood flow to the heart. In the second type, sudden cardiac death, the heart's electrical system abruptly stops working, causing death. It is unclear whether losing and regaining weight in adulthood also increases the risk of death from these heart diseases, so the investigators looked at this relationship among postmenopausal women. The study has several limitations. First, the study was observational, therefore it could only show association and not a cause and effect relationship. In addition, the study relied on self-reports, which could be inaccurate. Since sudden cardiac death occurred relatively infrequently, the cases that did occur could have resulted from chance. Finally, the study included only older women. "More research is needed before any recommendations can be made for clinical care regarding the risks of weight cycling, since these results apply only to postmenopausal women and not to younger-aged women or men," Rasla said. In the United States and worldwide, heart disease is the leading cause of death. Obesity is a major risk factor, along with high blood pressure and cholesterol, diabetes, physical inactivity, poor diet, and smoking. One way to lower your risk factors is by following the American Heart Association's Life's Simple 7 program, which recommends: (1) manage blood pressure; (2) control cholesterol; (3) reduce blood sugar; (4) get active; (5) eat better; (6) maintain normal weight; and (7) stop smoking. Co-authors are Marina Garas, D.O.; Mary B. Roberts, M.S.; Molly E. Waring, Ph.D.; Christine M. Albert, M.D., M.P.H.; Deepika Laddu, Ph.D.; Marcia L Stefanick, Ph.D.; David K. Garas, M.B.A.; and Charles B. Eaton, M.D., M.S. Author disclosures are on the abstract. This study is funded by the National Heart Lung and Blood Institute. Note: Scientific presentation time is 10:45 a.m. CT, Tuesday, Nov. 15 in the Science and Technology Hall, Population Science Section. Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www. .
News Article | November 13, 2016
NEW ORLEANS, Nov. 13, 2016 -- More than a third of advanced heart failure patients treated with a combination of an artificial heart assist device, called a left ventricular assist device, or LVAD, and intensive drug therapy have recovered their heart function enough to allow removal of the LVAD device, according to preliminary results of an ongoing study presented at the American Heart Association's Scientific Sessions 2016. The multicenter trial called RESTAGE, includes 40 patients (67.5 percent men, average age 34.9 years) at six different centers, with very advanced or end stage heart failure. Within the first 209 days, three patients did not survive long enough to get the therapy and one had the device removed. The remaining 36 patients were implanted with an LVAD (HeartMate II) and prescribed an aggressive combination of drugs (Lisinopril 40 mg, spironolactone 25 mg, digoxin 125 mic and losartan 150 mg daily and coreg 25 mg bid). All of the patients were so disabled from heart failure that the initial intent with the LVAD was to use it until they could receive a heart transplant or to leave the device in for the rest of their lives. "This suggests that even very advanced heart failure can be reversed using these heart pumps, particularly when combined with additional drug therapy, avoiding the need for heart transplantation for these patients and making the donor heart available for another needy individual," said Emma J. Birks, M.D., lead author of the study and professor of medicine at the University of Louisville in Louisville, Kentucky. Researchers tested the 36 patients' heart function to determine if any had improved heart function enough from the therapy to have the pumps removed, or if their heart function remained poor and needed a heart transplant or to remain on the pump. "The fact that this could be done in several centers suggests that using the device with this drug combination to reverse heart failure is possible on a larger scale. It has previously been thought that these devices rarely recover heart function enough to allow them to be removed, but this study suggests that this can occur in a much bigger number than originally thought, particularly if combined with drug therapy," Birks said. Co-authors are Eduardo Rame, M.D.; Snehal R Patel, M.D.; Craig Selzman, M.D.; Chris Cunningham, Ph.D.; Randall Starling, M.D., M.P.H.; John Um, M.D.; Daniel Goldstein, M.D.; Mark Slaughter, M.D.; Pavan Alturi, M.D.; Daniel Spevack, M.D.; David Farrar, Ph.D.; Brian D. Lowes, M.D.; and Stavros G. Drakos, M.D., Ph.D. Author disclosures are on the abstract. This study is funded by St Jude Medical. Note: Actual scientific presentation time is 2 p.m. CT, Sunday, Nov.13, 2016 in the Science and Technology Hall, Clinical Science Section. Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www. .
Ellis M.V.,Science Section
Australian Zoologist | Year: 2016
Nest boxes have been widely used across the world to provide shelter for animal species, often to restore areas following the loss of natural tree hollows. While the microclimates of installed nest boxes have been studied, limited attention has been paid to whether microclimate is influenced by nest box size, shape and entrance dimensions. In this study the temperature and humidity patterns were recorded within six nest box designs that were exposed to direct sunshine.AII were constructed of 19 mm plywood but varied in length by a factor of 2X, in volume by 3.5X and in entrance areas by 5X. All next boxes behaved the same thermally, closely following ambient during the night, but during the day they heated to 5 °C warmer than ambient by mid-afternoon. Fluctuations in humidity varied, with small nest boxes with large entrances being closer to ambient humidity than those with small entrances or large volumes. Overall, nest box size and shape had no detectable influence on the internal temperature fluctuations, but did to a slight extent on humidity patterns. Construction material and nest box placement are the likely drivers of the temperature and humidity patterns within nest boxes, and need to be the focus of efforts to keep nest boxes habitable when deployed, and designs should be selected on the basis of the target animal's preferences for size and shape.