News Article | May 14, 2016
In an attempt to understand the riddles of science, the White House will now begin a National Microbiome Initiative, a program that aims to unify all microbe culture research. In October 2015, more than 40 scientists from different scientific backgrounds came together and proposed the creation of a Unified Microbiome Initiative Consortium (UMIC). The initiative would bring together cutting-edge research and discoveries that would benefit health care, the environment and even create renewable energy. "Microbes are everywhere," said Pamela Silver, a Harvard's Wyss Institute for Biologically Inspired Engineering researcher. "Therefore understanding microbiomes, whther they be the ones that live in and on our bodies or the ones in the environment, is essential to understanding life." The White House announced the initiative on May 13 to jumpstart microbe research that would encompass all those that are found in animals, air, plants, soil and water. The government is hoping that gaining more information would give insight into how to fight disease, increase food production, and fight climate change. The National Microbiome Initiative (PDF) will work with other organizations interested in the research, including University of Michigan and Juvenile Diabetes Research Foundation (JDRF), One Codex, The BioCollective, the University of California, and Bill and Melinda Gates Foundation. The program will have a total of $521 million in funding, with $121 million from the federal government and $400 million funding from private organizations. While most people think that bacteria cause decay and death, there exists a huge trove of good microbes that are essential to human existence. White House Office of Science and Technology associate director for science Jo Handelsman explained that life on land became possible because ancient ocean-dwelling microbes released oxygen into the atmosphere. Handelsman explained that humans need bacteria to survive. "We wouldn't be here without these bacteria," said Handelsman. "Our health, our behavior and even our longevity are all affected by these bacteria." Alterations in human microbiomes cause diseases, including allergies, asthma, autism, diabetes, and even obesity, said Microbiology Professor Martin Blaser, who also serves as director of the New York University Langone Medical Center's Human Microbiome Program. When people take antibiotics to cure diseases, good bacteria is also eliminated along with the bad bacteria. Scientists still need to learn from these microbiomes. A Tech Times' report has stated about 99.999 percent of the 1 trillion microbial species in the world are yet to be discovered. With the program, the scientists are hoping to map the microbes, alter them, and identify how it can help address some of the maladies that affect human existence. Some experts believe that understanding microbiomes could also help solve crimes. Forensic scientists can use the microbial trail left by people as they go to places, much like how detectives solve crime using DNA and fingerprints left behind by criminals. © 2017 Tech Times, All rights reserved. Do not reproduce without permission.
News Article | November 7, 2016
Certain proteins in the blood of children can predict incipient type 1 diabetes, even before the first symptoms appear. A team of scientists at the Helmholtz Zentrum München, partners in the German Center for Diabetes Research (DZD), reported these findings in the Diabetologia journal. The work was based on two large studies that are intended to explain the mechanisms behind the development of type 1 diabetes (BABYDIAB and BABYDIET*). The study participants are children who have a first-degree relative with type 1 diabetes and who consequently have an increased risk of developing the disease due to the familial predisposition. This autoimmune process does not develop from one day to the next, however: Often the young patients go through longer asymptomatic preliminary stages that see the formation of the first antibodies against the child's own insulin-producing cells in the pancreas; these are the so-called autoantibodies. Biomarkers that indicate whether and when this is the case and how quickly the clinical symptoms will appear could significantly improve the treatment of patients at-risk. A team of scientists, led by Dr. Stefanie Hauck, head of the Research Unit Protein Science and the Core Facility Proteomics, and Prof. Dr. Anette-G. Ziegler, Director of the Institute of Diabetes Research (IDF) at the Helmholtz Zentrum München, analyzed blood samples from 30 children with autoantibodies who had developed type 1 diabetes either very rapidly or with a very long delay. The researchers compared the data with data on children who displayed neither autoantibodies nor diabetes symptoms. In a second step with samples from another 140 children, the researchers confirmed the protein composition differences that they found in this approach. "Altogether, we were able to identify 41 peptides** from 26 proteins that distinguish children with autoantibodies from those without," reports Dr. Christine von Toerne, a scientist in the Research Unit Protein Science who shared first authorship of the work with Michael Laimighofer, a doctoral candidate in Jan Krumsiek's junior research group at the Institute of Computational Biology. Striking in their evaluations: A large number of these proteins are associated with lipid metabolism. "Two peptides -- from the proteins apolipoprotein M and apolipoprotein C-IV -- were particularly conspicuous and were especially differently expressed in the two groups," von Toerne adds. In autoantibody-positive children, it was furthermore possible to reach a better estimate of the speed of the diabetes development using the peptide concentrations of three proteins (hepatocyte growth factor activator, complement factor H and ceruloplasmin) in combination with the age of the particular child. The researchers are confident that the protein signatures they have discovered will be helpful as biomarkers for future diagnostics. "The progression of type 1 diabetes into a clinical disease takes place over a period of time that varies from individual to individual and that at this time is insufficiently predictable," explains Prof. Ziegler. "The biomarkers that we have identified allow a more precise classification of this presymptomatic stage and they are relatively simple to acquire from blood samples." * The BABYDIAB study, which was established in 1989 as the world's first diabetes prospective birth cohort, is a pioneering study in the field of type 1 diabetes pathogenesis research. More than 1650 children of parents with type 1 diabetes have been observed since their birth, or for a period of 25 years. The objective of the BABYDIAB study is to determine when islet autoantibodies first appear, which genetic factors and environmental factors influence their development, and which characteristics of the autoantibodies are most strongly associated with the development of type 1 diabetes. The participants in the study are reexamined every three years by means of blood samples and questionnaires. The BABYDIET is examining the influence of food containing gluten on the development of type 1 diabetes. Of the 2,441 children included in the two studies, so far 124 have developed a precursor to diabetes. 82 of these meanwhile display a clinical disease (as of November 2014). ** Peptides are molecules that, like proteins, are constructed from amino acids. However, they are smaller and to some extent result as fragments during protein breakdown. The transition is therefore relatively fluid. The study was financed by the Juvenile Diabetes Research Foundation (JDRF), which has headquarters in the USA. The number of new cases of type 1 diabetes each year continues to rise. New immunotherapeutic approaches aim at stopping this development. A precise assessment of the individual stage of disease development is an important criterion for the targeted use of new treatments. The described study shows that children already display proteomic changes in the blood during the presymptomatic stage. This information allows a better assessment of the time until clinical manifestation of the disease. Recently scientists in the Protein Science Research Unit were also able to identify biomarkers for the precursor to type 2 diabetes: https:/ Von Toerne, C. & Laimighofer, M. et al. (2016): Peptide serum markers in islet autoantibody-positive children. Diabetologia, doi: 10.1007/s00125-016-4150-x http://link. The presence of certain proteins in blood samples can predict incipient type 1 diabetes. The researchers identify these in their measurements using so-called peptide peaks (see selection in red). Source: Helmholtz Zentrum München The Helmholtz Zentrum München, the German Research Center for Environmental Health, pursues the goal of developing personalized medical approaches for the prevention and therapy of major common diseases such as diabetes and lung diseases. To achieve this, it investigates the interaction of genetics, environmental factors and lifestyle. The Helmholtz Zentrum München is headquartered in Neuherberg in the north of Munich and has about 2,300 staff members. It is a member of the Helmholtz Association, a community of 18 scientific-technical and medical-biological research centers with a total of about 37,000 staff members. http://www. The independent Research Unit Protein Science (PROT) investigates the composition of protein complexes and their integration into cellular processes and protein networks. One focus is the analysis of the interaction of genetic variance and environmental factors in neurodegenerative and metabolic diseases. The aim of this research is to identify biological systems and disease-associated disorders on a systemic level, thus contributing to a molecular understanding of diseases. http://www. The Core Facility Proteomics is an instrumental analysis platform at the Helmholtz Zentrum München. It provides interested research groups with access to comprehensive proteome analyses conducted with highly sensitive mass spectrometers. The portfolio ranges from technical and scientific consultation during project design and sample preparation to the development of optimized analysis methods to actual sample measurement and data evaluation. The Institute of Diabetes Research (IDF) focuses on the pathogenesis and prevention of type 1 diabetes and type 2 diabetes and the long-term effects of gestational diabetes. A major project is the development of an insulin vaccination against type 1 diabetes. The IDF conducts long-term studies to examine the link between genes, environmental factors and the immune system for the pathogenesis of type 1 diabetes. Findings of the BABYDIAB study, which was established in 1989 as the world's first prospective birth cohort study, identified risk genes and antibody profiles. These permit predictions to be made about the pathogenesis and onset of type 1 diabetes and will lead to changes in the classification and the time of diagnosis. The IDF is part of the Helmholtz Diabetes Center (HDC). http://www. The German Center for Diabetes Research (DZD) is a national association that brings together experts in the field of diabetes research and combines basic research, translational research, epidemiology and clinical applications. The aim is to develop novel strategies for personalized prevention and treatment of diabetes. Members are Helmholtz Zentrum München - German Research Center for Environmental Health, the German Diabetes Center in Düsseldorf, the German Institute of Human Nutrition in Potsdam-Rehbrücke, the Paul Langerhans Institute Dresden of the Helmholtz Zentrum München at the University Medical Center Carl Gustav Carus of the TU Dresden and the Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Zentrum München at the Eberhard-Karls-University of Tuebingen together with associated partners at the Universities in Heidelberg, Cologne, Leipzig, Lübeck and Munich. https:/
News Article | November 15, 2016
INDIANAPOLIS, IN--(Marketwired - November 15, 2016) - USA Funds® announces the election of Edward R. Schmidt as chairman of its board of trustees, for a three-year term beginning Jan. 1, 2017. Schmidt has served on the USA Funds board for nearly 20 years. He is a member of the board's compensation committee and serves as chair of its governance committee. "I look forward to working with my fellow trustees and USA Funds' management to help more students finish what they start when they enroll in postsecondary education programs and to ensure they are ready to launch into rewarding careers," Schmidt said. Schmidt is president & CEO of Silver Creek Partners LLC, based in suburban Indianapolis. He is a retired partner of the Indianapolis-based law firm Krieg, DeVault LLP and the former executive vice president, general counsel and corporate secretary of USA Group Inc. Schmidt received a bachelor's degree from Susquehanna University, where he serves as vice chair of the board of trustees. He received his law degree from the University of Notre Dame, where he serves as a member of the Law School Advisory Council. Schmidt is a member of the American, Indiana and Indianapolis Bar Associations. In addition to serving on the board of trustees of Susquehanna University, he also serves on the boards of Indiana Hemophilia & Thrombosis Center, HCEI Inc., as well as the board of chancellors of the Indiana State Chapter of JDRF (the Juvenile Diabetes Research Foundation). He was a founding board member of the Lumina Foundation for Education board, serving from 2000 to 2009. Schmidt will succeed Ike G. Batalis, who is completing his three-year term as chairman of the USA Funds board. Batalis will continue to serve on the USA Funds board. USA Funds is a nonprofit organization that supports Completion With a Purpose®, building a more purposeful path for America's students to and through college and on to rewarding careers and successful lives. USA Funds pursues its nonprofit mission through philanthropic activities and partnerships, policy research, and programs and services that enhance preparation for, access to and success in higher education. Learn more at www.usafunds.org.
News Article | February 15, 2017
Sonny Stancarone, CEO of Sonny's Luxury Art Case Pianos, a premiere Long Island restoration house for pre-owned art case Steinways and other brand name pianos, is pledging to donate $100,000, or 10 percent of the final price of a million-dollar Steinway he has offered for sale, to the Juvenile Diabetes Research Foundation Long Island Chapter to help in its quest to find a cure for juvenile diabetes. “I hope by doing this it will bring attention to the importance of finding a cure for this devastating illness, and the money we raise will help families cope with this condition and improve the quality of their lives,“ said Stancarone, a longtime piano entrepreneur and piano dealer. “Millions of people around the world live with type 1 diabetes, a life-threatening autoimmune disease that strikes both children and adults. There is no way to prevent it, and at present, no cure. JDRF works every day to change this by amassing grassroots support, deep scientific knowledge and strong industry and academic partnerships to fund research. Sonny’s contribution will go a long way to supporting our efforts,” said Joann Flick, director of development at JDRF Long Island Chapter. The million-dollar Steinway, known as the “Prince’s Love Piano,” was purchased by a Prussian prince in 1900 from the Steinway Hamburg, Germany, factory. The prince commissioned a master artist to create a series of King Louis XV “Vernis Martin” style love scenes on the piano to immortalize his love for his princess. The piano itself is a Hamburg Steinway Model A – one of the finest instruments money could buy then and now. The piano is part of Sonny’s luxury art case pianos collection and was purchased and restored by Sonny's Art Case Pianos over the past year. See photos and video tour of this piano here http://tinyurl.com/zvkpgct. Stancarone chose the JDRF for his donation, he said, because “the public is generally not aware of what a difficult illness type 1 diabetes is to manage with its daily regimen of blood sugar level monitoring, insulin injections or insulin pump adjustments, exacting dietary restrictions and meal scheduling, all of which even when performed perfectly can still result in catastrophe when sugar levels go too low or too high. Swings in blood sugar levels can cause mood changes, inability to concentrate, urgent cravings for sugary foods and can be debilitating – even fatal.” In particular, Stancarone believes families with young children and infants who have juvenile diabetes struggle because children cannot always communicate what they are experiencing, leaving parents not knowing when to make any necessary adjustments to help their child function normally. “I'd like to encourage others to donate to this important cause at http://www.jdrf.org,” he added. “Even small donations are greatly appreciated and can go a long way.” About Sonny’s Pianos Sonny’s Luxury Art Case Pianos, located in Bohemia, Long Island in New York, is one of the premiere restoration houses for pre-owned decorative art case Steinways and other brand name pianos. Sonny buys and restores luxury and traditional-style pre-owned Steinways and other pianos, selling them to discriminating clients in a worldwide market. Sonny’s team of furniture specialists, piano technicians and artists return the sound and appearance of these majestic instruments to their original elegant and beautiful condition. Sonny is donating 10% of the final sale price of the Million Dollar Steinway and another hand painted masterpiece in his collection called the “Green Chi Steinway,“ priced at $125,000, to the Juvenile Diabetes Research Foundation (JDRF) Long Island Chapter, that funds research for treatments and therapies for Type 1 Diabetes. To learn more, visit Sonny’s Bohemia, Long Island showroom or view videos and photos of his inventory at http://www.SonnysPianoTV.com/artcase. Private showings of Sonny’s Luxury Art Case Pianos are available by appointment only, by calling 631-475-8046. See recent Newsday Feature Video about Sonny's Art Case Pianos https://youtu.be/qfLHEKkRt28 To read the article click here http://sonnyspianotv.com/pdf/Newsday.pdf or on the Newsday PDF attachment. About JDRF JDRF is the leading global charitable, non-profit organization funding type 1 diabetes (T1D) research. Its 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 in research funding since its inception. It is an organization built on a grassroots model of people connecting in their local communities, collaborating regionally for efficiency and broader fundraising impact, and uniting on a national stage to pool resources, passion, and energy. It collaborates with academic institutions, policymakers, and corporate and industry partners to develop and deliver a pipeline of innovative therapies to people living with T1D. Its staff and volunteers throughout the United States and its six international affiliates are dedicated to advocacy, community engagement and its vision of a world without T1D. For more information, please visit jdrf.org or follow it on Twitter: @JDRF.
News Article | February 16, 2017
Alpha cells in the pancreas can be induced in living mice to quickly and efficiently become insulin-producing beta cells when the expression of just two genes is blocked, according to a study led by researchers at the Stanford University School of Medicine. Studies of human pancreases from diabetic cadaver donors suggest that the alpha cells' "career change" also occurs naturally in diabetic humans, but on a much smaller and slower scale. The research suggests that scientists may one day be able to take advantage of this natural flexibility in cell fate to coax alpha cells to convert to beta cells in humans to alleviate the symptoms of diabetes. "It is important to carefully evaluate any and all potential sources of new beta cells for people with diabetes," said Seung Kim, MD, PhD, professor of developmental biology and of medicine. "Now we've discovered what keeps an alpha cell as an alpha cell, and found a way to efficiently convert them in living animals into cells that are nearly indistinguishable from beta cells. It's very exciting." Kim is the senior author of the study, which will be published online Feb. 16 in Cell Metabolism. Postdoctoral scholar Harini Chakravarthy, PhD, is the lead author. "Transdifferentiation of alpha cells into insulin-producing beta cells is a very attractive therapeutic approach for restoring beta cell function in established Type 1 diabetes," said Andrew Rakeman, PhD, the director of discovery research at JDRF, an organization that funds research into Type 1 diabetes. "By identifying the pathways regulating alpha to beta cell conversion and showing that these same mechanisms are active in human islets from patients with Type 1 diabetes, Chakravarthy and her colleagues have made an important step toward realizing the therapeutic potential of alpha cell transdifferentiation." Rakeman was not involved in the study. Cells in the pancreas called beta cells and alpha cells are responsible for modulating the body's response to the rise and fall of blood glucose levels after a meal. When glucose levels rise, beta cells release insulin to cue cells throughout the body to squirrel away the sugar for later use. When levels fall, alpha cells release glucagon to stimulate the release of stored glucose. Although both Type 1 and Type 2 diabetes are primarily linked to reductions in the number of insulin-producing beta cells, there are signs that alpha cells may also be dysfunctional in these disorders. "In some cases, alpha cells may actually be secreting too much glucagon," said Kim. "When there is already not enough insulin, excess glucagon is like adding gas to a fire." Because humans have a large reservoir of alpha cells, and because the alpha cells sometimes secrete too much glucagon, converting some alpha cells to beta cells should be well-tolerated, the researchers believe. The researchers built on a previous study in mice several years ago that was conducted in a Swiss laboratory, which also collaborated on the current study. It showed that when beta cells are destroyed, about 1 percent of alpha cells in the pancreas begin to look and act like beta cells. But this happened very slowly. "What was lacking in that initial index study was any sort of understanding of the mechanism of this conversion," said Kim. "But we had some ideas based on our own work as to what the master regulators might be." Chakravarthy and her colleagues targeted two main candidates: a protein called Arx known to be important during the development of alpha cells and another called DNMT1 that may help alpha cells "remember" how to be alpha cells by maintaining chemical tags on its DNA. The researchers painstakingly generated a strain of laboratory mice unable to make either Arx or DNMT1 in pancreatic alpha cells when the animals were administered a certain chemical compound in their drinking water. They observed a rapid conversion of alpha cells into what appeared to be beta cells in the mice within seven weeks of blocking the production of both these proteins. To confirm the change, the researchers collaborated with colleagues in the laboratory of Stephen Quake, PhD, a co-author and professor of bioengineering and of applied physics at Stanford, to study the gene expression patterns of the former alpha cells. They also shipped the cells to collaborators in Alberta, Canada, and at the University of Illinois to test the electrophysiological characteristics of the cells and whether and how they responded to glucose. "Through these rigorous studies by our colleagues and collaborators, we found that these former alpha cells were -- in every way -- remarkably similar to native beta cells," said Kim. The researchers then turned their attention to human pancreatic tissue from diabetic and nondiabetic cadaver donors. They found that samples of tissue from children with Type 1 diabetes diagnosed within a year or two of their death include a proportion of bi-hormonal cells -- individual cells that produce both glucagon and insulin. Kim and his colleagues believe they may have caught the cells in the act of converting from alpha cells to beta cells in response to the development of diabetes. They also saw that the human alpha cell samples from the diabetic donors had lost the expression of the very genes -- ARX and DNMT1 -- they had blocked in the mice to convert alpha cells into beta cells. "So the same basic changes may be happening in humans with Type 1 diabetes," said Kim. "This indicates that it might be possible to use targeted methods to block these genes or the signals controlling them in the pancreatic islets of people with diabetes to enhance the proportion of alpha cells that convert into beta cells." Kim is a member of Stanford Bio-X, the Stanford Cardiovascular Institute, the Stanford Cancer Institute and the Stanford Child Health Research Institute. Researchers from the University of Alberta, the University of Illinois, the University of Geneva and the University of Bergen are also co-authors of the study. The research was supported by the National Institutes of Health (grants U01HL099999, U01HL099995, UO1DK089532, UO1DK089572 and UC4DK104211), the California Institute for Regenerative Medicine, the Juvenile Diabetes Research Foundation, the Center of Excellence for Stem Cell Genomics, the Wallenberg Foundation, the Swiss National Science Foundation, the NIH Beta-Cell Biology Consortium, the European Union, the Howard Hughes Medical Institute, the H.L. Snyder Foundation, the Elser Trust and the NIH Human Islet Resource Network. Stanford's Department of Developmental Biology also supported the work. The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://med. . The medical school is part of Stanford Medicine, which includes Stanford Health Care and Stanford Children's Health. For information about all three, please visit http://med. .
News Article | December 7, 2016
Douglas Melton allowed himself a brief moment of celebration. After 23 years of trying, he had finally managed to grow tissue in the laboratory that could replace the cell clusters, or islets, in the pancreas that are destroyed by type 1 diabetes (T1D) — the autoimmune disease that affects two of his children. Melton, co-director of the Harvard Stem Cell Institute in Cambridge, Massachusetts, had transformed embryonic stem cells into the specialized β-cells found in islets that sense glucose and secrete insulin to help to control blood sugar1. The ramifications were huge. The ability to produce a potentially limitless supply of β-cells meant that people with T1D would no longer need to receive islet transplants from deceased donors — an option that can help only a few hundred patients per year because of the dearth of donor organs. Most of the millions of adults and children living with T1D have to monitor their glucose levels continually and inject themselves with insulin every day. But after throwing a party for his lab group — at which Melton gave everyone blue winter hats emblazoned with his signature 'Skittle diagram', a schematic of colourful circles showing the developmental progression from stem cell to β-cell — reality set in. Even though he could now grow millions of β-cells in a single flask, an achievement for which he would be recognized with the 2016 Ogawa-Yamanaka Stem Cell Prize, Melton now faced a new challenge: how to protect implanted cells from the autoimmune attack that had destroyed the original cells. “Suddenly that problem loomed very large,” says Melton, “because now it was the problem. To prevent rejection of the islets — both because the cells come from unrelated donors and because of the recipients' islet-directed autoimmunity — patients have to take life-long courses of immune-suppressing drugs. But these medicines come with serious side effects, including increased risk of infection and cancer. Melton wanted to avoid these agents, which meant he needed some sort of device or material that would shield implanted β-cells — lab-grown or donor — from the immune system, while allowing nutrients such as glucose, insulin and oxygen into and out of these cells. “The dream is to be able to build some kind of immuno-isolation device that will allow people to get the benefit of the cells without having to suppress their immune system,” explains one of Melton's collaborators, Daniel Anderson, a bioengineer at the Massachusetts Institute of Technology (MIT) in Cambridge. That dream has eluded academics, entrepreneurs and big pharmaceutical companies for more than 40 years. Thanks to the new-found ability to make β-cells from scratch, however, researchers now have a consistent and reliable cell source. This means that they can methodically compare different encapsulation systems side by side, rather than tinkering through trial and error with whatever leftover β-cells they could get their hands on — the “dregs of material”, as Melton puts it. And this rational engineering approach is leading to improvements in the design of both large and small cell-safeguarding techniques. Some companies, including the regenerative-medicine heavyweight ViaCyte, based in San Diego, California, are loading thousands of β-cells into macroencapsulation devices that are as big as the palm of your hand. Others, like the start-up Sigilon, based in Cambridge, Massachusetts, are parcelling up individual bundles of β-cells into microscopic shells smaller than a mustard seed. With both strategies, “we're at this inflection point” where success is within reach, says Julia Greenstein, vice-president of discovery research at JDRF in New York City, a non-profit formerly known as the Juvenile Diabetes Research Foundation. “We've seen a much more scientifically directed approach to the problem than ever before.” For many years, the most popular capsule material for transplanted β-cells has been a seaweed extract called alginate. It's been tested in rodents, dogs, monkeys and even humans in a few pilot clinical studies. The human trials showed that the material was safe, even in people who were not taking immunosuppressant drugs. But the therapeutic benefit was marginal because, within weeks of implantation, the alginate would usually begin to attract immune cells such as macrophages and neutrophils. This led to the deposition of fibrotic scar tissue that gummed up the capsules, choking off the cells inside. This type of immune reaction was different from the one that originally destroyed the patients' β-cells, but it was equally damaging to the prospects of this therapeutic approach. Seeking a derivative of alginate that could evade immune detection altogether, Anderson teamed up with his MIT colleague Robert Langer. The researchers systematically screened close to 800 chemical offshoots of alginate in mice. They found one variety — triazole–thiomorpholine dioxide alginate — that seemed to go completely unnoticed by the immune system2. Tiny spheres of this super-alginate survived for up to six months when implanted in macaques. And, when loaded with Melton's stem-cell-derived β-cells, the capsules could restore typical levels of blood sugar in a mouse model of T1D, with no signs of an immune reaction3. “We demonstrated, for the first time, a material that remains fibrosis-free when implanted in the body,” says Omid Veiseh, a biomaterials researcher who worked on the project as a postdoc at MIT. “There hasn't been anything like this.” Veiseh will start his own lab in 2017 at Rice University in Houston, Texas. But until then, he is sticking around in Cambridge to help get Sigilon off the ground. Named after the Spanish word for stealth, Sigilon launched this year with US$37.5 million in funding to commercialize the new alginate for a variety of biomedical applications. These include two potential ways to treat T1D. One is microencapsulated cell therapy. By 2018, Sigilon intends to show that this technology works in people using donor islets, and it is looking to partner with cell-therapy companies about then testing a stem-cell-derived β-cell enveloped in its alginate. The second approach is to use the material to coat parts of bionic pancreas systems that enter the body (see 'Bionic versus beta'). “One way or another,” says Sigilon president and chief executive Paul Wotton, patients with T1D will “benefit from this platform.” In the microencapsulation field, size matters. In tests with the super-alginate, the MIT team used capsules with a diameter of 1.5 millimetres, which it has demonstrated are much less immunogenic than the 0.5-mm capsules that researchers in the diabetes cell-therapy field have conventionally used4. But a tripling of the diameter means a nearly 30-fold increase in the volume of each capsule. And given the large number of capsules required to contain the hundreds of millions of β-cells needed to control a person's diabetes, there are few places in the body where the therapy could be implanted. The capsules probably won't fit under the skin or in another easily retrievable location — and regulatory agencies have insisted, as a safety measure, that any stem-cell-derived diabetes therapy implanted in patients should be fully recoverable. That's why Alice Tomei, a bioengineer at the University of Miami in Florida, has developed what she calls a “shrink-wrapping technology”, which uses microfluidics to apply a thin biocompatible coating to clusters of cells to make the smallest possible capsule — one that's only about 0.2 mm across5. Her material of choice, polyethylene glycol, may be more immune-reactive than Sigilon's super-alginate, but Tomei argues that her thinly wrapped cells will be small enough to implant in more accessible spots in the body. Tomei is evaluating her technology using Melton's stem-cell-derived β-cells, in collaboration with start-up Semma Therapeutics in Cambridge, Massachusetts. Melton launched Semma in 2015 with the biotech investor and entrepreneur Robert Millman. (Millman's wife came up with the name: a combination of Sam and Emma, the names of Melton's two diabetic children.) Although Semma has its own encapsulation technology through the acquisition of drug-delivery-technology company Cytosolv, it is also looking for partners such as Tomei to test a range of encapsulation systems with the company's stem cells. “Anyone who's got a device, we'll work with them,” says Millman, Semma's chief executive, “because even with the best cells, if we don't have the right device it'll fail.” Another of Semma's collaborators is Beta-O Technologies, a company based in Rosh-Haayin, Israel, that has been working on encapsulated cell therapies for T1D for more than a decade. As the name suggests, Beta-O was created to develop a way of delivering oxygen to implanted cells — a problem that's especially acute with larger macroencapsulation devices, which impose a larger barrier than capsule technologies between the blood supply that carries the oxygen and the energetically hungry β-cells. The company's initial prototype was a chamber about the size of a hockey puck that is implanted under the skin and requires daily injections with oxygen. As proof of principle, Beta-O tested this device by loading it with donor islets and implanting it in five patients in Germany6 and Sweden. The results were encouraging: the cells remained alive and healthy for months. Beta-O is working on its second-generation device, which, according to chief executive Yuval Avni, will be able to hold more cells and require oxygen injections only once a week. But the company needs a more reliable cell source, and Avni has high hopes for Melton's cells. Melton's original recipe for making β-cells was cumbersome. It took 35 days of carefully swapping 5 different growth media and mixing in 11 different factors, including sugars and proteins. According to Felicia Pagliuca, a former postdoc in Melton's lab who now leads cell-biology research and development at Semma, she and her team have dramatically streamlined the protocol. “We are leaps and bounds further from where we were,” she says. And they have a strategy for getting the cells into clinical trials, even before an encapsulation device is ready. The plan is to make β-cells from induced pluripotent stem cells created from people who need insulin, but whose bodies don't attack their own cells, which happens in people with T1D. Since there would be no tissue mismatch or chance of autoimmune reaction, those cells could then be implanted back into the patients without any immune-suppressing drugs or barrier technologies. Semma is focused on three patient populations, none of which have autoimmunity: people with a form of type 2 diabetes called lean diabetes, in which β-cells have stopped working; individuals who have had their pancreases surgically removed because of problems such as chronic inflammation; and patients with an insulin-dependent form of cystic fibrosis. The company hopes to test its cells in one of these populations in three to four years; trials with any sort of encapsulated device for people with T1D will follow at a later point. But this means that Semma might be playing catch-up with its competitor ViaCyte. Earlier this year, the firm absorbed one of its chief rivals, a division of Johnson & Johnson called BetaLogics, while also announcing promising early data from the first human trial of an encapsulated stem-cell-derived product for T1D. ViaCyte's PEC-EnCap device is made up of a semi-permeable pouch, about the size of a sticking plaster, that contains thousands of pancreatic precursor cells, each derived from embryonic stem cells. The company uses precursor cells, rather than fully mature β-cells, because these cells are hardier under the low-oxygen conditions that follow implantation, when the packets haven't yet integrated with the blood system. Over the past 2 years, ViaCyte has implanted its devices under the skin of about 20 patients without immunosuppression. In many recipients, the pancreatic precursors have grown into insulin-producing β-cells — although these cells often die after a few months, owing to a fibrotic immune reaction on the device exterior. “That's a proof of feasibility that this is achievable, but we still have a lot of work to do,” says ViaCyte's chief executive, Paul Laikind. “The goal now is to reduce or delay that foreign-body response long enough for the cells to engraft.” ViaCyte hopes to achieve this by modifying either the encapsulation device or some other aspect of the treatment protocol before it moves into the next phase of testing with a full therapeutic doses of its product. By then, perhaps, Melton's β-cells could also be ready for testing in patients with T1D. Melton is confident that with the right delivery system, these cells can cure his children's illness. “It just makes sense to me,” Melton says, “that if you can make the cell that's missing in a person we ought to be able to find a way to put that cell back into people.”
News Article | November 30, 2016
Fit4D, a New York City-based health technology company, announced today that former Prudential Healthcare President, Sam Havens, and Susan Duffy, former McCann Healthcare President, have joined its Board of Strategic Advisors. Both Sam and Susan will advise Fit4D as it continues to deliver on its mission of empowering people with diabetes. Fit4D has demonstrated success in improving the health of people with diabetes through its technology-enabled services. The appointment of both Sam and Susan demonstrates Fit4D’s commitment to further accelerate its growth through its pharmaceutical, payer and provider distribution channels. “Sam has years of healthcare experience, beginning at Prudential and then leading and advising 15 payer and health IT companies,” said David Weingard, CEO of Fit4D. “We are excited to have him join the Fit4D team as we scale patient volumes within regional and national health plans. Susan’s experience delivering impactful solutions to pharmaceutical clients will support our continued innovation in diabetes and non-diabetes market segments. Fit4D is a technology-enabled health coaching solution that scales the reach of expert certified diabetes educators (CDEs), allowing them to manage a patient population more than five times larger than traditional inpatient settings. Fit4D clients include pharmaceutical companies with a branded drug or device seeking to improve initiation and adherence, and payers looking to improve health outcomes and quality measures. The company’s team of CDEs across the country leverage the proprietary technology platform to engage patients with a personalized plan that addresses the individual barriers one faces when learning to self-manage the condition. Coaching topics include basic education about the condition, tips and tactics to initiate therapy and improve medication adherence, the importance of preventive care, nutrition, exercise, advice to overcome psychosocial barriers and more. “I am honored to join the Fit4D Board of Advisors,” said Sam Havens, former Prudential Healthcare President and board member of Blue Cross Blue Shield of Rhode Island and TelaDoc. “I am tremendously excited to make an impact guiding the growth of the company as it continues to leverage its technology platform in the market.” “Fit4D is an innovative health IT company,” said Susan Duffy, former President of McCann Healthcare. “I’m thrilled to join the team and help expand their reach so they can help more people through their expert health coaching.” Fit4D’s mission is to improve the lives of people living with diabetes worldwide. Fit4D delivers scalable and effective patient programs through an optimized mix of its technology platform and human-based touch points. The Fit4D clinical team of certified diabetes educators (CDEs) is comprised of dietitians, exercise physiologists, nurses, and social workers, who are passionate about empowering people with diabetes to live rich, healthy and fulfilling lives. Fit4D’s Fortune 500 clients include pharmaceutical, payer, provider and wellness companies. Fit4D has also engaged in numerous joint initiatives with the Juvenile Diabetes Research Foundation, American Diabetes Association, and Diabetes Research Institute.
News Article | February 28, 2017
Fit4D, a New York City-based health technology company, announced today that Jeff Becker, J.D., founding partner at Epstein Becker & Green, will join its Board of Directors. Fit4D has demonstrated success in improving the health of people with diabetes through its technology-enabled services. By appointing Mr. Becker to the board, Fit4D demonstrates its continued commitment to bring industry thought leaders into its team to further accelerate its growth through its pharmaceutical, payer and provider clients. Jeff Becker co-founded Epstein Becker & Green in 1973 and provides strategic advice and legal guidance to a wide range of health care organizations. Mr. Becker was selected by his peers for inclusion in the Best Lawyers in America (1995 to 2017) and selected as one of the leading health care attorneys in New York by Chambers USA. “We are honored to have Jeff Becker join the Fit4D board,” said David Weingard, CEO of Fit4D. “Today’s healthcare landscape is complex and Jeff’s business and legal acumen is critical to successfully navigating this landscape while achieving our business and social mission." “I am tremendously excited to join the Fit4D team and support the company improving the health of people with diabetes. Fit4D’s technology-enabled services deliver innovation and measurable value to its clients and I look forward to contributing to the company’s ongoing success,” said Jeff Becker. Fit4D is a technology-enabled health coaching solution that scales the reach of expert certified diabetes educators (CDEs), allowing them to manage a patient population more than five times larger than traditional inpatient settings. Fit4D clients include pharmaceutical companies with a branded drug or device seeking to improve initiation and adherence, and payers looking to improve health outcomes and quality measures. The company’s team of CDEs across the country leverage the Fit4D technology platform to engage patients with a personalized plan that addresses the individual barriers one faces when learning to self-manage the condition. Coaching topics include diabetes education, tips and tactics to initiate therapy and improve medication adherence, the importance of preventive care, nutrition, exercise, advice to overcome psycho-social barriers and more. About Fit4D Fit4D’s mission is to improve the lives of people living with diabetes worldwide. Fit4D delivers scalable and effective patient programs through an optimized mix of its technology platform and human-based touch points. The Fit4D clinical team of certified diabetes educators (CDEs) is comprised of dietitians, exercise physiologists, nurses, and social workers, who are passionate about empowering people with diabetes to live rich, healthy and fulfilling lives. Fit4D’s Fortune 500 clients include pharmaceutical, payer, provider and wellness companies. Fit4D has also engaged in numerous joint initiatives with the Juvenile Diabetes Research Foundation, American Diabetes Association, and the Diabetes Research Institute.
News Article | November 2, 2016
Type 1 diabetes patients may one day be able to monitor their blood glucose levels and even control their insulin infusions via a transparent sensor on a contact lens, a new Oregon State University study suggests. The sensor uses a nanostructured transistor — specifically an amorphous indium gallium oxide field effect transistor, or IGZO FET — that can detect subtle glucose changes in physiological buffer solutions, such as the tear fluid in eyes. Type 1 diabetes, formerly known as juvenile diabetes, can lead to serious health complications unless glucose levels are carefully controlled. Problems can include retinopathy, blindness, neuropathy, kidney and cardiac disease. Researchers in the OSU College of Engineering say sensors they fabricated using the IGZO FET will be able to transmit real-time glucose information to a wearable pump that delivers the hormones needed to regulate blood sugar: insulin and glucagon. The sensor and pump would, in effect, act as an artificial pancreas. “We have fully transparent sensors that are working,” says Greg Herman, an OSU professor of chemical engineering and corresponding author on this study. “What we want to do next is fully develop the communication aspect, and we want to use the entire contact lens as real estate for sensing and communications electronics. “We can integrate an array of sensors into the lens and also test for other things: stress hormones, uric acid, pressure sensing for glaucoma, and things like that. We can monitor many compounds in tears — and since the sensor is transparent, it doesn’t obstruct vision; more real estate is available for sensing on the contact lens.” The FET’s closely packed, hexagonal, nanostructured network resulted from complimentary patterning techniques that have the potential for low-cost fabrication. Those techniques include colloidal nanolithography and electrohydrodynamic printing, or e-jet, which is somewhat like an inkjet printer that creates much finer drop sizes and works with biological materials instead of ink. The findings by postdoctoral scholar Xiaosong Du, visiting scholar Yajuan Li and,Herman were recently published online in the journal Nanoscale. The Juvenile Diabetes Research Foundation provided primary funding for the research. Google has been working on a glucose-monitoring contact lens but its version is not fully transparent. “It’s an amperometric sensor and you can see the chips — that means it has to be off to the side of the contact lens,” Herman says. “Another issue is the signal is dependent on the size of the sensor and you can only make it so small or you won’t be able to get a usable signal. With an FET sensor, you can actually make it smaller and enhance the output signal by doing this.” This research builds on earlier work by Herman and other OSU engineers that developed a glucose sensor that could be wrapped around a catheter, such as one used to administer insulin from a pump. “A lot of type 1 diabetics don’t wear a pump,” Herman says. “Many are still managing with blood droplets on glucose strips, then using self-injection. Even with the contact lens, someone could still manage their diabetes with self-injection. The sensor could communicate with your phone to warn you if your glucose was high or low.” The transparent FET sensors, Herman says, might ultimately be used for cancer detection, by sensing characteristic biomarkers of cancer risk. Their high sensitivity could also measure things such as pulse rate, oxygen levels, and other aspects of health monitoring that require precise control.
News Article | November 4, 2016
SCOTTSDALE, Ariz.--(BUSINESS WIRE)--STORE Capital Corporation (NYSE: STOR), an internally managed net-lease real estate investment trust (REIT) that invests in Single Tenant Operational Real Estate, is proud to support the Juvenile Diabetes Research Foundation (JDRF) as Gold Sponsor of the 2016 Promise Ball Gala: “An Evening of Gratitude” being held November 12, 2016, in Scottsdale, Arizona. Christopher H. Volk, President and CEO of STORE Capital, and his family are this year’s honorees. “Our f