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MEDFORD/SOMERVILLE, Mass. (May 23, 2017) Researchers have succeeded in permanently rewriting flatworms' regenerative body shape by resetting their internal bioelectric pattern memory, causing even normal-appearing flatworms to harbor the "code" to regenerate as two-headed worms. The findings, published today in Biophysical Journal (Cell Press), suggest an alternative to genomic editing for large-scale regenerative control, according to the authors. The research, led by scientists at Tufts University's Allen Discovery Center and its Department of Biology, addresses the forces that determine the shape to which an animal's body regenerates when severely damaged, shows that it is possible to permanently alter the target morphology of an animal with a wild-type genomic sequence, and reveals that alternative body patterns can be encoded within animals with normal anatomy and histology. The research also provides clues about why certain individuals have different biological outcomes when exposed to the same treatment as others in their group. "With this work, we now know that bioelectric properties can permanently override the default body shape called for by a genome, that regenerative target morphology can be edited to diverge from the current anatomy, and that bioelectric networks can be a control point for investigating cryptic, previously-unobservable phenotypes," said the paper's corresponding author, Michael Levin, Ph.D., Vannevar Bush professor of biology and director of the Allen Discovery Center at Tufts and the Tufts Center for Regenerative and Developmental Biology. The findings are important because advances in regenerative medicine require an understanding of the mechanisms by which some organisms repair damage to their bodies, said Levin. "Bioelectricity has a powerful instructive role as a mediator in the reprogramming of anatomical structure, with many implications for understanding the evolution of form and the path to regenerative therapies," he added. Researchers worked with planaria (Dugesia japonica) -- flatworms that are known for their regenerative capacity. When cut into pieces, each fragment of flatworm regenerates what it is missing to complete its anatomy. Normally, regeneration produces an exact copy of the original, standard worm. Building on previous work in which Levin and colleagues demonstrated it was possible to cause flatworms to grow heads and brains of another species of flatworm by altering their bioelectric circuits, the researchers briefly interrupted the flatworms' bioelectric networks. They did so by using octanol (8 OH) to temporarily interrupt gap junctions, which are protein channels -- electrical synapses -- that enable cells to communicate with each other locally and by forming networks across long distances, passing electrical signals back and forth. Twenty five percent of the amputated trunk fragments regenerated into two-headed flatworms, while 72 percent regenerated into normal-appearing, one-headed worms; approximately 3 percent of the trunk fragments did not develop properly. At first, the researchers assumed that the single-headed treated flatworms had not been affected by the treatment, as is common when the function of a biological system is altered by any experimental treatment or environmental event. However, when the flatworms with normal body shape were then amputated repeatedly over several months in normal spring water, they produced the same ratio of two-headed worms to one-headed worms. The flatworms' pattern memory had been altered, although this was not apparent in their intact state and was revealed only upon regeneration. The research showed that the altered target morphology -- the shape to which the worms regenerate upon damage -- was encoded not in their histology, molecular marker expression, or stem cell distribution, but rather in a bioelectric pattern that instructs one of two possible anatomical outcomes after subsequent damage. "The altered regenerative body plan is stored in the bioelectric networks in the cells of seemingly normal planaria, and the body-wide bioelectric gradients serve as a kind of pattern memory," said Fallon Durant, the paper's first author and a Ph.D. student in the Integrative Graduate Education and Research Traineeship (IGERT) program at the Department of Biology and the Allen Discovery Center at Tufts University. "Bioelectric signals can act as a switch that not only can change body plan anatomy but also undo those changes when reversed." Other authors on the paper are Junji Morokuma, research associate, and Katherine Williams, undergraduate, both in the Tufts University Department of Biology; Dany Spencer Adams, Ph.D., research professor in the Department of Biology and the Center for Regenerative and Developmental Biology; and Christopher Fields, an independent researcher. Work was supported by the Allen Discovery Center program through The Paul G. Allen Frontiers Group, the G. Harold and Leila Y. Mathers Charitable Foundation, the Templeton World Charity Foundation, and the National Science Foundation. Durant, F., Morokuma, J., Fields, C., Williams, K., Spencer Adams, D., Levin, M. "Long-term, stochastic editing of regenerative anatomy via targeting endogenous bioelectric gradients." Biophysical Journal. Published May 23, 2017. DOI: 10.1016/j.bpj.2017.04.011 Tufts University, located on campuses in Boston, Medford/Somerville and Grafton, Massachusetts, and in Talloires, France, is recognized among the premier research universities in the United States. Tufts enjoys a global reputation for academic excellence and for the preparation of students as leaders in a wide range of professions. A growing number of innovative teaching and research initiatives span all Tufts campuses, and collaboration among the faculty and students in the undergraduate, graduate and professional programs across the university's schools is widely encouraged.


News Article | April 27, 2017
Site: www.eurekalert.org

Vanderbilt University Medical Center (VUMC) cancer researcher James Goldenring, M.D., Ph.D., has received a two-year, $200,000 grant from the DeGregorio Family Foundation in Pleasantville, New York, to begin clinical trials of a potential approach for reversing precancerous stomach lesions. Stomach cancer is the fourth leading cause of cancer-related deaths worldwide after lung, liver and colorectal cancers. In the United States, 28,000 people will be diagnosed with stomach cancer this year, and nearly 11,000 will die from the disease, according to the American Cancer Society. Goldenring said the grant will support an international collaborative trial with colleagues at Yonsei University Medical Center in Seoul, Korea, to test the effectiveness of the drug Selumetinib to reverse pre-cancerous lesions in patients following endoscopic resection of stage I gastric cancer. Koreans have one of the world's highest incidences of gastric cancer. "I am extremely grateful for the support that we have received from the DeGregorio Family Foundation," said Goldenring, the Paul W. Sanger Professor of Experimental Surgery at Vanderbilt University School of Medicine. "It is often difficult to obtain support for trials that require clinical collaboration at international sites." "We are very excited to partner with Dr. Goldenring and his colleagues at Vanderbilt University," said Lynn DeGregorio, president of the DeGregorio Family Foundation. "We look forward to the day when we can say we had a part in eradicating stomach cancer." The foundation was established in 2006 after a 10th member of the DeGregorio family succumbed to stomach cancer and was found to have had a rare gene mutation that causes the disease and other common cancers. Selumetinib blocks MEK, an enzyme downstream of Ras, a signaling protein that regulates cell growth and survival. Abnormal Ras activation, possibly triggered by other signaling molecules, is associated with up to one-third of all human cancers and recently was identified in a large percentage of gastric cancers. A year ago, Goldenring reported in Gastroenterology that Selumetinib, a drug recently approved for use in patients with advanced thyroid cancer, halted and reversed neoplastic progression in a mouse model of activated Ras induction of metaplasia and precancerous lesions in the stomach. It appears that underneath the abnormal metaplastic cells hides a lineage of normal progenitor cells, which can regenerate the normal mucosal layer of the stomach, Goldenring said. When the consequences of abnormal Ras activation were blocked by Selumetinib, normal cells pushed the abnormal tissue out of the mucosa. The grant will support a study of MEK inhibition in patients who have had local endoscopic removal of a stage I gastric cancer. These patients have a 2 to 5 percent per year incidence of developing a second cancer in the stomach because a large amount of metaplastic mucosa remains. Astra-Zeneca Corporation will provide the Selumetinib for the trial. Few clinical trials have focused on the elimination of discrete precancerous cells through drug treatment, Goldenring said. The protocol for treatment with Selumetinib will evaluate the drug's efficacy for resolving pre-cancerous metaplasia in humans. If short-term treatment with Selumetinib is successful in these patients, broader studies will be needed to evaluate the consequences on both cancer recurrence and long-term survival, he said. Goldenring is professor of Surgery and Cell & Developmental Biology, vice-chair for Surgical Research in the Section of Surgical Sciences and co-director of the Epithelial Biology Center at VUMC. He also is a staff physician at the Veterans Affairs Medical Center (Tennessee Valley Healthcare System, Nashville campus).


"The March of Dimes believes Dr. Allis's research has opened a door to finding new ways to diagnose, prevent and eventually cure complex conditions such as preterm birth," says Joe Leigh Simpson, MD, senior vice president of Research and Grants at the March of Dimes. Premature birth (before 37 weeks of pregnancy) is the most significant health problem facing mothers and babies today, the March of Dimes says. Premature birth and its complications are the leading cause of death among babies in the United States and children under age 5 around the world. Babies who survive an early birth often have lifelong health problems such as cerebral palsy, vision and hearing loss, and intellectual disabilities. Dr. Simpson noted scientists working at the network of five March of Dimes Prematurity Research Centers around the country are leveraging Dr. Allis's sentinel discoveries in epigenetics to determine what turns genes on and off, especially away from the healthy/normal state.  "This cutting-edge research in March of Dimes Prematurity Research Centers can be expected to accelerate determination of the causes of preterm birth," he said. Dr. Allis will deliver the 22nd annual March of Dimes Prize Lecture on May 8 at the Moscone Convention Center during the 2017 Pediatric Academy Societies annual meeting. He will receive the Prize at a gala black-tie dinner and ceremony that evening at the Hotel Nikko, emceed by CBS sportscaster Greg Gumbel, a member of the March of Dimes national Honorary Board of Trustees. Linda Giudice, MD, PhD, Distinguished Professor and Robert B. Jaffe, MD Endowed Professor in the Reproductive Sciences at the University of California, San Francisco School of Medicine, is scheduled to deliver the Appreciation. Stacey D. Stewart, president of the March of Dimes, will preside at the ceremony. The March of Dimes and Richard B. Johnston, Jr., MD Prize in Developmental Biology has been awarded annually since 1996 to honor investigators whose research has profoundly advanced the science that underlies the understanding of birth defects. The March of Dimes created the Prize as a tribute to Dr. Jonas Salk shortly before his death in 1995. Dr. Salk received March of Dimes support for his work on the polio vaccine. The Prize is a cash award of $250,000 and a silver medal in the design of the Roosevelt dime, honoring President Franklin D. Roosevelt, March of Dimes founder. The March of Dimes is the leading nonprofit organization for pregnancy and baby health. For more than 75 years, moms and babies have benefited from March of Dimes research, education, vaccines, and breakthroughs. For the latest resources and health information, visit our websites marchofdimes.org and nacersano.org. If you have been affected by prematurity or birth defects, visit our shareyourstory.org community to find comfort and support. For detailed national, state and local perinatal statistics, visit peristats.org. You can also find us on Facebook or follow us on Instagram and Twitter. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/2017-march-of-dimes-prize-awarded-to-dr-c-david-allis-for-groundbreaking-research-300452393.html


— Established expert in housing market and faithful philanthropist, Kenny Slaught advocates for scientific research development and technological advancement to enhance global health treatment methods in response to urgent international development calls in a timely and most effective manner. Having earned a degree in business and economics from the University of California, Santa Barbara, Slaught has served on the UCSB Foundation Board of Trustees since 1996. The prominent real estate developer has recently praised the University on his blog at KennySlaught.com, as the notable institution was announced the Grand Challenges Explorations grant winner last year in May. David Low, a professor in UCSB’s Department of Molecular, Cellular, and Developmental Biology, will pursue an innovative global health and development research project titled “Strategy for development of enteric pathogen-specific phage”. Low’s research focuses on a new way to deal with serious bacterial pathogens that are becoming resistant to many once-powerful antibiotics. He will engineer phage to selectively target and destroy several pathogenic bacteria to prevent enteric diseases in infants. They will engineer different versions of the T2 lytic bacteriophage that bind multiple different regions of the BamA protein found on the surface of several pathogenic bacteria, which will ensure they only infect these target bacteria. They will test the different phage for capacity to kill pathogenic E. coli and Shigella, and whether they cause resistance. Kenny Slaught notes that Grand Challenges Explorations (GCE) funds individuals worldwide to explore ideas that can break the mold in how the humanity approaches persistent global health and development challenges. GCE is a $100 million initiative funded by the Bill & Melinda Gates Foundation and was launched in 2008. More than 1,186 projects in over 61 countries have received GCE grants. Anyone from any organization can apply for the GCE grant program. There is a short two-page online application and no preliminary data required. Initial grants of $100,000 are awarded two times a year. A successful project has the opportunity to receive a follow-on grant of up to $1 million. “These grants are meant to spur on new discoveries that could ultimately save millions of lives,” said Chris Wilson, director of Global Health Discovery at the Bill & Melinda Gates Foundation. “GCE winners are expanding the pipeline of ideas for serious global health and development challenges where creative thinking is most urgently needed.” Where human lives are concerned, Slaught is convinced medical research and practice need expanding horizons for timely and holistic global health interventions. Founder of Investec Real Estate Companies, Kenny Slaught has been in the industry for more than four decades. A dedicated investment strategist, he manages more than 3 million square feet of property throughout California. With total transactions valued above $1.2 billion, Investec has grown to become one of Santa Barbara’s leading real estate firms. An avid philanthropist, Mr. Slaught is involved with many non-profit and community organizations, including Hospice of Santa Barbara, the Music Academy of the West. Contributing to the benefit of youth in the area, he dedicates considerable time to these and other worthy causes. For more information, please visit http://www.KennySlaughtNews.com


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

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. .


— California’s notable real estate investor, Kenny Slaught continues to support the notion of robust empirical research and its critical impact on public health policies and practices. Driven by his passion for learning excellence and empowering communities through education, he has been an active member and supporter of UCSB Foundation, who recently posted on his blog at KennySlaught.com that “The University of California Santa Barbara announced on May 26, 2016 that it is a Grand Challenges Explorations grant winner.” David Low, a professor in UCSB’s Department of Molecular, Cellular, and Developmental Biology, will pursue an innovative global health and development research project titled “Strategy for development of enteric pathogen-specific phage”. Low’s research focuses on a new way to deal with serious bacterial pathogens that are becoming resistant to many once-powerful antibiotics. According to Kenny Slaught, “He will engineer phage to selectively target and destroy several pathogenic bacteria to prevent enteric diseases in infants”. David Low was awarded his bachelor’s degree in biology from UC San Diego, his master’s degree in microbiology from San Diego State University and his Ph.D. in cellular biochemistry from UC Irvine. As a postdoctoral scholar at Stanford University he conducted research in molecular microbiology in the lab of Stanley Falkow, now a professor emeritus in microbiology and immunology. Low joined the UCSB faculty in 1998 after 13 years as a professor at the University of Utah Health Sciences Center. He was elected a fellow of the American Academy of Microbiology in 2013 and of the American Association for the Advancement of Science in 2003. In 2011, Guillermo Bazan, a professor in the Department of Chemistry and Biochemistry, was one of the winners of the GCE grant. Bazan’s award was for the study of how semiconducting molecules that penetrate the membranes of living organisms can facilitate the conversion of wastewater into energy. The Bill and Melinda Gates Foundation was interested in the possibility of using this technology to alleviate the emerging world’s problem with sanitation, which presents a significant health hazard and negatively impacts people’s dignity. Founder of Investec Real Estate Companies, Kenny Slaught has been in the industry for more than four decades. A dedicated investment strategist, he manages more than 3 million square feet of property throughout California. With total transactions valued above $1.2 billion, Investec has grown to become one of Santa Barbara’s leading real estate firms. An avid philanthropist, Mr. Slaught is involved with many non-profit and community organizations, including Santa Barbara Bowl Foundation and the Music Academy of the West. Contributing to the benefit of youth in the area, he dedicates considerable time to these and other worthy causes. For more information, please visit http://www.KennySlaughtNews.com


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

The mystery of what controls the range of developmental clocks in mammals -- from 22 months for an elephant to 12 days for a opossum -- may lie in the strict time-keeping of pluripotent stem cells for each unique species. Developmental clocks are of high importance to regenerative medicine, since many cells types take long periods to grow to maturity, limiting their usefulness to human therapies. The regenerative biology team at the Morgridge Institute for Research, led by stem cell pioneer and UW-Madison professor James Thomson, is studying whether stem cell differentiation rates can be accelerated in the lab and made available to patients faster. In a study published in February online editions of the journal Developmental Biology, Morgridge scientists tested the stringency of the developmental clock in human stem cells during neural differentiation. First, they closely compared the differentiation rates of the cells growing in dishes compared to the known growth rates of human cells in utero. Second, they grew the human stem cells within a mouse host, surrounded by factors -- such as blood, growth hormones and signaling molecules -- endemic to a species that grows much more rapidly than humans. In both cases -- lab dish or different species -- the cells did not waver from their innate timetable for development, without regard to environmental changes. "What we found remarkable was this very intrinsic process within cells," said lead author Chris Barry, a Morgridge assistant scientist. "They have self-coding clocks that do not require outside stimulus from the mother or the uterus or even neighboring cells to know their pace of development." While the study suggests that cellular timing is a stubborn process, the Thomson lab is exploring a variety of follow-up studies on potential factors that could help cells alter their pace, Barry said. One aspect of the study that's immediately valuable across biology is the realization that how stem cells behave in the dish aligns almost precisely with what happens in nature. "The promising thing is that we can take species of stem cells, put them in tissue culture, and more confidently believe that events we're seeing are probably happening in the wild as well," Barry said. "That is potentially great news for studying embryology in general, understanding what's going on in the womb and disease modeling for when things can go wrong." It also opens up potential avenues in embryology that would have been inconceivable otherwise -- for example, using stem cells to accurately study the embryology of whales and other species with much longer (or shorter) gestation rates than humans. In order to accurately compare development timing across species with wildly different gestation rates -- nine months compared to three weeks -- the team used an algorithm called Dynamic Time Warping, originally developed for speech pattern recognition. This algorithm will stretch or compress the time frame of one species to match up with similar gene expression patterns in the other. Using this process, they identified more than 3,000 genes that regulate more rapidly in mice and found none that regulate faster in human cells. The impact of solving the cell timing puzzle could be enormous, Barry said. For example, cells of the central nervous system take months to develop to a functional state, far too long to make them therapeutically practical. If scientists can shorten that timing to weeks, cells could potentially be grown from individual patients that could counteract grave diseases such as Parkinson's, Multiple Sclerosis, Alzheimer's, Huntington's disease and spinal cord injuries. "If it turns out these clocks are universal across different cell types," said Barry, "you are looking at broad-spectrum impact across the body."


News Article | February 27, 2017
Site: phys.org

Developmental clocks are of high importance to regenerative medicine, since many cells types take long periods to grow to maturity, limiting their usefulness to human therapies. The regenerative biology team at the Morgridge Institute for Research, led by stem cell pioneer and UW-Madison professor James Thomson, is studying whether stem cell differentiation rates can be accelerated in the lab and made available to patients faster. In a study published in February online editions of the journal Developmental Biology, Morgridge scientists tested the stringency of the developmental clock in human stem cells during neural differentiation. First, they closely compared the differentiation rates of the cells growing in dishes compared to the known growth rates of human cells in utero. Second, they grew the human stem cells within a mouse host, surrounded by factors—such as blood, growth hormones and signaling molecules—endemic to a species that grows much more rapidly than humans. In both cases—lab dish or different species—the cells did not waver from their innate timetable for development, without regard to environmental changes. "What we found remarkable was this very intrinsic process within cells," says lead author Chris Barry, a Morgridge assistant scientist. "They have self-coding clocks that do not require outside stimulus from the mother or the uterus or even neighboring cells to know their pace of development." While the study suggests that cellular timing is a stubborn process, the Thomson lab is exploring a variety of follow-up studies on potential factors that could help cells alter their pace, Barry says. One aspect of the study that's immediately valuable across biology is the realization that how stem cells behave in the dish aligns almost precisely with what happens in nature. "The promising thing is that we can take species of stem cells, put them in tissue culture, and more confidently believe that events we're seeing are probably happening in the wild as well," Barry says. "That is potentially great news for studying embryology in general, understanding what's going on in the womb and disease modeling for when things can go wrong." It also opens up potential avenues in embryology that would have been inconceivable otherwise—for example, using stem cells to accurately study the embryology of whales and other species with much longer (or shorter) gestation rates than humans. In order to accurately compare development timing across species with wildly different gestation rates—nine months compared to three weeks—the team used an algorithm called Dynamic Time Warping, originally developed for speech pattern recognition. This algorithm will stretch or compress the time frame of one species to match up with similar gene expression patterns in the other. Using this process, they identified more than 3,000 genes that regulate more rapidly in mice and found none that regulate faster in human cells. The impact of solving the cell timing puzzle could be enormous, Barry says. For example, cells of the central nervous system take months to develop to a functional state, far too long to make them therapeutically practical. If scientists can shorten that timing to weeks, cells could potentially be grown from individual patients that could counteract grave diseases such as Parkinson's, Multiple Sclerosis, Alzheimer's, Huntington's disease and spinal cord injuries. "If it turns out these clocks are universal across different cell types," says Barry, "you are looking at broad-spectrum impact across the body." Explore further: Researchers turn stem cells into somites, precursors to skeletal muscle, cartilage and bone


News Article | February 25, 2017
Site: news.yahoo.com

Today marks the 20th anniversary of the announcement of Dolly the sheep, the first mammal cloned from an adult cell. Her creation left a lasting impact on both the public and the field of developmental biology, experts say. At the time, other researchers had managed to clone mammals by splitting embryos in a test tube and implanting them in adults. However, none had successfully used an adult somatic (body) cell to clone a mammal. Researchers at the Roslin Institute in Scotland were finally able to produce Dolly — cloned from the udder cell of an adult sheep — after 276 attempts, according to the National Human Genome Research Institute (NHGRI). "For a developmental biologist, the ability to clone an advanced mammal was thought to be impossible," Lawrence Brody, director of the Division of Genomics and Society at the NHGRI, told Live Science. Although Dolly was born in July 1996, Researchers announced Dolly's existence on Feb. 22, 1997. The delay in the announcement was due to the time needed to amass sufficient data on the project, check the data, write and get the manuscript published, said Bruce Whitelaw, the head of the Division of Developmental Biology at the Roslin Institute. [5 Fascinating Findings About Stem Cells] Although British biologist John Gurdon had cloned frogs from the skin cells of adult frogs in 1958, researchers after him had failed to clone mammals such as mice, rats and pigs, despite trying for decades, Brody said. He added that many researchers began to feel there had to be "something different about mammals in the way their genome and genetic blueprints are packaged," and that cloning them would be impossible. However, Dolly's creation "told us that was all wrong," Brody said. That breakthrough would be crucial in the years to come. "It is rare that a single scientific story can have such a rapid, then sustained, impact" on science, Whitelaw said. Dolly had a massive scientific impact, especially through driving stem cell research and therapy, Whitelaw told Live Science. Ian Wilmut, the scientist who led the team that created Dolly, similarly told Live Science that research on Dolly led to both unexpected and very important results. "The birth of Dolly and the new understanding of the opportunity to change the functioning of cells made researchers consider other possible ways of modifying cells," Wilmut said. Later, in 2006, researchers in Japan found that introducing a set of four proteins into these skin cells led to a portion of them to "become very similar to embryo stem cells," where they had the ability to then differentiate into different adult cell types, Wilmut said. "The whole stem-cell investigation was really stimulated by the fact that Dolly was able to be born, and stem cells still are quite promising as a means to be able to repair human tissues when they're damaged," Brody said. "We're obviously not there yet, but it is something that could be traced back to the success of Dolly." There is also a link between the Dolly experiments and the so-called CRISPR technologies that allow scientists to edit genomes, Brody said: Both are breakthroughs of enormous magnitude, and could help researchers figure out ways to repair damaged or diseased tissues, he said. [Unraveling the Human Genome: 6 Molecular Milestones] Another important result of the Dolly experiments is that they put science in the spotlight. "Dolly captured the world's imagination and allowed the world to hear about science," Brody said. "It's rare that the general public gets enamored [with] science, and it was clearly enamored with Dolly". The creation of Dolly also brought up important conversations about the ethical limitations of manipulating human cells and embryos, laying the groundwork for similar conversations today, Brody said. Dolly died in February 2003, at age 6. (A typical life span for a sheep is about 10 to 12 years.) She had both offspring and clone "sisters," which were derived from the same batch of cells as Dolly. However, none of her offspring are alive today, Wilmut told Live Science. (Whitelaw also mentioned that the Roslin Institute no longer keeps sheep, as the funding for this program has run out.) Since Dolly's creation, numerous other mammals have been cloned successfully, including mice, cattle, deer, horses and rats, according to the NHGRI.


News Article | March 1, 2017
Site: marketersmedia.com

— With research and technologies growing in popularity like never before, scholars and practitioners see innovation solutions combined with knowledge management as the key to improving global health care and human wellbeing. California-based entrepreneur and philanthropist, Kenny Slaught, acknowledges the value of scientific innovations in addressing international development needs. Having earned a degree in business and economics from the University of California, Santa Barbara, he has served on the UCSB Foundation Board of Trustees since 1996. The prominent real estate developer has recently praised the University on his blog at KennySlaught.com, as the notable institution was announced the Grand Challenges Explorations grant winner last year in May. David Low, a professor in UCSB’s Department of Molecular, Cellular, and Developmental Biology, will pursue an innovative global health and development research project titled “Strategy for development of enteric pathogen-specific phage”. Low’s research focuses on a new way to deal with serious bacterial pathogens that are becoming resistant to many once-powerful antibiotics. He will engineer phage to selectively target and destroy several pathogenic bacteria to prevent enteric diseases in infants. They will engineer different versions of the T2 lytic bacteriophage that bind multiple different regions of the BamA protein found on the surface of several pathogenic bacteria, which will ensure they only infect these target bacteria. They will test the different phage for capacity to kill pathogenic E. coli and Shigella, and whether they cause resistance. Kenny Slaught notes that Grand Challenges Explorations (GCE) funds individuals worldwide to explore ideas that can break the mold in how the humanity approaches persistent global health and development challenges. GCE is a $100 million initiative funded by the Bill & Melinda Gates Foundation and was launched in 2008. More than 1,186 projects in over 61 countries have received GCE grants. Anyone from any organization can apply for the GCE grant program. There is a short two-page online application and no preliminary data required. Initial grants of $100,000 are awarded two times a year. A successful project has the opportunity to receive a follow-on grant of up to $1 million. “These grants are meant to spur on new discoveries that could ultimately save millions of lives,” said Chris Wilson, director of Global Health Discovery at the Bill & Melinda Gates Foundation. “GCE winners are expanding the pipeline of ideas for serious global health and development challenges where creative thinking is most urgently needed.” Where human lives are concerned, Slaught is convinced medical research and practice need expanding horizons for timely and holistic global health interventions. Founder of Investec Real Estate Companies, Kenny Slaught has been in the industry for more than four decades. A dedicated investment strategist, he manages more than 3 million square feet of property throughout California. With total transactions valued above $1.2 billion, Investec has grown to become one of Santa Barbara’s leading real estate firms. An avid philanthropist, Mr. Slaught is involved with many non-profit and community organizations, including Hospice of Santa Barbara, the Music Academy of the West. Contributing to the benefit of youth in the area, he dedicates considerable time to these and other worthy causes. For more information, please visit http://www.KennySlaughtNews.com

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