- Human genome and mouse studies identify new precise genetic links

Newswise Working with genetically engineered mice and the genomes of thousands of people with schizophrenia, researchers at Johns Hopkins say they now better understand how both nature and nurture can affect ones risks for schizophrenia and abnormal brain development in general.

The researchers reported in the March 2 issue of Cell that defects in a schizophrenia-risk genes and environmental stress right after birth together can lead to abnormal brain development and raise the likelihood of developing schizophrenia by nearly one and half times.

Our study suggests that if people have a single genetic risk factor alone or a traumatic environment in very early childhood alone, they may not develop mental disorders like schizophrenia, says Guo-li Ming, M.D., Ph.D., professor of neurology and member of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine. But the findings also suggest that someone who carries the genetic risk factor and experiences certain kinds of stress early in life may be more likely to develop the disease.

Pinpointing the cause or causes of schizophrenia has been notoriously difficult, owing to the likely interplay of multiple genes and environmental triggers, Ming says. Searching for clues at the molecular level, the Johns Hopkins team focused on the interaction of two factors long implicated in the disease: Disrupted-in-Schizophrenia 1 (DISC1) protein, which is important for brain development, and GABA, a brain chemical needed for normal brain function.

To find how these factors impact brain development and disease susceptibility, the researchers first engineered mice to have reduced levels of DISC1 protein in one type of neuron in the hippocampus, a region of the brain involved in learning, memory and mood regulation. Through a microscope, they saw that newborn mouse brain cells with reduced levels of DISC1 protein had similar sized and shaped neurons as those from mice with normal levels of DISC1 protein. To change the function of the chemical messenger GABA, the researchers engineered the same neurons in mice to have more effective GABA. Those brain cells looked much different than normal neurons, with longer appendages or projections. Newborn mice engineered with both the more effective GABA and reduced levels of DISC1 showed the longest projections, suggesting, Ming said, that defects in both DISC1 and GABA together could change the physiology of developing neurons for the worse.

Meanwhile, other researchers at University of Calgary and at the National Institute of Physiological Sciences in Japan had shown in newborn mice that changes in environment and routine stress can impede GABA from working properly during development. In the next set of experiments, the investigators paired reducing DISC1 levels and stress in mice to see if it could also lead to developmental defects. To stress the mice, the team separated newborns from their mothers for three hours a day for ten days, then examined neurons from the stressed newborns and saw no differences in their size, shape and organization compared with unstressed mice. But when they similarly stressed newborn mice with reduced DISC1 levels, the neurons they saw were larger, more disorganized and had more projections than the unstressed mouse neurons. The projections, in fact, went to the wrong places in the brain.

Next, to see if their results in mice correlated to suspected human schizophrenia risk factors, the researchers compared the genetic sequences of 2,961 schizophrenia patients and healthy people from Scotland, Germany and the United States. Specifically, they determined if specific variations of DNA letters found in two genes, DISC1 and a gene for another protein, NKCC1, which controls the effect of GABA, were more likely to be found in schizophrenia patients than in healthy individuals. They paired 36 DNA letter changes in DISC1 and two DNA letter variations in NKCC1 one DNA letter change per gene in all possible combinations. Results showed that if a persons genome contained one specific combination of single DNA letter changes, then that person is 1.4 times more likely than people without these DNA changes to develop schizophrenia. Having these single DNA letter changes in either one of these genes alone did not increase risk.

Now that we have identified the precise genetic risks, we can rationally search for drugs that correct these defects, says Hongjun Song, Ph.D., co-author, professor of neurology and director of the Stem Cell Program at the Institute for Cell Engineering.

Other authors of the paper from Johns Hopkins are Ju Young Kim, Cindy Y. Liu, Fengyu Zhang, Xin Duan, Zhexing Wen, Juan Song, Kimberly Christian and Daniel R. Weinberger. Emer Feighery, Bai Lu and Joseph H. Callicott from the National Institute of Mental Health, Dan Rujescu of Ludwig-Maximilians-University, and David St Clair of the University of Aberdeen Royal Cornhill Hospital are additional authors.

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Genetic Risk and Stressful Early Infancy Join to Increase Risk for Schizophrenia

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Public release date: 26-Mar-2012 [ | E-mail | Share ]

Contact: Karen N. Peart karen.peart@yale.edu 203-432-1326 Yale University

Obese youths with particular genetic variants may be more prone to fatty liver disease, a leading cause of chronic liver disease in children and adolescents in industrialized countries, according to new findings by Yale School of Medicine researchers.

The study, which focused on three ethnic groups, is published in the March issue of the journal Hepatology.

Led by Nicola Santoro, M.D., associate research scientist in the Department of Pediatrics at Yale School of Medicine, the authors measured the hepatic, or liver, fat content of children using magnetic resonance imaging. The study included 181 Caucasian, 139 African-American and 135 Hispanic children who were, on average, age 13.

"We observed that a common genetic variant known as Patatin-like phospholipase domain containing protein-3 (PNPLA3) working with a regulatory protein called glucokinase (GCKR), was associated with increased triglycerides, very low-density lipoproteins levels, and fatty liver," said Santoro.

Santoro explained that his observations could help unravel the genetic mechanisms that contribute to liver fat metabolism. "This may drive the decisions about future drug targets to treat hypertriglyceridemia and non-alcoholic fatty liver disease," he said.

Childhood obesity is a global health concern. Experts say nonalcoholic fatty liver disease is now the leading cause of chronic liver disease in children and adolescents in industrialized countries.

"Our findings confirm that obese youths with genetic variants in the GCKR and PNPLA3 genes may be more susceptible to fatty liver disease," said Santoro, who is cautious about automatically extending this observation to the overall population.

"Our data refer to a population of obese children and adolescents," he said. "I think that further studies in a larger sample size involving lean subjects and adults may help to further define in more details these associations."

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Researchers unravel genetic mechanism of fatty liver disease in obese children

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By George Winslow -- Broadcasting & Cable, 3/26/2012 5:41:01 PM Pixeldust Studios has produced around eight minutes of original animation sequences that will be used in a one-hour episode of PBS's Nova series called "Cracking Your Genetic Code" that will air on March 28.

The PBS special will explore the medical benefits of the genetic revolution and some of the ethical questions raised by these new technologies. To help tell that story, Pixeldust created animated sequences showing the science behind genes, chromosomes and DNA as well as how certain medications and drugs work in the human body.

"Pixeldust did an amazing job coming up with creative ways to visualize the human genome," noted Sarah Holt, producer for Nova/PBS & Holt Productions in a statement. "Their animators skillfully took the audience inside a human cell, past human chromosomes, and into DNA that is coiled inside the nucleus. The animation was sophisticated and artistically gorgeous to look at, but also helped the audience grasp difficult concepts in genomics [while laboring]...to ensure the accuracy of the scientific details."

Ricardo Andrade, founder and executive creative director at Pixeldust added in a statement that they used "warm colors" to give the "work a more organic look." The studio also consulted with a noted cell biologist to ensure the scientific accuracy of the images.

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PBS' 'Nova' Applies Pixeldust to Genetics

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(RTTNews.com) - Myriad Genetics Inc. (MYGN) announced that the Supreme Court of the United States remanded the case of The Association for Molecular Pathology, et al., v. Myriad Genetics Inc., et al to the Federal Circuit Court of Appeals.

The company said that as a result of this decision by the Supreme Court, the United States Court of Appeals for the Federal Circuit will reconsider their decision dated July 29, 2011, which upheld Myriad's gene patents.

In that decision, the Federal Circuit declared that the composition of matter claims covering isolated DNA of the BRCA 1 and BRCA 2 genes are patent-eligible under Section 101 of the United States Patent Act.

"While, this case should not have any direct impact to Myriad and its operations because of our extensive patent estate, it has great importance to the medical, pharmaceutical, biotechnology and other commercial industries, as well as the hundreds of millions of people whose lives are bettered by the products these industries develop based on the promise of strong patent protection," said Peter Meldrum, President and CEO of Myriad Genetics.

"Thus, we are prepared to vigorously defend the patent claims granted to Myriad by the U.S. Patent and Trademark Office and believe that we will be successful," said Peter Meldrum.

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Myriad Genetics Says Supreme Court Of United States Remands Gene Patenting Case

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LOS ANGELES--(BUSINESS WIRE)--

Response Genetics, Inc. (Nasdaq:RGDX - News), a company focused on the development and commercialization of molecular diagnostic tests for cancer, announced today the addition of Stephanie H. Astrow, Ph.D., as the Companys Vice President for Research and Development. In her role, Dr. Astrow will be responsible for leading the companys research and development programs, as well as identifying and incorporating new technologies into the services that the Company provides to the medical community.

With her strong background in the oncology molecular diagnostics industry we believe Stephanie is the perfect fit to lead our R&D efforts, said Thomas Bologna, Chairman and Chief Executive Officer of Response Genetics. Stephanies track record of identifying and developing biomarker assays and driving scientific innovation to expand business will be a tremendous asset to us and we are looking forward to her contributions.

Dr. Astrow brings extensive experience in molecular diagnostics research and development as well as operational experience to her role at Response Genetics. Most recently, Dr. Astrow was Scientific Director for Oncology at Quest Diagnostics, the largest global provider of diagnostic testing. At Quest, she played a key role in expanding business by introducing new assays and services, as well as coordinating development strategy for companion diagnostics with key pharmaceutical companies. Prior to her work at Quest, Dr. Astrow served as Vice President and Director of Oncology at Pathway Diagnostics, and Vice President, Scientific Director of Impath, Inc. Dr. Astrow received a Bachelor of Arts in Biology and Medicine at Brown University, and her Ph.D. in Molecular and Cell Biology from the University of California, Berkeley. She also holds a Masters of Business Administration from Pepperdine University.

Dr. Astrow, commenting on her appointment said, I couldnt be more excited to be joining Response Genetics, a company that matches my background and interests very well. I look forward to putting my skills and experience to work in helping people with cancer, and being part of a company that is both patient-centric and well suited to prosper in the exciting field of personalized diagnostics.

About Response Genetics, Inc.

Response Genetics Inc. (RGI) is a CLIA-certified clinical laboratory focused on the development and sale of molecular diagnostic tests for cancer. RGIs principal customers include oncologist, pathologists and hospitals. In addition to diagnostic testing services, the Company generates revenue from the sales of its analytical testing services of clinical trial specimens to the pharmaceutical industry. RGI was founded in 1999 and its principal headquarters are located in Los Angeles, California. For additional information, please visit http://www.responsegenetics.com.

Forward-Looking Statement Notice

Except for the historical information contained herein, this press release and the statements of representatives of RGI related thereto contain or may contain, among other things, certain forward-looking statements, within the meaning of the Private Securities Litigation Reform Act of 1995.

Such forward-looking statements involve significant risks and uncertainties. Such statements may include, without limitation, statements with respect to the Companys plans, objectives, projections, expectations and intentions, such as the ability of the Company to continue to execute on its business strategy and operations, the ability to expand our test panels, the ability , and other statements identified by words such as projects, may, could, would, should, believes, expects, anticipates, estimates, intends, plans or similar expressions.

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Response Genetics, Inc. Announces Appointment of Stephanie Astrow, Ph.D., as Vice President, Research and Development

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Seattle Genetics Announces Pivotal ADCETRIS™ (Brentuximab Vedotin) Hodgkin Lymphoma Study Published in Journal of ...

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SILVER SPRING, Md.--(BUSINESS WIRE)--

Nuvilex, Inc. (OTCQB:NVLX), an emerging international biotechnology provider of cell and gene therapy solutions through its associate SG Austria, announced today a significant advance in gene therapy with a new, unique, and specialized system for induction of gene expression in encapsulated cells.

In a recent publication in the Journal of Controlled Release, SG Austria and its research partners described a new system for induction of gene expression, or the means for stimulating a gene to be expressed within cells, including those that have been encapsulated and implanted in the body.

The process described in the publication involves the stimulation of pre-programmed living cells, encapsulated using the Cell-in-a-Box technology, to express therapeutic genes under the control of a heat shock protein inducible promoter. This is done by simultaneously co-encapsulating pre-programmed cells and magnetic nanoparticles, which are much smaller than the cells. When subjected to an alternating magnetic field, the magnetic nanoparticles inside the capsules vibrate, producing heat. This results in a localized, temporary increase in temperature inside the capsules. This heat causes specialized heat shock proteins in the cells to induce expression of the therapeutic gene(s).

Although both cell and gene therapies have an enormous range of potential applications, a critical issue in modern molecular biology has been to be able to regulate and control gene expression. Therefore, many systems have been created to regulate gene expression. Those gene expression systems currently available mostly rely on small molecules such as hormones or antibiotics as inducers. Unfortunately, administration of some of these inducers is difficult to control, the effects on gene regulation are typically slow, and they do not easily shut off once turned on. The new system developed by SG Austria and its partners will allow doctors in the future to more accurately control both dosage and the synthesis of specific proteins for treating a disease.

Dr. Robert Ryan, CEO of Nuvilex, said: "We are excited by this latest development, since fine-tuned heating of the encapsulated cells by nanoparticles by a localized magnetic field will allow carefully regulated gene expression within a short time. All of this can be done from outside the body they have been placed in. This system has great versatility and potential for advancing cell and gene therapy approaches, substantially increasing the value and dramatically expanding the capabilities of our live cell encapsulation technology."

About Nuvilex

Nuvilex, Inc. (OTCQB:NVLX) is an emerging international biotechnology provider of live, clinically useful, therapeutically valuable, encapsulated cells as well as services for encapsulating live cells for the research and medical communities. Through substantial effort, the aspects of our corporate activities alone and in concert with SG Austria continue to move toward agreement completion and ultimately a strong future together. Our companys ultimate clinical offerings will include cancer, diabetes and other treatments using the companys industry-leading cell and gene therapy expertise and cutting-edge, live-cell encapsulation technology.

Safe Harbor Statement

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 involving risks and uncertainties including product demand, market competition, and Nuvilexs ability to meet current or future plans which may cause actual results, events, and performances, expressed or implied, to vary and/or differ from those contemplated or predicted. Investors should study and understand all risks before making an investment decision. Readers are recommended not to place undue reliance on forward-looking statements or information. Nuvilex is not obliged to publicly release revisions to any forward-looking statement to reflect events or circumstances afterward, or to disclose unanticipated occurrences, except as required under applicable laws.

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Nuvilex Announces Advance in Gene Therapy for Encapsulated Living Cells Using Magnetic Nanoparticles

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Public release date: 24-Mar-2012 [ | E-mail | Share ]

Contact: Beth Casteel bcasteel@acc.org 240-328-4549 American College of Cardiology

CHICAGO -- A new study found that using a patient's own bone marrow cells may help repair damaged areas of the heart caused by heart failure, according to research presented today at the American College of Cardiology's 61st Annual Scientific Session. The Scientific Session, the premier cardiovascular medical meeting, brings cardiovascular professionals together to further advances in the field.

Millions of Americans suffer from heart failure, the weakening of the heart muscle and its inability to pump blood effectively throughout the body. If medications, surgery, or stents fail to control the disease, doctors often have few treatment options to offer.

This is the largest study to date to look at stem cell therapy, using a patient's own stem cells, to repair damaged areas of the heart in patients with chronic ischemic heart disease and left ventricular dysfunction. Researchers found that left ventricular ejection fraction (the percentage of blood leaving the heart's main pumping chamber) increased by a small but significant amount (2.7 percent) in patients who received stem cell therapy. The study also revealed that the improvement in ejection fraction correlated with the number of CD34+ and CD133+ cells in the bone marrow information that will be helpful in evaluating and designing future therapies and trials.

"This is the kind of information we need in order to move forward with the clinical use of stem cell therapy," said Emerson Perin, MD, PhD, director of clinical research for cardiovascular medicine at the Texas Heart Institute and the study's lead investigator.

This multi-center study was conducted by the Cardiovascular Cell Therapy Research Network and took place between April 2009 and 2011. At five sites, 92 patients were randomly selected to receive stem cell treatment or placebo. The patients, average age 63, all had chronic ischemic heart disease and an ejection fraction of less than 45 percent along with heart failure and/or angina, and were no longer candidates for revascularization.

"Studies such as these are able to be completed much faster because of the team approach of the network," said Sonia Skarlatos, PhD, deputy director of the division of cardiovascular sciences at the National, Heart, Lung and Blood Institute, and program director of the network.

Bone marrow was aspirated from the patients and processed to obtain just the mononuclear fraction of the marrow. In patients randomly selected to receive stem cell therapy, doctors inserted a catheter into the heart's left ventricle to inject a total of 3 ccs comprising 100 million stem cells into an average of 15 sites that showed damage on the electromechanical mapping image of the heart. Dr. Perin said the procedure is relatively quick and painless, involving only an overnight stay at the hospital.

The study used electromechanical mapping of the heart to measure the voltage in areas of the heart muscle and create a real-time image of the heart.

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Stem cell therapy possibly helpful in heart failure patients

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Public release date: 25-Mar-2012 [ | E-mail | Share ]

Contact: Michael Bernstein m_bernstein@acs.org 619-525-6268 (March 23-28, San Diego Press Center) 202-872-6042

Michael Woods m_woods@acs.org 619-525-6268 (March 23-28, San Diego Press Center) 202-872-6293 American Chemical Society

SAN DIEGO, March 25, 2012 Medicine's recipe for keeping older people active and functioning in their homes and workplaces and healing younger people injured in catastrophic accidents may include "noodle gels" and other lab-made invisible filaments that resemble uncooked spaghetti with nanoscale dimensions, a scientist said here today at the 243rd National Meeting & Exposition of the American Chemical Society (ACS). The world's largest scientific society, ACS is meeting here this week with reports on more than 11,000 reports on new advances in science on its schedule.

Samuel I. Stupp, Ph.D., who presented an ACS plenary lecture, explained that the synthetic pasta-like objects actually are major chemistry advances for regenerative medicine that his research team has accomplished. Regenerative medicine is an emerging field that combines chemistry, biology and engineering. It focuses on the regeneration of tissues and organs for the human body, to repair or replace those damaged through illness, injury, aging or birth defects. Those tissues range from cartilage in joints damaged by arthritis to heart muscle scarred by a heart attack and nerves severed in auto accidents.

"A graying of the population is underway in industrialized countries," Stupp said. "In the U.S., we have the 'baby boom' generation 75 million people born between 1946 and 1964, who now are reaching their mid-60s. At the same time, people are living longer into their 80s, 90s and even 100s. With that comes an expectation of a better quality of life. It's also an economic issue because with lifespan rising, we're going to have to think about how to provide healthcare and keep people functional for longer periods of time, perhaps to keep them in the workforce longer."

Stupp explained that advances in regenerative medicine also hold promise to improve people's lives at any age. For example, a young person could survive a car accident, but emerge with a spinal cord injury and be paralyzed. Also, cardiovascular disease and heart attacks are a leading cause of premature death around the world. Cartilage wears away and does not regenerate on its own in the body, leading to painful osteoarthritis. Some bones do not mend correctly. And the millions of people with diabetes face complications, including blocked blood vessels that result in an increased risk of heart attacks and limb amputations. Regenerative medical techniques could coax cells to grow and repair all of these types of damage, said Stupp, who is with Northwestern University. He is Board of Trustees Professor of Chemistry, Materials Science and Engineering, and Medicine and director of the Institute for BioNanotechnology in Medicine.

One type of spaghetti-like filament developed by Stupp's team is a nanostructure of small bits of protein that glue themselves together spontaneously. These nanofilaments are so small that more than 50,000 would fit across the width of a human hair, and they can serve as smart scaffolds for many uses. For example, Stupp attached to these fibers signaling substances that mimic a powerful substance called VEGF that can promote the formation of new blood vessels. The VEGF-mimic caused new blood vessels to form in mice (stand-ins for humans) with blood vessel damage.

"When VEGF itself was used in clinical trials on humans, it didn't work, despite a lot of laboratory research that suggested otherwise," said Stupp. "The problem was that VEGF was quickly broken down in the body. The nanofilament scaffold, however, lasts in the body for weeks, which allows the VEGF-mimic more time to grow vessels." Eventually, the nanofilaments break down and disappear, leaving only the new blood vessels behind.

In other research, his group developed so-called "noodle gels," which are nanofibers that form long, noodle-like gels when they are heated, cooled and then squeezed out from a pipette (much like frosting from a piping bag) into salty water. These gels can be more than half an inch long and are visible with the naked eye.

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'Noodle gels' or 'spaghetti highways' could become tools of regenerative medicine

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By Prue Salasky

3:48 p.m. EDT, March 23, 2012

UVA recently performed the first two stem cell transplants in Virginia, using non-embryonic stem cells from umbilical cord blood. The Stem Cell Transplant Program offers both bone marrow and stem cell transplants, with a focus on cord blood, to treat leukemia, lymphoma, Hodkin's disease and other blood diseases.

The outcome isn't known yet, but in both patients the stem cells began producing new cells 14 days after the transplant instead of the 24 to 28 days it usually takes.

The cord blood comes from placentas that otherwise would be discarded following childbirth; its benefits include sidestepping ethical issues of embryonic stem cells; they're easier and faster to collect than stem cells from other sources; and they are immune tolerant (this means that they won't attack other cells in the body and match doesn't have to be exact).

Speed is important because there is a narrow window of opportunity to perform a transplant when a patient's disease is in remission.

The program is led by Mary Laughlin, who heads up a team of 29, including 4 other transplant physicians who started seeing patients in September. The program had anticipated doing 15 transplants in first year; now expects to do 100.

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Health Notes: UVA performs first stem cell transplants in Virginia

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HOUSTON -

Doctors from the Texas Heart Institute at St. Luke's Episcopal Hospital have found that patients with heart failure may be able to repair the damaged areas of the heart with stem cells from the patient's own bone marrow.

Doctors presented the findings at the American College of Cardiologys 61st Annual Scientific Session Saturday.

The results are from a multi-center clinical study that measured the possible benefits of using a patients own bone marrow cells to repair damaged areas of the heart suffering from severe heart failure, a condition that affects millions of Americans.

The study, which was the largest such investigation to date, found that the hearts of the patients receiving bone marrow derived stem cells showed a small but significant increase in the ability to pump oxygenated blood from the left ventricle, the hearts main pumping chamber, to the body.

The expectation is that the study will pave the way for potential new treatment options and will be important to designing and evaluating future clinical trials.

This is exactly the kind of information we need to move forward with the clinical use of stem cell therapy, said Emerson Perin, MD, PhD, Director of Clinical Research for Cardiovascular Medicine at THI, and one of the studys lead investigators.

The bone-marrow derived stem cells are helpful to the injured heart when they are themselves biologically active, added Dr. James T. Willerson, the studys principal investigator and President and Medical Director of THI.

This study moves us one step closer to being able to help patients with severe heart failure who have no other alternatives.

The study was conducted by the Cardiovascular Cell Therapy Research Network, the national consortium to conduct such research funded by the National Institutes of Healths National Heart, Lung, and Blood Institute.

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Stem cell, heart heath study

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ScienceDaily (Mar. 22, 2012) Researchers at the University of Bonn artificially derive brain stem cells directly from the connective tissue of mice.

Scientists at the Life & Brain Research Center at the University of Bonn, Germany, have succeeded in directly generating brain stem cells from the connective tissue cells of mice. These stem cells can reproduce and be converted into various types of brain cells. To date, only reprogramming in brain cells that were already fully developed or which had only a limited ability to divide was possible. The new reprogramming method presented by the Bonn scientists and submitted for publication in July 2011 now enables derivation of brain stem cells that are still immature and able to undergo practically unlimited division to be extracted from conventional body cells. The results have now been published in the current edition of the journal Cell Stem Cell.

The Japanese stem cell researcher Professor Shinya Yamanaka and his team produced stem cells from the connective tissue cells of mice for the first time in 2006; these cells can differentiate into all types of body cells. These induced pluripotent stem cells (iPS cells) develop via reprogramming into a type of embryonic stage. This result made the scientific community sit up and take notice. If as many stem cells as desired can be produced from conventional body cells, this holds great potential for medical developments and drug research. "Now a team of scientists from the University of Bonn has proven a variant for this method in a mouse model," report Dr. Frank Edenhofer and his team at the Institute of Reconstructive Neurobiology (Director: Dr. Oliver Brstle) of the University of Bonn. Also involved were the epileptologists and the Institute of Human Genetics of the University of Bonn, led by Dr. Markus Nthen, who is also a member of the German Center for Neurodegenerative Diseases.

Edenhofer and his co-workers Marc Thier, Philipp Wrsdrfer and Yenal B. Lakes used connective tissue cells from mice as a starting material. Just as Yamanaka did, they initiated the conversion with a combination of four genes. "We however deliberately targeted the production of neural stem cells or brain stem cells, not pluripotent iPS multipurpose cells," says Edenhofer. These cells are known as somatic or adult stem cells, which can develop into the cells typical of the nervous system, neurons, oligodendrocytes and astrocytes.

The gene "Oct4" is the central control factor

The gene "Oct4" is a crucial control factor. "First, it prepares the connective tissue cell for reprogramming, later, however, Oct4 appears to prevent destabilized cells from becoming brain stem cells" reports the Bonn stem cell researcher. While this factor is switched on during reprogramming of iPS cells over a longer period of time, the Bonn researchers activate the factor with special techniques for only a few days. "If this molecular switch is toggled over a limited period of time, the brain stem cells, which we refer to as induced neural stem cells (iNS cells), can be reached directly," said Edenhofer. "Oct4 activates the process, destabilizes the cells and clears them for the direct reprogramming. However, we still need to analyze the exact mechanism of the cellular conversion."

The scientists at the University of Bonn have thus found a new way to reprogram cells, which is considerably faster and also safer in comparison to the iPS cells and embryonic stem cells. "Since we cut down on the reprogramming of the cells via the embryonic stage, our method is about two to three times faster than the method used to produce iPS cells," stresses Edenhofer. Thus the work involved and the costs are also much lower. In addition, the novel Bonn method is associated with a dramatically lower risk of tumors. As compared to other approaches, the Bonn scientists' method stands out due to the production of neural cells that can be multiplied to a nearly unlimited degree.

Low risk of tumor and unlimited self renewal

A low risk of tumor formation is important because in the distant future, neural cells will replace defective cells of the nervous system. A vision of the various international scientific teams is to eventually create adult stem cells for example from skin or hair root cells, differentiate these further for therapeutic purposes, and then implant them in damaged areas. "But that is still a long way off," says Edenhofer. However, the scientists have a rather urgent need today for a simple way to obtain brain stem cells from the patient to use them to study various neurodegenerative diseases and test drugs in a Petri dish. "Our work could form the basis for providing practically unlimited quantities of the patient's own cells." The current study was initially conducted on mice. "We are now extremely eager to see whether these results can also be applied to humans," says the Bonn scientist.

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New shortcut for stem cell programming

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24-03-2012 07:46 This is the harvest of adipose tissue for combination with bone marrow aspirate concentrate for stem cell therapy

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Adipose harvest for stem cell therapy by Dr Adelson - Video

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25-03-2012 10:22 Dr Adelson aspirates bone marrow for concentration for stem cell therapy for musculoskeletal pain conditions

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bone marrow aspiration for stem cell therapy by Dr Adelson - Video

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(RTTNews.com) - An important clinical trial, which evaluated the use of autologous bone-marrow-cell therapy in patients with chronic ischemic heart failure, has failed to meet the prespecified end points of improvement in most measures of heart function, according to the results presented at the American College of Cardiology 2012 Scientific Sessions.

The trial dubbed, FOCUS - a phase II study, is the largest study to date to investigate if a patient's own bone marrow cells improved myocardial perfusion, reduced left ventricular end-systolic volume or enhanced maximal oxygen consumption in patients with coronary artery disease or LV dysfunction, and limiting heart failure or angina. The FOCUS trial was undertaken by the National Heart, Lung, and Blood Institute-sponsored Cardiovascular Cell Therapy Research Network.

Ninety two patients with chronic ischemic heart disease , having a left ventricular ejection fraction of 45% or less, a perfusion defect by single-photon emission tomography, or SPECT, who were no longer candidates for revascularization, were enrolled in the trial. Sixty one patients in the study were administered bone marrow cells through transendocardial injections while thirty one patients were administered placebo.

An assessment of primary endpoints at 6 months has revealed that there is no statistically significant difference between the treatment group and placebo arm in left ventricular end-systolic volume assessed by echocardiography, maximal oxygen consumption, and reversibility on SPECT. The secondary outcomes, including percent myocardial defect, total defect size, fixed defect size, regional wall motion, and clinical improvement, also has not exhibited any difference between the two arms.

However, according to the study authors, exploratory analyses have revealed that left ventricular ejection fraction improved in the treatment group compared with the placebo group by 2.7%.

The authors, led by Emerson Perin, concluded that the findings provide evidence for further studies to determine the relationship between the composition and function of bone marrow product and clinical end points. Understanding these relationships will improve the design and interpretation of future studies of cardiac cell therapy, the authors noted.

The results were published online March 24 in the Journal of the American Medical Association.

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Bone Marrow Stem Cell Therapy Trial - Clues, But No Answers

Recommendation and review posted by Bethany Smith

3/25/2012 10:50 AM ET (RTTNews) - An important clinical trial, which evaluated the use of autologous bone-marrow-cell therapy in patients with chronic ischemic heart failure, has failed to meet the prespecified end points of improvement in most measures of heart function, according to the results presented at the American College of Cardiology 2012 Scientific Sessions.

The trial dubbed, FOCUS - a phase II study, is the largest study to date to investigate if a patient's own bone marrow cells improved myocardial perfusion, reduced left ventricular end-systolic volume or enhanced maximal oxygen consumption in patients with coronary artery disease or LV dysfunction, and limiting heart failure or angina. The FOCUS trial was undertaken by the National Heart, Lung, and Blood Institute-sponsored Cardiovascular Cell Therapy Research Network.

Ninety two patients with chronic ischemic heart disease , having a left ventricular ejection fraction of 45% or less, a perfusion defect by single-photon emission tomography, or SPECT, who were no longer candidates for revascularization, were enrolled in the trial. Sixty one patients in the study were administered bone marrow cells through transendocardial injections while thirty one patients were administered placebo.

An assessment of primary endpoints at 6 months has revealed that there is no statistically significant difference between the treatment group and placebo arm in left ventricular end-systolic volume assessed by echocardiography, maximal oxygen consumption, and reversibility on SPECT. The secondary outcomes, including percent myocardial defect, total defect size, fixed defect size, regional wall motion, and clinical improvement, also has not exhibited any difference between the two arms.

However, according to the study authors, exploratory analyses have revealed that left ventricular ejection fraction improved in the treatment group compared with the placebo group by 2.7%.

The authors, led by Emerson Perin, concluded that the findings provide evidence for further studies to determine the relationship between the composition and function of bone marrow product and clinical end points. Understanding these relationships will improve the design and interpretation of future studies of cardiac cell therapy, the authors noted.

The results were published online March 24 in the Journal of the American Medical Association.

by RTT Staff Writer

For comments and feedback: editorial@rttnews.com

View post:
FOCUS : Bone Marrow Cell Therapy Trial Fails To Meet Goals

Recommendation and review posted by Bethany Smith

25 March 2012 Last updated at 13:00 ET By Eleanor Bradford BBC Scotland Health Correspondent

Scientists have discovered a gene which may make some people more susceptible to flu.

The gene was found by Edinburgh University researchers working with the Wellcome Trust Sanger Institute near Cambridge.

It may explain why apparently healthy people have needed intensive care after contracting swine flu, while others were unaware they had been infected.

The findings have been published in the journal Nature.

An analysis of the DNA of 60 patients in intensive care with flu revealed an unusually high number with a variant in a gene called IFITM3.

This gene produced a protein which hinders the spread of the flu virus in the lungs. The variant in this gene means less protein is produced and the flu virus can spread more easily.

Although the genetic variation is normally rare, it was 19-times more common than expected in people who needed hospital treatment.

Dr Kenneth Baillie, an expert in genetics and critical care at Edinburgh University's Roslin Institute, said: "During the pandemic it was very unusual for a healthy person to become desperately sick with flu but it did happen to some people.

"It was a mystery why it affected those people so severely when most people were hardly affected at all. This research explains a fraction of why those individuals were so susceptible."

Link:
Gene clue found for flu mystery

Recommendation and review posted by Bethany Smith

* Gene appears to determine people's ability to fight flu

* People could be screened for gene

* It may help develop new medicines for other viruses too

LONDON, March 25 (Reuters) - A genetic discovery could help explain why flu makes some people seriously ill or kills them, while others seem able to bat it away with little more than a few aches, coughs and sneezes.

In a study published in the journal Nature on Sunday, British and American researchers said they had found for the first time a human gene that influences how people respond to flu infections, making some people more susceptible than others.

The finding helps explain why during the 2009/2010 pandemic of H1N1 or "swine flu", the vast majority of people infected had only mild symptoms, while others - many of them healthy young adults - got seriously ill and died.

In future, the genetic discovery could help doctors screen patients to identify those more likely to be brought down by flu, allowing them to be selected for priority vaccination or preventative treatment during outbreaks, the researchers said.

It could also help develop new vaccines or medicines against potentially more dangerous viruses such as bird flu.

Paul Kellam of Britain's Sanger Institute, who co-led the study and presented the findings in a telephone briefing, said the gene, called ITFITM3, appeared to be a "crucial first line of defence" against flu.

When IFITM3 was present in large quantities, the spread of the virus in lungs was hindered, he explained. But when IFITM3 levels were lower, the virus could replicate and spread more easily, causing more severe symptoms.

Read this article:
Scientists find gene that can make flu a killer

Recommendation and review posted by Bethany Smith

25 March 2012 Last updated at 13:39 ET

Scientists have identified a genetic flaw that may explain why some people get more ill with flu than others.

Writing in Nature, the researchers said the variant of the IFITM3 gene was much more common in people hospitalised for flu than in the general population.

It controls a malformed protein, which makes cells more susceptible to viral infection.

Experts said those with the flaw could be given the flu jab, like other at-risk groups.

Researchers removed the gene from mice. They found that when they developed flu, their symptoms were much worse than those seen in mice with the gene.

Evidence from genetic databases covering thousands of people showed the flawed version of the gene is present in around one in 400 people.

The scientists, who came from the UK and US, then sequenced the IFITM3 genes of 53 patients who were in hospital with flu.

Three were found to have the variant - a rate of one in 20.

The researchers say these findings now need to be replicated in bigger studies. And they add it is probably only part of the genetic jigsaw that determines a person's response to flu.

Read the original:
'Severe flu' gene flaw identified

Recommendation and review posted by Bethany Smith

Public release date: 25-Mar-2012 [ | E-mail | Share ]

Contact: Michael Bernstein m_bernstein@acs.org 619-525-6268 (March 23-28, San Diego Press Center) 202-872-6042

Michael Woods m_woods@acs.org 619-525-6268 (March 23-28, San Diego Press Center) 202-872-6293 American Chemical Society

SAN DIEGO, March 25, 2012 Just as aspiring authors often read hundreds of books before starting their own, scientists are using decades of knowledge garnered from sequencing or "reading" the genetic codes of thousands of living things to now start writing new volumes in the library of life. J. Craig Venter, Ph.D., one of the most renowned of those scientists, described the construction of the first synthetic cell and many new applications of this work today at the 243rd National Meeting & Exposition of the American Chemical Society (ACS), the world's largest scientific society, which is underway this week.

In a plenary talk titled, "From Reading to Writing the Genetic Code," Venter described a fundamental shift in his field of genomics, and its promise for producing synthetic life that could help provide 21st century society with new fuels, medicines, food and nutritional products, supplies of clean water and other resources. Venter, a pioneer in the field, led the team at Celera Genomics that went head-to-head with the government-and-foundation-funded Human Genome Project in the race to decode the human genome. This quest, in which the 23,000 human genes were deciphered, ended with the teams declaring a tie and publishing simultaneous publications in 2001.

"Genomics is a rapidly evolving field and my teams have been leading the way from reading the genetic code deciphering the sequences of genes in microbes, humans, plants and other organisms to writing code and constructing synthetic cells for a variety of uses. We can now construct fully synthetic bacterial cells that have the potential to more efficiently and economically produce vaccines, pharmaceuticals, biofuels, food and other products."

The work Venter described at the ACS session falls within an ambitious new field known as synthetic biology, which draws heavily on chemistry, metabolic engineering, genomics and other traditional scientific disciplines. Synthetic biology emerged from genetic engineering, the now-routine practice of inserting one or two new genes into a crop plant or bacterium. The genes can make tomatoes, for instance, ripen without softening or goad bacteria to produce human insulin for treating diabetes. Synthetic biology, however, involves rearranging genes on a much broader scale that of a genome, which is an organism's entire genetic code to reprogram entire organisms and even design new organisms.

Venter and his team at the not-for-profit J. Craig Venter Institute (JCVI), which has facilities in Rockville, Maryland, and San Diego, announced in 2010 that they had constructed the world's first completely synthetic bacterial cell. Using computer-designed genes made on synthesizer machines from four bottles of chemicals, the scientists arranged those genes into a package, a synthetic chromosome. When inserted into a bacterial cell, the chromosome booted up the cell and was capable of dividing and reproducing.

In the ACS talk, Venter described progress on major projects, including developing new synthetic cells and engineering genomes to produce biofuels, vaccines, clean water, food and other products. That work is ongoing at both JCVI and at his company, Synthetic Genomics Inc. (SGI). A project at SGI for instance, aims to engineer algae cells to capture carbon dioxide and use it as a raw material for producing new fuels. Another group uses synthetic genomic advances with the goal of making influenza vaccines in hours rather than months to better respond to sudden mutations in those viruses.

Venter also described his work in sequencing the first draft human genome in 2001 while he and his team were at Celera Genomics, as well as the work on his complete diploid genome published in 2007 by scientists at JCVI, along with collaborators at The Hospital for Sick Children in Toronto and the University of California, San Diego. In addition to continued analysis of Venter's genome, he and his team are also studying the human microbiome, the billions of bacteria that live in and on people, and how these microbes impact health and disease.

Read more from the original source:
J. Craig Venter, Ph.D., describes biofuels, vaccines and foods from made-to-order microbes

Recommendation and review posted by Bethany Smith

ScienceDaily (Mar. 25, 2012) A genetic finding could help explain why influenza becomes a life-threating disease to some people while it has only mild effects in others. New research led by the Wellcome Trust Sanger Institute has identified for the first time a human gene that influences how we respond to influenza infection.

People who carry a particular variant of a gene called IFITM3 are significantly more likely to be hospitalised when they fall ill with influenza than those who carry other variants, the team found. This gene plays a critical role in protecting the body against infection with influenza and a rare version of it appears to make people more susceptible to severe forms of the disease. The results are published in the journal Nature.

A central question about viruses is why some people suffer badly from an infection and others do not. IFITM3 is an important protein that protects cells against virus infection and is thought to play a critical role in the immune system's response against such viruses as H1N1 pandemic influenza, commonly known as 'swine flu'. When the protein is present in large quantities, the spread of the virus in lungs is hindered, but if the protein is defective or absent, the virus can spread more easily, causing severe disease.

"Although this protein is extremely important in limiting the spread of viruses in cells, little is known about how it works in lungs," explains Aaron Everitt, first author from the Wellcome Trust Sanger Institute. "Our research plays a fundamental part in explaining how both the gene and protein are linked to viral susceptibility."

The antiviral role of IFITM3 in humans was first suggested by studies using a genetic screen, which showed that the protein blocked the growth of influenza virus and dengue virus in cells. This led the team to ask whether IFITM3 protected mice from viral infections. They removed the IFITM3 gene in mice and found that once they contracted influenza, the symptoms became much more severe compared to mice with IFITM3. In effect, they found the loss of this single gene in mice can turn a mild case of influenza into a fatal infection.

The researchers then sequenced the IFITM3 genes of 53 patients hospitalised with influenza and found that some have a genetic mutant form of IFITM3, which is rare in normal people. This variant alters the IFITM3 gene and makes cells more susceptible to viral infection.

"Since IFITM3 appears to be a first line defender against infection, our efforts suggest that individuals and populations with less IFITM3 activity may be at increased risk during a pandemic and that IFITM3 could be vital for defending human populations against other viruses such as avian influenza virus and dengue virus" says Dr. Abraham Brass, co-senior author and Assistant Professor at the Ragon Institute of MGH, MIT and Harvard and the Gastrointestinal Unit of Massachusetts General Hospital.

This research was a collaboration between institutes in the United States and the United Kingdom. The samples for this study were obtained from the MOSAIC consortium in England and Scotland, co-ordinated from the Centre for Respiratory Infection (CRI) at Imperial College London, and the GenISIS consortium in Scotland at the Roslin Institute of University of Edinburgh. These were pivotal for the human genetics component of the work.

"Collectively, these data reveal that the action of a single antiviral protein, IFITM3, can profoundly alter the course of the flu and potentially other viruses in both human and mouse," explains Professor Paul Kellam, co-senior author from the Wellcome Trust Sanger Institute. "To fully understand how both the protein and gene control our susceptibility to viral infections, we need to study the mechanisms of the gene variant more closely.

"Our research is important for people who have this variant as we predict their immune defences could be weakened to some virus infections. Ultimately as we learn more about the genetics of susceptibility to viruses, then people can take informed precautions, such as vaccination to prevent infection."

Visit link:
Genetics of flu susceptibility: Why the flu is life-threatening for some, and quite mild for others

Recommendation and review posted by Bethany Smith

Public release date: 25-Mar-2012 [ | E-mail | Share ]

Contact: Aileen Sheehy as22@sanger.ac.uk 44-122-349-2368 Wellcome Trust Sanger Institute

A genetic finding could help explain why influenza becomes a life-threating disease to some people while it has only mild effects in others. New research led by the Wellcome Trust Sanger Institute has identified for the first time a human gene that influences how we respond to influenza infection.

People who carry a particular variant of a gene called IFITM3 are significantly more likely to be hospitalised when they fall ill with influenza than those who carry other variants, the team found. This gene plays a critical role in protecting the body against infection with influenza and a rare version of it appears to make people more susceptible to severe forms of the disease. The results are published in the journal Nature.

A central question about viruses is why some people suffer badly from an infection and others do not. IFITM3 is an important protein that protects cells against virus infection and is thought to play a critical role in the immune system's response against such viruses as H1N1 pandemic influenza, commonly known as 'swine flu'. When the protein is present in large quantities, the spread of the virus in lungs is hindered, but if the protein is defective or absent, the virus can spread more easily, causing severe disease.

"Although this protein is extremely important in limiting the spread of viruses in cells, little is known about how it works in lungs," explains Aaron Everitt, first author from the Wellcome Trust Sanger Institute. "Our research plays a fundamental part in explaining how both the gene and protein are linked to viral susceptibility."

The antiviral role of IFITM3 in humans was first suggested by studies using a genetic screen, which showed that the protein blocked the growth of influenza virus and dengue virus in cells. This led the team to ask whether IFITM3 protected mice from viral infections. They removed the IFITM3 gene in mice and found that once they contracted influenza, the symptoms became much more severe compared to mice with IFITM3. In effect, they found the loss of this single gene in mice can turn a mild case of influenza into a fatal infection.

The researchers then sequenced the IFITM3 genes of 53 patients hospitalised with influenza and found that some have a genetic mutant form of IFITM3, which is rare in normal people. This variant gene encodes a shortened version of the protein which makes cells more susceptible to viral infection.

"Since IFITM3 appears to be a first line defender against infection, our efforts suggest that individuals and populations with less IFITM3 activity may be at increased risk during a pandemic and that IFITM3 could be vital for defending human populations against other viruses such as avian influenza virus and dengue virus" says Dr. Abraham Brass, co-senior author and Assistant Professor at the Ragon Institute and Gastrointestinal Unit of Massachusetts General Hospital.

This research was a collaboration between institutes in the United States and the United Kingdom. The samples for this study were obtained from the MOSAIC consortium in England and Scotland, co-ordinated from the Centre for Respiratory Infection (CRI) at Imperial College London, and the GenISIS consortium in Scotland at the Roslin Institute of the University of Edinburgh. These were pivotal for the human genetics component of the work.

The rest is here:
Genetics of flu susceptibility

Recommendation and review posted by Bethany Smith

25-03-2012 10:22 Dr Adelson aspirates bone marrow for concentration for stem cell therapy for musculoskeletal pain conditions

Read more from the original source:
bone marrow aspiration for stem cell therapy by Dr Adelson - Video

Recommendation and review posted by simmons

24-03-2012 07:46 This is the harvest of adipose tissue for combination with bone marrow aspirate concentrate for stem cell therapy

Here is the original post:
Adipose harvest for stem cell therapy by Dr Adelson - Video

Recommendation and review posted by simmons

3/25/2012 10:50 AM ET (RTTNews) - An important clinical trial, which evaluated the use of autologous bone-marrow-cell therapy in patients with chronic ischemic heart failure, has failed to meet the prespecified end points of improvement in most measures of heart function, according to the results presented at the American College of Cardiology 2012 Scientific Sessions.

The trial dubbed, FOCUS - a phase II study, is the largest study to date to investigate if a patient's own bone marrow cells improved myocardial perfusion, reduced left ventricular end-systolic volume or enhanced maximal oxygen consumption in patients with coronary artery disease or LV dysfunction, and limiting heart failure or angina. The FOCUS trial was undertaken by the National Heart, Lung, and Blood Institute-sponsored Cardiovascular Cell Therapy Research Network.

Ninety two patients with chronic ischemic heart disease , having a left ventricular ejection fraction of 45% or less, a perfusion defect by single-photon emission tomography, or SPECT, who were no longer candidates for revascularization, were enrolled in the trial. Sixty one patients in the study were administered bone marrow cells through transendocardial injections while thirty one patients were administered placebo.

An assessment of primary endpoints at 6 months has revealed that there is no statistically significant difference between the treatment group and placebo arm in left ventricular end-systolic volume assessed by echocardiography, maximal oxygen consumption, and reversibility on SPECT. The secondary outcomes, including percent myocardial defect, total defect size, fixed defect size, regional wall motion, and clinical improvement, also has not exhibited any difference between the two arms.

However, according to the study authors, exploratory analyses have revealed that left ventricular ejection fraction improved in the treatment group compared with the placebo group by 2.7%.

The authors, led by Emerson Perin, concluded that the findings provide evidence for further studies to determine the relationship between the composition and function of bone marrow product and clinical end points. Understanding these relationships will improve the design and interpretation of future studies of cardiac cell therapy, the authors noted.

The results were published online March 24 in the Journal of the American Medical Association.

by RTT Staff Writer

For comments and feedback: editorial@rttnews.com

See the article here:
Bone Marrow Stem Cell Therapy Trial - Clues, But No Answers

Recommendation and review posted by simmons