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Stem Cell Therapy Safely Repairs Damaged Heart Muscle in …

Using stem cells to repair damaged heart muscle in patients with chronic heart failure is safe and beneficial, whether the cells come from patients own bone marrow or from a healthy volunteer, according to a preliminary study by researchers at the Johns Hopkins University School of Medicine and the University of Miami Miller School of Medicine. In a study of 31 patients, the therapy reduced heart muscle scar tissue and improved their quality of life. For many patients in the study, the therapy also enhanced their hearts pumping ability.

An article describing the study, “Comparison of Allogeneic vs. Autologous Bone Marrow-Derived Mesenchymal Stem Cells Delivered by Transendocardial Injection in Patients with Ischemic Cardiomyopathy,” is published in the Journal of the American Medical Association (JAMA) on Nov. 6. Results are scheduled to be presented that same day at the American Heart Association Scientific Sessions in Los Angeles.

The researchers say this is the first study to compare autologous stem cells, which are derived from the patients’ own bone marrow, to allogeneic stem cells, taken from the marrow of healthy volunteers, in patients with heart disease. The advantage of using allogeneic cells is the potential for developing an off-the-shelf therapy that could be delivered in a more timely way, rather than requiring a bone marrow biopsy from heart failure patients and waiting for the cells to be processed. Also, stem cells from the patients themselves may not be as robust.

All of the study patients had longstanding ischemic cardiomyopathy – chronic heart failure caused by a prior heart attack that blocked blood flow to the heart and damaged heart muscle. The condition affects about 70 percent of the six million people in the United States who suffer from heart failure.

“The primary focus of our study was to determine the safety of the therapy, specifically within 30 days of the treatment,” says Gary Gerstenblith, M.D., professor of medicine at the Johns Hopkins University School of Medicine and co-author of the study. “We found that the treatment was safe and also that many of the patients experienced significant improvement, whether they had received the allogeneic or the autologous stem cells,” he says.

Patients in the study were randomly selected to have either their own stem cells or donated cells injected directly into their heart muscle. They were monitored for treatment-associated complications, such as death, heart attack, stroke, hospitalization for worsening heart failure and dangerous heart arrhythmias. All of the patients were still alive 12 months after the treatment.

The researchers were especially interested in learning whether the patients immune system would recognize the allogeneic (donated) stem cells as foreign and mount an immune response to reject the cells. Only 3.7 percent of the patients receiving the donated cells had such a response. The cells were injected into the heart muscle just once during a cardiac catheterization procedure.

The particular cells used for the therapy, mesenchymal stem cells, are less likely to stimulate an immune response and rejection than most other stem cells. They have the ability to repair muscular tissues and to reduce inflammation.

Patients in the allogeneic and autologous groups were further divided according to the doses of the stem cells they received. Three different doses were tested: 20 million cells, 100 million cells and 200 million cells.

“We generally think the more the better, but in fact, the lowest dose of 20 million cells appeared to be the most effective at improving the hearts pumping ability as well as reducing the extent of scar tissue,” says Peter Johnston, M.D., assistant professor of medicine at Johns Hopkins and co-author of the study.

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Faculty and Staff of the Stem Cell Center at Texas Heart …

Principal Investigators

Assistant Medical Director Guilherme V. Silva, MD

See Publications for articles and presentations by Stem Cell Center physician/scientists.

Staff

Assistant Director Jennifer Chambers, RN, BSN, CCRC

Research Nurse Practitioner Amadita Rodriguez, MS, RN, ANP

Clinical Research James Chen, RN, BSN, CCRC Nichole Piece, RN , CCRC Kerry Blakeney, RN Dia Tisdel-Pickens,MHA Erica Delano, BS, CCRP

Coordinator Assistants Tracye Dauphin Sara Sampaio

Executive Assistant to Dr. Perin Tanya Rojas

Research Scientists Maria da Graca Cabreira, PhD Elton Migliati, DVM, MS, PhD

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High-intensity sound waves may aid regenerative medicine

6 hours ago A cross section through a histotripsy lesion created in bovine liver tissue with the liquified cellular contents washed out revealing the remaining extracellular matrix. The scale bar represents 5mm. Credit: T.Khoklova/UW

Researchers at the University of Washington have developed a way to use sound to create cellular scaffolding for tissue engineering, a unique approach that could help overcome one of regenerative medicine’s significant obstacles. The researchers will present their technique at the 168th meeting of the Acoustical Society of America (ASA), held October 27-31, 2014, at the Indianapolis Marriott Downtown Hotel.

The development of the new technique started with somewhat of a serendipitous discovery. The University of Washington team had been studying boiling histotripsy – a technique that uses millisecond-long bursts of high-intensity ultrasound waves to break apart tissue – as a method to eliminate cancerous tumors by liquefying them with ultrasound waves. After the sound waves destroy the tumors, the body should eliminate them as cellular waste. When the researchers examined these ‘decellularized’ tissues, however, they were surprised by what the boiling left intact.

“In some of our experiments, we discovered that some of the stromal tissue and vasculature was being left behind,” said Yak-Nam Wang, a senior engineer at the University of Washington’s Applied Physics Laboratory. “So we had the idea about using this to decellularize tissues for tissue engineering and regenerative medicine.”

The structure that remains after decellularizing tissues is known as the extracellular matrix, a fibrous network that provides a scaffold for cells to grow upon. Most other methods for decellularizing tissues and organs involve chemical and enzymatic treatments that can cause damage to the tissues and fibers and takes multiple days. Histrostipsy, on the other hand, offers the possibility of fast decellularization of tissue with minimal damage to the matrix.

“In tissue engineering, one of the holy grails is to develop biomimetic structures so that you can replace tissues with native tissue,” Wang said. Stripping away cells from already developed tissue could provide a good candidate for these structures, since the extracellular matrix already acts as the cellular framework for tissue systems, Wang said.

Due to its bare composition, the matrix also induces only a relatively weak immune response from the host. The matrix could then theoretically be fed with stem cells or cells from the same person to effectively re-grow an organ.

“The other thought is that maybe you could just implant the extracellular matrix and then the body itself would self-seed the tissues, if it’s just a small patch of tissue that you’re replacing,” Wang said. “You won’t have any immune issues, and because you have this biomimetic scaffold that’s closer to the native tissue, healing would be better, and the body would recognize it as normal tissue.”

Wang is currently investigating decellularization of kidney and liver tissue from large animals. Future work involves increasing the size of the decellularized tissues and assessing their in-vivo regenerative efficacy.

Explore further: The future of regenerative medicine

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HEMACORD, the First FDA-Licensed Stem Cell Product, Wins Prix Galien USA "Best Biotechnology Product" Award

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Identifying the source of stem cells

7 hours ago Amy Ralston, MSU biochemist and molecular biologist, has identified a possible source of stem cells, which can advance regenerative and fertility research. Credit: G.L. Kohuth

When most animals begin life, cells immediately begin accepting assignments to become a head, tail or a vital organ. However, mammals, including humans, are special. The cells of mammalian embryos get to make a different first choice to become the protective placenta or to commit to forming the baby.

It’s during this critical first step that research from Michigan State University has revealed key discoveries. The results, published in the current issue of PLOS Genetics, provide insights into where stem cells come from, and could advance research in regenerative medicine. And since these events occur during the first four or five days of human pregnancy, the stage in which the highest percentage of pregnancies are lost, the study also has significant implications for fertility research.

Pluripotent stem cells can become any cell in the body and can be created in two ways. First, they can be produced when scientists reprogram mature adult cells. Second, they are created by embryos during this crucial four-day window of a mammalian pregnancy. In fact, this window is uniquely mammalian, said Amy Ralston, MSU assistant professor of biochemistry and molecular biology, and lead author on the study.

“Embryos make pluripotent stem cells with 100 percent efficiency,” she said. “The process of reprogramming cells, manipulating our own cells to become stem cells, is merely 1 percent efficient. Embryos have it figured out, and we need to learn how they’re doing it.”

The researchers’ first discovery is that in mouse embryos, the gene, Sox2, appears to be acting ahead of other genes traditionally identified as playing crucial roles in stem cell formation. Simply put, this gene could determine the source of stem cells in mammals. Now researchers are trying to decipher why Sox2 is taking the lead role.

“Now we know Sox2 is the first indicator that a cell is pluripotent,” Ralston said. “In fact, Sox2 may be the pre-pluripotent gene. We show that Sox2 is detectable in just one or two cells of the embryo earlier than previously thought, and earlier than other known stem cell genes.”

The second discovery is that Sox2 has broader influence than initially thought. The gene appears to help coordinate the cells that make the fetus and the other cells that establish the pregnancy and nurture the fetus.

Future research will focus on studying exactly why Sox2 is playing this role. The team has strong insights, but they want to go deeper, Ralston said.

“Reprogramming is amazing, but it’s inefficient,” she said. “What we’ve learned from the embryo is how to improve efficiency, a process that could someday lead to generating stem cells for clinical purposes with a much higher success rate.”

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Shinya Yamanaka – Wikipedia, the free encyclopedia

Shinya Yamanaka ( , Yamanaka Shin’ya?, born September 4, 1962) is a Japanese Nobel Prize-winning stem cell researcher.[1][2][3] He serves as the director of Center for iPS Cell Research and Application and a professor at the Institute for Frontier Medical Sciences at Kyoto University; as a senior investigator at the UCSF-affiliated J. David Gladstone Institutes in San Francisco, California; and as a professor of anatomy at University of California, San Francisco (UCSF). Yamanaka is also a past president of the International Society for Stem Cell Research (ISSCR).

He received the Wolf Prize in Medicine in 2011 with Rudolf Jaenisch;[6] the Millennium Technology Prize in 2012 together with Linus Torvalds. In 2012 he and John Gurdon were awarded the Nobel Prize for Physiology or Medicine for the discovery that mature cells can be converted to stem cells.[7] In 2013 he was awarded the $3 million Breakthrough Prize in Life Sciences for his work.

Yamanaka was born in Higashisaka Japan in 1962. After graduating from Tennji High School attached to Osaka Kyoiku University,[8] he received his M.D. at Kobe University in 1987 and his PhD at Osaka City University Graduate School in 1993. After this, he went through a residency in orthopedic surgery at National Osaka Hospital and a postdoctoral fellowship at the Gladstone Institute of Cardiovascular Disease, San Francisco.

Afterwards he worked at the Gladstone Institutes in San Francisco, USA and Nara Institute of Science and Technology in Japan. Yamanaka is currently Professor at Kyoto University, where he directs its Center for iPS Research and Application. He is also a senior investigator at the Gladstone Institutes as well as the director of the Center for iPS Cell Research and Application.[9]

Between 1987 and 1989, Yamanaka was a resident in orthopedic surgery at the National Osaka Hospital. His first operation, was removing a benign tumor from his friend Shuichi Hirata, a task he could not complete after one hour, when a skilled surgeon would take ten minutes or so. Some seniors referred to him as “Jamanaka”, a pun on the Japanese word for obstacle.[10]

From 1993 to 1996, he was at the Gladstone Institute of Cardiovascular Disease. Between 1996 and 1999, he was an assistant professor at Osaka City University Medical School, but found himself mostly looking after mice in the laboratory, not doing actual research.[10]

His wife advised him to become a practicing doctor, but instead he applied for a position at the Nara Institute of Science and Technology. He stated that he could and would clarify the characteristics of embryonic stem cells, and this can-do attitude won him the job. From 19992003, he was an associate professor there, and started the research that would later win him the 2012 Nobel Prize. He became a full professor and remained at the institute in that position from 20032005. Between 2004 and 2010, Yamanaka was a professor at the Institute for Frontier Medical Sciences.[11] Currently, Yamanaka is the director and a professor at the Center for iPS Cell Research and Application at Kyoto University.

In 2006, he and his team generated induced pluripotent stem cells (iPS cells) from adult mouse fibroblasts.[1] iPS cells closely resemble embryonic stem cells, the in vitro equivalent of the part of the blastocyst (the embryo a few days after fertilization) which grows to become the embryo proper. They could show that his iPS cells were pluripotent, i.e. capable of generating all cell lineages of the body. Later he and his team generated iPS cells from human adult fibroblasts,[2] again as the first group to do so. A key difference from previous attempts by the field was his team’s use of multiple transcription factors, instead of transfecting one transcription factor per experiment. They started with 24 transcription factors known to be important in the early embryo, but could in the end reduce it to 4 transcription factors Sox2, Oct4, Klf4 and c-Myc.[1]

Yamanaka practiced judo (2dan black belt) and played rugby as a university student. He also has a history of running marathons. After a 20-year gap, he competed in the inaugural Osaka Marathon in 2011 as a charity runner with a time of 4:29:53. He also took part in the 2012 Kyoto Marathon to raise money for iPS research, finishing in 4:03:19. He also ran in the second Osaka Marathon on November 25, 2012.[12]

In 2007, Yamanaka was recognized as a “Person Who Mattered” in the Time Person of the Year edition of Time Magazine.[13] Yamanaka was also nominated as a 2008 Time 100 Finalist.[14] In June 2010, Yamanaka was awarded the Kyoto Prize for reprogramming adult skin cells to pluripotential precursors. Yamanaka developed the method as an alternative to embryonic stem cells, thus circumventing an approach in which embryos would be destroyed.

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Stem Cell Therapy | stem cells fraud – Video



Stem Cell Therapy | stem cells fraud
http://www.arthritistreatmentcenter.com Too good to be true. And I was fooled also Japanese stem cell breakthrough, a fraud Reported by Rob Stein in Shots, a prestigious scientific journal…

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Gene research centre develops new Downs test

A NEW test for Downs syndrome could spare mothers-to-be the stress of amniocentesis and other invasive procedures.

Oxford Gene Technologys method checks an unborn babys DNA simply by analysing a blood sample from its mum. More accurate than existing blood tests or ultrasound scans, it is also safer for the foetus.

The Begbroke Science Park firm, which specialises in genetic research, has adapted its technology to work in pre-natal clinics.

The test can be used instead of amniocentesis or chorionic villus sampling, where a needle is pushed through the stomach wall to collect amniotic fluid for testing.

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Microbiologist Dr John Anson, who is president of research and development at Oxford Gene Technology, said: Blood is tested using a microscope glass slide which is printed with tiny spots of DNA in a sequence designed to bond to specific regions of DNA.

The spots act like biological magnets, which means we can be very selective about which part of the foetuss DNA we analyse.

OGT has finished pre-clinical trials and will now go ahead with large-scale testing.

If successful, it could be granted approval within 12 months, paving the way for the test to become available in ante-natal clinics.

Dr Anson added: This test is less risky for the unborn baby, carries less chance of infection and is potentially cost-saving.

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Sanford Study Reveals Fetal Alcohol Spectrum Disorders Prevalence in U.S.

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Newswise SIOUX FALLS, S.D. Nearly 5 percent of U.S. children may be affected by fetal alcohol spectrum disorders, according to a new study co-authored by Sanford Researchs Gene Hoyme, M.D., and Amy Elliott, Ph.D., and published by Pediatrics.

The study, Prevalence and characteristics of fetal alcohol spectrum disorders, explored the incidence of fetal alcohol spectrum disorders (FASD) among first-grade students, or 6 to 7 year olds, in a representative Midwestern U.S. community, which was Sioux Falls. According to Hoyme, students were enrolled from all the elementary schools in Sioux Falls, both public and parochial. The study is the first school-based ascertainment study to be completed as a measure of FASD prevalence in American children.

FASD are a group of conditions that can occur in the children of mothers who drank alcohol during pregnancy. Characteristics are both physical and cognitive and can include abnormal facial features, smaller-than-average physical growth, poor coordination, learning disabilities and vision and hearing problems.

The research team gathered data on two groups of children related to physical growth, development, dysmorphology, cognition and behavior. The first group was made up of small children who were in the 25th percentile or less in height, weight and head circumference; the second group, or the control group, was randomly selected. The mothers of children from both groups were interviewed for maternal risk related to alcohol consumption while pregnant.

Around 2.4 percent to 4.8 percent of all the children studied were found to have some form of FASD based on cognitive and physical attributes. Furthermore, women who had affected children displayed higher levels of weekend binge drinking before discovering they were pregnant, sought prenatal care later and less frequently and noted the fathers of their children were frequent drinkers.

Previous estimates of fetal alcohol spectrum disorders put the occurrence at around 1 percent in the United States, said Hoyme. By actively assessing the children who were part of this study, our team was able to develop a more accurate figure for the prevalence of this disorder among the predominately middle class population of Sioux Falls and identify key risk factors that can predict it.

Hoyme is internationally known for his work with FASD and also serves as president of Sanford Research and chief academic officer for Sanford Health. He has led FASD research studies in South Africa for the past 15 years and helped establish the prevalence rate in South Africa, which remains the highest documented rate in the world. In 2012, Hoyme was the recipient of the National Organization on Fetal Alcohol Syndrome Excellence Award, joining the ranks of almost 40 past recipients that include Senator John McCain and the late Ted Kennedy.

Elliott leads the Center for Health Outcomes and Prevention Research at Sanford Research and is involved with national and international investigations about FASD and its consequences. Amy Baete and Jaymi Russo, research staff of the Center for Health Outcomes and Prevention, also contributed to the study.

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UCLA Gene Discovery Shows How Stem Cells Can Be Activated to Help Immune System Respond to Infection

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Newswise In a study led by Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research member Dr. Julian Martinez-Agosto, UCLA scientists have shown that two genes not previously known to be involved with the immune system play a crucial role in how progenitor stem cells are activated to fight infection. This discovery lays the groundwork for a better understanding of the role progenitor cells can play in immune system response and could lead to the development of more effective therapies for a wide range of diseases.

The two-year study was published online October 30, 2014 ahead of print in the journal Current Biology.

Progenitor cells are the link between stem cells and fully differentiated cells of the blood system, tissues and organs. This maturation process, known as differentiation, is determined in part by the original environment that the progenitor cell came from, called the niche. Many of these progenitors are maintained in a quiescent state or “standby mode” and are ready to differentiate in response to immune challenges (such as stress, infection or disease).

Dr. Gabriel Ferguson, a postdoctoral fellow in the lab of Dr. Martinez-Agosto and first author of the study, built upon the lab’s previous research that utilized the blood system of the fruit fly species Drosophila, showing that a specific set of signals must be received by progenitor cells to activate their differentiation into cells that can work to fight infection after injury. Dr. Ferguson focused on two genes previously identified in stem cells but not in the blood system, named Yorkie and Scalloped, and discovered that they are required in a newly characterized cell type called a lineage specifying cell. These cells then essentially work as a switch, sending the required signal to progenitor cells.

The researchers further discovered that when the progenitor cells did not receive the required signal, the fly would not make the mature cells required to fight infection. This indicates that the ability of the blood system to fight outside infection and other pathogens is directly related to the signals sent by this new cell type.

“The beauty of this study is that we now have a system in which we can investigate how a signaling cell uses these two genes Yorkie and Scalloped, which have never before been shown in blood, to direct specific cells to be made,” said Dr. Martinez-Agosto, associate professor of human genetics. “It can help us to eventually answer the question of how our body knows how to make specific cell types that can fight infection.”

Drs. Martinez-Agosto and Ferguson and colleagues next hope that future studies will examine these genes beyond Drosophila and extend to mammalian models, and that the system will be used by the research community to study the role of the genes Yorkie and Scalloped in different niche environments.

“At a biochemical level, there is a lot of commonality between the molecular machinery in Drosophila and that in mice and humans,” said Dr. Ferguson. “This study can further our shared understanding of how the microenvironment can regulate the differentiation and fate of a progenitor or stem cell.”

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Speech 1311- Genetic Engineering – Video



Speech 1311- Genetic Engineering
Genetic Engineering, Stem cells and Cloning.

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New guidelines for reproductive & developmental toxicity testing of oligonucleotide drugs

PUBLIC RELEASE DATE:

30-Oct-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, October 30, 2014Oligonucleotide-based therapeutics present unique challenges when it comes to testing their potential to cause reproductive and developmental harm. New consensus guidelines for toxicity testing that take into consideration the combined chemical and biological characteristics of these novel biopharmaceuticals are presented in Nucleic Acid Therapeutics, a peer-reviewed journal from Mary Ann Liebert, Inc. publishers. The article is available free on the Nucleic Acid Therapeutics website until November 30, 2014.

Joy Cavagnaro, Access BIO (Boyce, VA), Cindy Berman, Berman Consulting (Wayland, MA), Doug Kornbrust, Preclinisight (Reno, NV), Tacey White, Exponent (Philadelphia, PA), Sarah Campion, Pfizer (Groton, CT), and Scott Henry, Isis Pharmaceuticals (Carlsbad, CA), coauthored the white paper that highlights key points to consider in the design of scientifically valid and predictive toxicity studies. The authors summarize the findings of the Reproductive Subcommittee of the Oligonucleotide Safety Working Group (OSWG) in the article “Considerations for Assessment of Reproductive and Developmental Toxicity of Oligonucleotide-Based Therapeutics.”

“I highly commend this latest white paper from the OSWG to researchers and regulators alike involved in the development and implementation of oligonucleotide or antisense based interventions,” says Executive Editor Graham C. Parker, PhD, The Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine, Children’s Hospital of Michigan, Detroit, MI.

Nucleic Acid Therapeutics is under the editorial leadership of Co-Editors-in-Chief Bruce A. Sullenger, PhD, Duke Translational Research Institute, Duke University Medical Center, Durham, NC, and C.A. Stein, MD, PhD, City of Hope National Medical Center, Duarte, CA; and Executive Editor Graham C. Parker, PhD.

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About the Journal

Nucleic Acid Therapeutics is an authoritative, peer-reviewed journal published bimonthly in print and online that focuses on cutting-edge basic research, therapeutic applications, and drug development using nucleic acids or related compounds to alter gene expression. Nucleic Acid Therapeutics is the official journal of the Oligonucleotide Therapeutics Society. Complete tables of content and a sample issue may be viewed on the Nucleic Acid Therapeutics website.

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Is space tourism safe or do civilians risk health effects?

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30-Oct-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

Rochelle, NY, October 30, 2014Several companies are developing spacecraft designed to take ordinary citizens, not astronauts, on short trips into space. “Space tourism” and short periods of weightlessness appear to be safe for most individuals according to a series of articles on space biomedicine published in New Space, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The articles are available free on the New Space website until November 30, 2014.

James Vanderploeg, MD, MPH and colleagues, University of Texas Medical Branch, Galveston, coauthored an article outlining the research that has been done to identify the risks and challenges involved in human commercial spaceflight. The authors describe the development of wearable biomedical monitoring equipment for spaceflight participants and of a medical and physiological database. In addition, the suthors also discuss topics such as the risk of electromagnetic interference and ionizing radiation to implanted medical devices in the article “The Human Challenges of Commercial Spaceflight: An Overview of Medical Research Conducted by the University of Texas Medical Branch Through the Federal Aviation Administration Center of Excellence.”

“One of the most important areas of New Space research is to determine whether there are biomedical conditions that would disqualify ordinary citizens from a short ride to the edge of space. This first rigorous, peer-reviewed work on a broad range of volunteers indicates most people can take that brief trip,” concludes Editor-in-Chief of New Space Prof. Scott Hubbard, Stanford University, in the Editorial “Space Biomedicine — Who Can Travel to the Final Frontier?”

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About the Journal

New Space facilitates and supports the efforts of researchers, engineers, analysts, investors, business leaders, and policymakers to capitalize on the opportunities of commercial space ventures. Spanning a broad array of topics including technological advancements, global policies, and innovative applications, the journal brings the new space community together to address the challenges and discover new breakthroughs and trends in this epoch of private and public/private space discovery. The Journal is published quarterly online with Open Access options and in print. Complete table of contents are available on the New Space website.

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Genetic factors behind surviving or dying from Ebola shown in mouse study

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30-Oct-2014

Contact: Leila Gray leilag@uw.edu 206-685-0381 University of Washington Health Sciences/UW Medicine

A newly developed mouse model suggests that genetic factors are behind the mild-to-deadly range of reactions to the Ebola virus.

People exposed to Ebola vary in how the virus affects them. Some completely resist the disease, others suffer moderate to severe illness and recover, while those who are most susceptible succumb to bleeding, organ failure and shock.

In earlier studies of populations of people who have contracted Ebola, these differences are not related to any specific changes in the Ebola virus itself that made it more or less dangerous; instead, the body’s attempts to fight infection seems to determine disease severity.

In the Oct. 30 edition of Science, scientists describe strains of laboratory mice bred to test the role of an individual’s genetic makeup in the course of Ebola disease. Systems biologists and virologists Angela Rasmussen and Michael Katze from the Katze Laboratory at the University of Washington Department of Microbiology led the study in collaboration with the National Institutes of Health’s Rocky Mountain Laboratories in Montana and University of North Carolina at Chapel Hill.

Research on Ebola prevention and treatment has been hindered by the lack of a mouse model that replicates the main characteristics of human Ebola hemorrhagic fever. The researchers had originally obtained this genetically diverse group of inbred laboratory mice to study locations on mouse genomes associated with influenza severity.

The research was conducted in a highly secure, state-of-the-art biocontainment safety level 4 laboratory in Hamilton, Mont. The scientists examined mice that they infected with a mouse form of the same species of Ebola virus causing the 2014 West Africa outbreak. The study was done in full compliance with federal, state, and local safety and biosecurity regulations. This type of virus has been used several times before in research studies. Nothing was done to change the virus.

Interestingly, conventional laboratory mice previously infected with this virus died, but did not develop symptoms of Ebola hemorrhagic fever.

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Alnylam to Webcast Presentation at the Nomura Biotechnology Conference

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New study pinpoints complex genetic origins for autoimmune diseases

Scores of autoimmune diseases afflicting one in 12 Americans ranging from type 1 diabetes, to multiple sclerosis (MS), to rheumatoid arthritis, to asthma mysteriously cause the immune system to harm tissues within our own bodies. Now, a new study pinpoints the complex genetic origins for many of these diseases, a discovery that may lead to better diagnosis and ultimately to improved treatments.

A team of scientists from UC San Francisco, the Broad Institute of MIT and Harvard, and Yale School of Medicine developed a new mathematical tool to more deeply probe existing DNA databases. In so doing they discovered how certain DNA variations, when inherited, are likely to contribute to disease.

By applying their method to analyzing data from previous studies of 21 different autoimmune diseases, the research team has deepened scientific understanding of the genetic underpinnings of a wide range of these disorders. They also found the specific immune cells most responsible for the diseases. Their study is published online on October 29, 2014 in Nature.

The researchers examined a wealth of data from 39 large-scale studies called genome-wide association studies (GWAS). Teams of scientists in recent years have conducted GWAS typically enlisting thousands of study participants to identify large blocks of DNA within the human genome within which genetic variants are implicated as risk factors for common diseases. But examination of GWAS data to date has seldom pointed to altered proteins, as surprisingly few protein-encoding gene variants within these broad swaths of DNA have been associated with the diseases under investigation.

Instead, the genetic risks identified through GWAS more often appear to be associated with DNA variations that do not reside within genes. The nature of this risk has defied understanding until now, fueling a perception that few medical benefits have thus far emerged from large-scale studies of human genetic variation being conducted in the wake of the initial Human Genome Project.

In the new study the researchers found that the presence of specific genetic variants in different autoimmune diseases can alter patterns of activity of genes in particular ways that affect functions of the immune system. This was true despite the fact that the genetic variants are not within genes.

To make their discoveries, the researchers developed software and used next-generation sequencing techniques to probe “epigenetic” characteristics of specialized immune cells, in which gene activity is affected without changes to the DNA sequence itself within the affected genes.

The team discovered that a majority of key DNA changes associated with autoimmune diseases occur in functional bits of DNA known as “enhancers.”

Although DNA exists within cells as long, stringy molecules, DNA can bend back upon itself with the support of the chromosome’s structural proteins, so that one piece of DNA may interact with another. Enhancers fold in this way to bind to DNA switches that turn genes on. In general the enhancers identified in the Nature study as playing a role in autoimmune disease were DNA sequences that did not match DNA-sequence motifs previously thought to be essential to enhancers, and had not previously been seen as having any functional role.

“Once again, research is revealing new meaning in the world of DNA once thought of as junk short, seemingly random DNA sequences that in fact serve meaningful roles in human physiology,” said Alex Marson, MD, PhD, UCSF Sandler Faculty Fellow and the corresponding author for the study.

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Fertility Center & Applied Genetics Sarasota, Great 5 Star Review – Video



Fertility Center Applied Genetics Sarasota, Great 5 Star Review
http://GeneticsAndFertility.com Call: 941-342-1568 Fertility Center Applied Genetics Sarasota reviews New review: Thanks to Dr. Pabon and his staff, we were able to complete…

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Download Molecular Genetics of Bacteria, 4th Edition PDF – Video



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Download Molecular Genetics of Bacteria, 4th Edition PDF – Video

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Seattle Genetics Reports Third Quarter 2014 Financial Results

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Seattle Genetics Reports Third Quarter 2014 Financial Results

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Seattle Genetics beats Street 3Q forecasts

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Seattle Genetics beats Street 3Q forecasts

Recommendation and review posted by Bethany Smith

Cancer Genetics, Inc. to Report Third Quarter 2014 Financial Results on Monday, November 10

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Cancer Genetics, Inc. to Report Third Quarter 2014 Financial Results on Monday, November 10

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United Cannabis Corp. Signs Exclusive Licensing and Distribution Agreement With DNA Genetics

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United Cannabis Corp. Signs Exclusive Licensing and Distribution Agreement With DNA Genetics

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Genetics, not upbringing, main influencer in a childs IQ, study says

Published October 30, 2014

Can parents make their kids smarter? New research published in the journal Intelligence suggests they cant influence intelligence at least beyond their genetic contribution.

To answer the oft-asked question, professors at Florida State University, the University of Nebraska, West Illinois University, King Abdulaziz in Saudi Arabia, and Erasmus University in the Netherlands used an adoption-based research design.

The study authors drew participants from a representative sample of between 5,500-7,000 non-adopted youth and a sample of between 250-300 adopted children from the National Longitudinal Study of Adolescent Health.

Researchers first administered a Picture Vocabulary Test (PVT) to middle and high school students and then repeated the test when the participants were between the ages of 18 and 26. The PVT served as an IQ test in which participants had to identify photos of people, places and things. Researchers also analyzed their parents behaviors.

Researchers found that parental socialization had no detectable influence on childrens intelligence later in life.

Previous research that has detected parenting-related behaviors affect intelligence is perhaps incorrect because it hasnt taken into account genetic transmission, study author Kevin Beaver, a criminology professor at FSU, said in a press release.

Some studies suggest that parents who interact with their kids over family dinners or by reading them bedtimes stories can boost their childrens IQ, while other research suggests that childrens IQs are only a product of their genetics.

Analyzing children who shared no DNA with their adoptive parents eliminated the possibility that parental socialization influenced a childs intelligence.

In previous research, it looks as though parenting is having an effect on child intelligence, but in reality the parents who are more intelligent are doing these things and it is masking the genetic transformation of intelligence to their children, Beaver said.

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Genetics, not upbringing, main influencer in a childs IQ, study says

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Bethany Hamilton Wins Inaugural Battle for the Breasts Event

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Bethany Hamilton Wins Inaugural Battle for the Breasts Event

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Atlas Genetics Selected to Present at Cavendish Global Health Impact Forum

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Atlas Genetics Selected to Present at Cavendish Global Health Impact Forum

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