Health Ranger calls for increased science education in America to combat scientific illiteracy
Scientific illiteracy has run rampant across America, with many scientists, doctors and journalists unable to carry on intelligent conversations about toxic heavy metals or the difference between...

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(MENAFN - The Peninsula) Researchers at Weill Cornell Medical College in Qatar (WCMC-Q) have published the first genetic map of the date palm, paving the way for Qatar to become a leader in date palm genetics and biotechnology.

The map shows the order in which the date palm's chromosomes are placed and which chromosome is responsible for reproduction.

In theory, the information could one day allow growers to manipulate the development of seeds, creating more female fruit-bearing plants than male plants,which do not produce dates. It also places Qatar at the head of research into the date palm, an important food source for much of the Middle East. The map has been produced by the genomics group under the direction of Dr Joel Malek, Assistant Professor of Genetic Medicine, in collaboration with Dr Karsten Suhre, Professor of Physiology and Biophysics, and with help from colleagues at the Ministry of Environment's Biotechnology Centre and its Department of Agricultural Affairs.

The programme 'Establishing World Leadership in Date Palm Research in Qatar' (NPRP-EP X-014-4-001) was funded by Qatar National Research Fund's NPRP Exceptional Proposal programme that provided 4.5m for the research.

Dr Malek said, "This is us laying the foundation for establishing world leadership in date palm research. To be a world leader, you have to have infrastructure and I consider this a genetic infrastructure that will allow us to be the leaders when it comes date palm biotechnology."

Three years ago, he and his team produced a draft version of the date palm genome which paved the way for the more accurate map. To create the map, Dr Malek and Dr Suhre worked with the centre and the Department of Agricultural Affairs. The ministry provided 150 seeds from a female tree and they were then propagated by Ameena Al Malki at the centre. Once they were large enough, leaves and DNA were taken from the seedlings. A new process 'genotyping-by-sequencing' was applied which sequenced portions of the genomes of all seedlings. It allowed the researchers to look at the parent tree and ascertain how it passed her DNA to her offspring.

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Qatar- First date palm genetic map made

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Accident Personal Injury Testimonial - Martyn Prowel Solicitors
http://www.martynprowel.co.uk/ We have several years expertise in representing clients in all kinds of personal injury claims where people have been injured through no fault of their own....

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Steve Ramsbottom and the SCI BC Peer Program
On March 29, 2014 Steve Ramsbottom presented and spoke about the benefits of physical activity for your overall well-being at our annual SCI Forum. This even...

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Individualized Medicine: Holly #39;s Story
The Center for Regenerative Medicine finds answers for patients like Holly based on new ways to use your genome and provide the best treatment available. Lea...

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Individualized Medicine: Holly's Story - Video

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PUBLIC RELEASE DATE:

14-May-2014

Contact: Katie Delach katie.delach@uphs.upenn.edu 215-349-5964 University of Pennsylvania School of Medicine

PHILADELPHIA Breastfeeding, tubal ligation also known as having one's "tubes tied" and oral contraceptives may lower the risk of ovarian cancer for some women with BRCA gene mutations, according to a comprehensive analysis from a team at the University of Pennsylvania's Basser Research Center for BRCA and the Abramson Cancer Center. The findings, a meta-analysis of 44 existing peer-reviewed studies, are published in the Journal of the National Cancer Institute.

The researchers, from Penn's Perelman School of Medicine, found that breastfeeding and tubal ligation are associated with reduced rates of ovarian cancer in BRCA1 mutation carriers, and the use of oral contraceptives is associated with a reduced risk of ovarian cancer in patients with BRCA1 or BRCA 2 mutations. The analysis also helped better define factors that may increase risk among this population: Smoking, for instance, may raise the risk of breast cancer for patients with a BRCA2 mutation. Though the team cautions that more data are required before definitive conclusions about these variables can be made, the findings help to shed light on non-surgical risk reduction options for women who may not be ready to undergo prophylactic removal of their ovaries to cut their cancer risk.

"Our analysis reveals that heredity is not destiny, and that working with their physicians and counselors, women with BRCA mutations can take proactive steps that may reduce their risk of being diagnosed with ovarian cancer," says lead author Timothy R. Rebbeck, PhD, professor of Epidemiology and Cancer Epidemiology and Risk Reduction Program Leader at Penn Medicine's Abramson Cancer Center. "The results of the analysis show that there is already sufficient information indicating how some variables might affect the risk of cancer for these patients."

BRCA1 and BRCA2 are human genes that produce tumor-suppressing proteins. A woman's risk of developing breast or ovarian cancer is notably increased if she inherits a harmful mutation in either the BRCA1 gene or the BRCA2 gene from either parent. Fifty-five to 65 percent of women who inherit a harmful BRCA1 mutation, and about 45 percent of women who inherit a harmful BRCA2 mutation will develop breast cancer by age 70, compared to approximately 12 percent of women in the general population. Thirty-nine percent of women who inherit a harmful BRCA1 mutation and up to 17 percent of women who inherit a harmful BRCA2 mutation will develop ovarian cancer by age 70, compared to only 1.4 percent of women in the general population. Both BRCA mutations have also been associated with increased risks of several other types of cancer.

Though the study's findings point to a helpful role for birth control pills in cutting ovarian cancer risk, the relationship between oral contraceptives and breast cancer risk was ambiguous. The authors say women and their health care providers should weigh the potential benefits of oral contraceptives (reduction in ovarian cancer risk, avoidance of unintended pregnancy, and regulation of menstrual cycles, for instance) against the potential risks (such as blood clots or the possible increased risk of breast cancer). There was also insufficient evidence to draw conclusions about the relationships between breastfeeding and tubal ligation, respectively, and breast cancer. Future research aims to examine these issues as well as how other variables, such as alcohol consumption, affect the risk of breast and ovarian cancer for BRCA mutation carriers. Since BRCA testing is relatively new, researchers have struggled to conduct large studies to examine these trends due to limited availability of large numbers of prospectively identified BRCA1/2 mutation carriers.

"Patients deserve better cancer-risk reduction options than surgically removing their healthy breasts and ovaries," said Susan Domchek, MD, executive director of the Basser Research Center for BRCA and co-author on the new paper. "It's imperative that we continue examining and building upon past research in this area so that we can provide BRCA mutation carriers with options at every age, and at every stage of their lives."

###

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Newswise PHILADELPHIA Breastfeeding, tubal ligation also known as having ones tubes tied and oral contraceptives may lower the risk of ovarian cancer for some women with BRCA gene mutations, according to a comprehensive analysis from a team at the University of Pennsylvania's Basser Research Center for BRCA and the Abramson Cancer Center. The findings, a meta-analysis of 44 existing peer-reviewed studies, are published in the Journal of the National Cancer Institute.

The researchers, from Penn's Perelman School of Medicine, found that breastfeeding and tubal ligation are associated with reduced rates of ovarian cancer in BRCA1 mutation carriers, and the use of oral contraceptives is associated with a reduced risk of ovarian cancer in patients with BRCA1 or BRCA 2 mutations. The analysis also helped better define factors that may increase risk among this population: Smoking, for instance, may raise the risk of breast cancer for patients with a BRCA2 mutation. Though the team cautions that more data are required before definitive conclusions about these variables can be made, the findings help to shed light on non-surgical risk reduction options for women who may not be ready to undergo prophylactic removal of their ovaries to cut their cancer risk.

Our analysis reveals that heredity is not destiny, and that working with their physicians and counselors, women with BRCA mutations can take proactive steps that may reduce their risk of being diagnosed with ovarian cancer, says lead author Timothy R. Rebbeck, PhD, professor of Epidemiology and Cancer Epidemiology and Risk Reduction Program Leader at Penn Medicine's Abramson Cancer Center. The results of the analysis show that there is already sufficient information indicating how some variables might affect the risk of cancer for these patients."

BRCA1 and BRCA2 are human genes that produce tumor-suppressing proteins. A woman's risk of developing breast or ovarian cancer is notably increased if she inherits a harmful mutation in either the BRCA1 gene or the BRCA2 gene from either parent. Fifty-five to 65 percent of women who inherit a harmful BRCA1 mutation, and about 45 percent of women who inherit a harmful BRCA2 mutation will develop breast cancer by age 70, compared to approximately 12 percent of women in the general population. Thirty-nine percent of women who inherit a harmful BRCA1 mutation and up to 17 percent of women who inherit a harmful BRCA2 mutation will develop ovarian cancer by age 70, compared to only 1.4 percent of women in the general population. Both BRCA mutations have also been associated with increased risks of several other types of cancer.

Though the study's findings point to a helpful role for birth control pills in cutting ovarian cancer risk, the relationship between oral contraceptives and breast cancer risk was ambiguous. The authors say women and their health care providers should weigh the potential benefits of oral contraceptives (reduction in ovarian cancer risk, avoidance of unintended pregnancy, and regulation of menstrual cycles, for instance) against the potential risks (such as blood clots or the possible increased risk of breast cancer). There was also insufficient evidence to draw conclusions about the relationships between breastfeeding and tubal ligation, respectively, and breast cancer. Future research aims to examine these issues as well as how other variables, such as alcohol consumption, affect the risk of breast and ovarian cancer for BRCA mutation carriers. Since BRCA testing is relatively new, researchers have struggled to conduct large studies to examine these trends due to limited availability of large numbers of prospectively identified BRCA1/2 mutation carriers.

Patients deserve better cancer-risk reduction options than surgically removing their healthy breasts and ovaries, said Susan Domchek, MD, executive director of the Basser Research Center for BRCA and co-author on the new paper. Its imperative that we continue examining and building upon past research in this area so that we can provide BRCA mutation carriers with options at every age, and at every stage of their lives.

Penn's Tara M. Friebel, MPH, is also an author of the paper.

Funding for the study was supported by the National Institutes of Health (R01-CA102776 and P50-CA083638) and the Basser Research Center for BRCA, the nation's first and only comprehensive center focused on prevention and treatment of BRCA-related cancers. In 2012, University of Pennsylvania alumni Mindy and Jon Gray gave a $25 million gift to establish the Basser Center in honor of Mindys sister, Faith Basser, who passed away at the age of 44 of ovarian cancer. Recently, the Grays committed an additional $5 million gift to support BRCA-related pancreatic cancer research as well as launch an external grants program to help advance science around the globe focused on BRCA-related research.

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Leadership

Michael Bamshad, MD Professor Division Chief

The Division of Genetic Medicine is committed to providing an outstanding level of patient care, education and research. The faculty have diverse interests and are drawn from several disciplines including clinical genetics, molecular genetics, biochemical genetics, human embryology/teratology and neurology.

A large clinical program of medical genetics operates from Seattle Childrens Hospital staffed by faculty from the Division. These clinical activities concentrate on pediatric genetics but also encompass adult and fetal consultations. At Seattle Children's full IP consultations are available and general genetics clinics occur regularly. Consultative services are also provided to the University of Washington Medical Center and Swedish Hospital. In addition, a variety of interdisciplinary clinical services are provided at Childrens including cardiovascular genetics, skeletal dysplasia, neurofibromatosis, craniofacial genetics, gender disorders, neurogenetics and biochemical genetics as well as others. A very large regional genetics service sponsored by state Departments of Health are provided to multiple outreach clinical sites in both Alaska and Washington.

Our research holds the promise for both continued development of improved molecular diagnostic tools and successful treatment of inherited diseases. Research in the Division is highly patient-driven. It often begins with a physician identifying a particular patients problems and subsequently taking that problem into a laboratory setting for further analysis. The Division has a strong research focus with established research programs in medical genetics information systems, neurogenetic disorders, fetal alcohol syndrome, neuromuscular diseases, human teratology, population genetics/evolution and gene therapy.

The Division offers comprehensive training for medical students, residents, and postdoctoral fellows in any of the areas of our clinical and research programs relevant to medical genetics. Medical Genetics Training Website

Margaret L.P. Adam, MD Associate Professor mpa5@u.washington.edu

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PUBLIC RELEASE DATE:

14-May-2014

Contact: Steve Graff stephen.graff@uphs.upenn.edu 215-301-5221 University of Pennsylvania School of Medicine

PHILADELPHIAWhile large genetic testing panels promise to uncover clues about patients' DNA, a team of researchers from Penn Medicine's Abramson Cancer Center (ACC)has found that those powerful tests tend to produce more questions than they answer. In a study of 278 women with early onset breast cancer who did not have the BRCA genes, the researchers found that only 2.5 percent of the patients had inherited mutations that were actually clinically actionable. Experts don't yet know how to interpret most of the mutations discovered by the testknown as massively parallel gene sequencing.

Results of the study, led by author Kara Maxwell, MD, PhD, a fellow in the division of Hematology-Oncology in the Perelman School of Medicine at the University of Pennsylvania, will be presented during the annual meeting of the American Society of Clinical Oncology (ASCO) in Chicago in early June (Abstract #1510).

Large genetic testing panels sometimes reveal mutations in genes that are associated with an increased risk in developing cancer. BRCA 1 and BRCA 2 genes are prime examples, where women can opt for mastectomies and ovary removal surgerywhich research shows slashes their risk of developing those cancers). However, there is not yet guidance for clinicians on how to care for patients who exhibit other types of mutations, such as CHEK2 and ATM. These are known as variants of unknown significance (VUS).

"We're in a time where the testing technology has outpaced what we know from a clinical standpoint. There's going to be a lot of unknown variants that we're going to have to deal with as more patients undergo large genetic testing panels," said Maxwell. "It's crucial that we figure out the right way to counsel women on these issues, because it can really provoke a lot of anxiety for a patient when you tell them, 'We found a change in your DNA and we don't know what it means.'"

The team, which includes Susan Domchek, MD, the Basser Professor in Oncology and director of the Basser Research Center for BRCA in Penn's ACC, and Katherine Nathanson, MD, an associate professor in the division of Translational Medicine and Chief Oncogenomics Physician for the ACC, studied 278 patients who had been diagnosed with breast cancer under the age of 40, were not carriers of the BRCA1 or BRCA2 mutations, and had no family history of ovarian cancer.

The researchers performed massively parallel gene sequencing to detect 22 known or proposed breast cancer susceptibility genes in each woman. Though the testing did reveal multiple variants of genes that are known to confer increased risk of breast cancer in patients who develop the disease young, only 2.5 percent of patients tested were found to have mutations that are actionable under current treatment guidelines, including TP53, CDKN2A, MSH2, and MUTYH.

In all, the sequencing revealed reportable variants in over 30 percent of the patients.

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Large panel genetic testing produces more questions than answers in breast cancer

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Before you enjoy your next slice of gouda or wedge of brie, you might take a moment to think of all the organisms that have nibbled it before you. Cheeses get the flavors you love from the bacteria and fungi that live on and inside them. And thanks to genetic testing, those microscopic workers are toiling in anonymity no longer.

Some cheese microorganisms have effects you can easily see. Bacteria leave behind bubbles of carbon dioxide in Swiss. Mold sends blue veins through Stilton. But except for fresh varieties like ricotta or goat cheese, every cheese you taste has been ripened by microbes. Some are starter bacteria added to the milk at the beginning of the process; others are smeared on the outside of the cheese after its formed, or allowed to land and grow there naturally from the environment. As these microbes break down the cheeses fats and proteins, the molecules they leave behind create its flavor.

Most studies focusing on cheese surface bacteria [have] focused on soft cheese, says Stephan Schmitz-Esser, a researcher at the Institute for Milk Hygiene at the University of Veterinary Medicine in Vienna, Austria. He and his coauthors decided to investigate a hard cheese instead: Vorarlberger Bergkse, which well call VB. This artisanal Austrian cheese starts with raw cows milk (from Alpine pastures, Schmitz-Esser notes) and a certain set of added bacterial cultures.* The cheese ripens for 3 to 18 months while its outside is washed or brushed periodically with salt. Finally its sold in wheels weighing nearly 70 pounds.

Schmitz-Esser visited three Austrian cheese facilities, with a total of seven cheese-ripening cellars. From each cellar, he gathered scrapings from the rinds of 25 to 30 cheese wheels and pooled them into one sample.Then the researchers sequenced the RNA within each sample to look for recognizable bacterial and fungal genes.

On the genus level, Schmitz-Esser says, most of the microorganisms they found (such asBrevibacterium, Brachybacterium, and Corynebacterium)are similar to those seen in other cheeses. But within these broad types of bacteria, the species living on VB make up a unique community, different from other cheeses. Several of the bacteria that turned up may even be new species, the authors write.

(Four out of the seven samples also included small amounts of DNA from a bug: namely, the miteAcarus immobilis. Certain cheeses are traditionally ripened by mites, the authors point outbut lets not dwell on that any longer.)

Each of the three cheese-making facilities had a different microbial signature. When cheeses were broken down by ageyounger batches, which had been ripening for less than six months, versus older onesthere was also a significant difference between their microbial communities. Our results suggest that facilities may have an influence on cheese microbes, Schmitz-Esser says. But the most distinct changes were found with respect to ripening time.

Surprisingly, the most abundant species on VB cheese wereHalomonas bacteria. In the past, these bacteria were thought to show that a dairy facility just wasnt clean. But the salt-loving microbes, which come from the ocean, may reach cheeses via brine treatments. We think that [Halomonas]may have an important role in cheese ripening, Schmitz-Esser says. But for now, the evidence is only circumstantial. We currently dont know anything about the function of Halomonas.

In the long term, Schmitz-Esser hopes studies like this one can lead to even better cheese. Clearly the microbial communities are key to flavor production, he says.Figuring out how different microbes contribute to cheese ripeninghow their actions create those signature flavorscould help cheese producers create exactly what they want. For now, though, the first step is to identify who is there.

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Genetic Test Shows Who's Who in Cheese Bacteria (and Fungus)

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Dyann Wirth (2013) Malaria: "Genetics and Global Health"
Professor Dyann Wirth (Harvard School of Public Health) gave this seminar on Genetics and Global Health in Barcelona on 8 May 2013. The talk was the second of the Global Health Lectures series,...

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Dyann Wirth (2013) Malaria: "Genetics and Global Health" - Video

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anon113973 Post 5

this is good and all, but you will never be able to figure everything out. We are just not God, my thoughts on trying to perfect every little thing the human mind tries to figure out? Just leave that 1 percent alone.

@ Georgesplane- A few years past the turn of the millennium, scientists from the U.S Department of Energy, the National Human Genome Research Institute, and the International Human genome Sequencing Consortium completed the mapping of the human genome. The Human Genome is the map of human genetics; a complete list of the 3 billion base pairs that make up human DNA.

The mapping and sequencing of the genome is 99% complete, but scientists are still working on determining what every gene does (the other 1% cannot be mapped until new technologies are invented). As scientists learn more about the purpose of the different base pairs and genes, they will be able to develop better drugs, create better diagnostic tools, and better manage genetic diseases.

Just like anything else, though, the understanding of genetics can open the window for potential harm. With the advancement of bioengineering, comes the potential for bioengineered threats. This is why the bulletin of Atomic Scientists have added biosecurity to the list of threats monitored in the overview of the doomsday clock.

What is the Human Genome? Is this part of the study of genetics? If so, has the government or researchers finished mapping the Human Genome? Additionally, what is the significance of the Human Genome? Is it going to allow us to change our genetics, orwhat exactly is the genome going to be used for?

The study of human haplogroup population genetics focuses on tracing haplogroups of Y-chromosome (paternal) and mitochondrial (maternal) DNA. This study shows a very high amount of commonalities in haplogroups among people groups of surprising geographic distance. This field, although still advancing from its early stages, indicates a common ancestor for all human beings (Mitochondrial Eve) from whom all mitochondrial DNA is derived.

In the past, geneticists have made the fatal error of assigning value to certain traits over others and assuming an inequity in the quality of life based on which genes a person has inherited. Such misconceptions led to Eugenics and the belief in Racial Superiority. It is helpful to recognize the fact that, although genes differ, they allow us humans to complement each other very well, with a recognition that greater diversity is both effective and beautiful.

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What is Genetics? (with pictures) - wiseGEEK

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Newswise NEW BRUNSWICK, N.J. The National Institute on Drug Abuse (NIDA) has awarded a five-year contract worth up to $19 million to RUCDR Infinite Biologics, a unit of Rutgers Human Genetics Institute of New Jersey. The worlds largest university-based biorepository, RUCDR Infinite Biologics is located on Rutgers Busch Campus in Piscataway.

Under the new contract, RUCDR will expand and enhance the services it provides through its NIDA Center for Genetic Studies, which it has supported for the past 15 years. The Center provides genomic services to NIDA-funded researchers.

Because the Rutgers operation has been continuously acquiring new equipment and systems, and refining the techniques its staff employs, the genomic testing and analysis for NIDA studies will be significantly more sophisticated than in previous years, according to Jay Tischfield, CEO and founder of RUCDR Infinite Biologics and the Duncan and Nancy Macmillan Distinguished Professor of Genetics at Rutgers.

Under this new contract with NIDA, we will be utilizing innovative technologies to support research, such as microarray typing and high-throughput sequencing for genomic and epigenomic analyses, Tischfield said. We also will support NIDA projects that employ induced pluripotent stem cells to facilitate the molecular and cellular study of brain development and addiction processes.

The NIDA Center for Genetic Studies is a scientific resource for informing the human molecular genetics of drug addiction. The center stores clinical and diagnostic data, pedigree information and biomaterials (including DNA, plasma, cryopreserved lymphocytes and/or cell lines) from human subjects participating in studies that form the NIDA Genetics Consortium.

The contract includes receiving data along with blood samples or other biospecimens from funded grants and/or contracts supporting research on the genetics of addiction and addiction vulnerability; processing these data and materials to create databases, serum, DNA, RNA and cell lines; distributing all data and materials in the NIDA Human Genetics Initiative to qualified investigators; and maintaining storage of data and biomaterials.

RUCDR has a similar agreement with the National Institute of Mental Health to support the NIMH Center for Collaborative Genomics Research on Mental Disorders, which provides services to NIMH-funded scientists studying mental disorders. A $44.5 million, five-year cooperative agreement renewal was awarded in 2013.

About RUCDR Infinite Biologics RUCDR Infinite Biologics offers a complete and integrated selection of biological sample processing, analysis and biorepository services to government agencies, academic institutions, foundations and biotechnology and pharmaceutical companies within the global scientific community. RUCDR Infinite Biologics provides DNA, RNA and cell lines with clinical data to hundreds of research laboratories for studies on mental health and developmental disorders, drug and alcohol abuse, diabetes and digestive, liver and kidney diseases. RUCDR completed an $11.8 million expansion and renovation of its facilities last year. Read more at http://www.rucdr.org.

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Newswise May 13, 2014 (BRONX, NY) Healthy stem cells work to restore or repair the bodys tissues, but cancer stem cells have a more nefarious mission: to spawn malignant tumors. Cancer stem cells were discovered a decade ago, but their origins and identity remain largely unknown.

Today, the Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research at Albert Einstein College of Medicine of Yeshiva University hosted its second Stem Cell Symposium, focusing on cancer stem cells. Leading scientists from the U.S., Canada and Belgium discussed the latest advances in the field and highlighted the challenges of translating this knowledge into targeted cancer treatments.

These exceptional scientists are pioneers in the field and have made enormous contributions to our understanding of the biology of stem cells and cancer, said Paul Frenette, M.D., director and chair of Einsteins Stem Cell Institute and professor of medicine and of cell biology. Hopefully this symposium will spark productive dialogues and collaborations among the researchers who attend.

The presenters were:

Cancer Stem Cells and Malignant Progression, Robert A. Weinberg, Ph.D., Daniel K. Daniel K. Ludwig Professor for Cancer Research Director, Ludwig Center of the Massachusetts Institute of Technology; Member, Whitehead Institute for Biomedical Research Towards Unification of Cancer Stem Cell and Clonal Evolution Models of Intratumoral Heterogeneity, John Dick, Ph.D., Canada Research Chair in Stem Cell Biology and senior scientist, Princess Margaret Cancer Center, University Health Network; professor of molecular genetics, University of Toronto Normal and Neoplastic Stem Cells, Irving L. Weissman, M.D., Director, Institute for Stem Cell Biology and Regenerative Medicine and Director, Stanford Ludwig Center for Cancer Stem Cell Research and Medicine; Professor of Pathology and Developmental Biology, Stanford University School of Medicine Cell Fate Decisions During Tumor Formation, Leonard I. Zon, M.D., Grousbeck Professor of Pediatric Medicine, Director, Stem Cell Research Program, Howard Hughes Medical Institute/Boston Children's Hospital, Harvard Medical School Skin Stem Cells in Silence, Action and Cancer, Elaine Fuchs, Ph.D., Rebecca C. Lancefield Professor, Laboratory of Mammalian Cell Biology and Development, Howard Hughes Medical Institute/The Rockefeller University Mechanism Regulating Stemness in Skin Cancer, Cdric Blanpain, M.D., Ph.D., professor of stem cell and developmental biology, WELBIO, Interdisciplinary Research Institute, Universit Libre de Bruxelles Mouse Models of Malignant GBM: Cancer Stem Cells and Beyond, Luis F. Parada, Ph.D., professor and chairman, Diana K and Richard C. Strauss Distinguished Chair in Developmental Biology; Director, Kent Waldrep Foundation Center for Basic Neuroscience Research; Southwestern Ball Distinguished Chair in Nerve Regeneration Research, University of Texas Southwestern Medical Center

***

About Albert Einstein College of Medicine of Yeshiva University

Albert Einstein College of Medicine of Yeshiva University is one of the nations premier centers for research, medical education and clinical investigation. During the 2013-2014 academic year, Einstein is home to 734 M.D., 236 Ph.D. students, 106 students in the combined M.D./Ph.D. program, and 353 postdoctoral research fellows. The College of Medicine has more than 2,000 full-time faculty members located on the main campus and at its clinical affiliates. In 2013, Einstein received more than $155 million in awards from the National Institutes of Health (NIH). This includes the funding of major research centers at Einstein in diabetes, cancer, liver disease, and AIDS. Other areas where the College of Medicine is concentrating its efforts include developmental brain research, neuroscience, cardiac disease, and initiatives to reduce and eliminate ethnic and racial health disparities. Its partnership with Montefiore Medical Center the University Hospital and academic medical center for Einstein, advances clinical and translational research to accelerate the pace at which new discoveries become the treatments and therapies that benefit patients. Through its extensive affiliation network involving Montefiore, Jacobi Medical CenterEinsteins founding hospital, and five other hospital systems in the Bronx, Manhattan, Long Island and Brooklyn, Einstein runs one of the largest residency and fellowship training programs in the medical and dental professions in the United States. For more information, please visit http://www.einstein.yu.edu, read our blog, follow us on Twitter, like us on Facebook, and view us on YouTube.

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Using new stem cell technology, scientists at the Salk Institute have shown that neurons generated from the skin cells of people with schizophrenia behave strangely in early developmental stages, providing a hint as to ways to detect and potentially treat the disease early.

The findings of the study, published online in April's Molecular Psychiatry, support the theory that the neurological dysfunction that eventually causes schizophrenia may begin in the brains of babies still in the womb.

"This study aims to investigate the earliest detectable changes in the brain that lead to schizophrenia," says Fred H. Gage, Salk professor of genetics. "We were surprised at how early in the developmental process that defects in neural function could be detected."

Currently, over 1.1 percent of the world's population has schizophrenia, with an estimated three million cases in the United States alone. The economic cost is high: in 2002, Americans spent nearly $63 billion on treatment and managing disability. The emotional cost is higher still: 10 percent of those with schizophrenia are driven to commit suicide by the burden of coping with the disease.

Although schizophrenia is a devastating disease, scientists still know very little about its underlying causes, and it is still unknown which cells in the brain are affected and how. Previously, scientists had only been able to study schizophrenia by examining the brains of patients after death, but age, stress, medication or drug abuse had often altered or damaged the brains of these patients, making it difficult to pinpoint the disease's origins.

The Salk scientists were able to avoid this hurdle by using stem cell technologies. They took skin cells from patients, coaxed the cells to revert back to an earlier stem cell form and then prompted them to grow into very early-stage neurons (dubbed neural progenitor cells or NPCs). These NPCs are similar to the cells in the brain of a developing fetus.

The researchers generated NPCs from the skin cells of four patients with schizophrenia and six people without the disease. They tested the cells in two types of assays: in one test, they looked at how far the cells moved and interacted with particular surfaces; in the other test, they looked at stress in the cells by imaging mitochondria, which are tiny organelles that generate energy for the cells.

On both tests, the Salk team found that NPCs from people with schizophrenia differed in significant ways from those taken from unaffected people.

In particular, cells predisposed to schizophrenia showed unusual activity in two major classes of proteins: those involved in adhesion and connectivity, and those involved in oxidative stress. Neural cells from patients with schizophrenia tended to have aberrant migration (which may result in the poor connectivity seen later in the brain) and increased levels of oxidative stress (which can lead to cell death).

These findings are consistent with a prevailing theory that events occurring during pregnancy can contribute to schizophrenia, even though the disease doesn't manifest until early adulthood. Past studies suggest that mothers who experience infection, malnutrition or extreme stress during pregnancy are at a higher risk of having children with schizophrenia. The reason for this is unknown, but both genetic and environmental factors likely play a role.

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Harvard scientists have merged stem cell and organ-on-a-chip technologies to grow, for the first time, functioning human heart tissue carrying an inherited cardiovascular disease. The research appears to be a big step forward for personalized medicine because it is working proof that a chunk of tissue containing a patient's specific genetic disorder can be replicated in the laboratory.

The work, published in May 2014 in Nature Medicine, is the result of a collaborative effort bringing together scientists from the Harvard Stem Cell Institute, the Wyss Institute for Biologically Inspired Engineering, Boston Children's Hospital, the Harvard School of Engineering and Applied Sciences, and Harvard Medical School. It combines the organs-on-chips expertise of Kevin Kit Parker, PhD, and stem cell and clinical insights by William Pu, MD.

A release from Harvard explains that using their interdisciplinary approach, the investigators modeled the cardiovascular disease Barth syndrome, a rare X-linked cardiac disorder caused by mutation of a single gene called Tafazzin, or TAZ. The disorder, which is currently untreatable, primarily appears in boys, and is associated with a number of symptoms affecting heart and skeletal muscle function.

The researchers took skin cells from two Barth syndrome patients, and manipulated the cells to become stem cells that carried these patients' TAZ mutations. Instead of using the stem cells to generate single heart cells in a dish, the cells were grown on chips lined with human extracellular matrix proteins that mimic their natural environment, tricking the cells into joining together as they would if they were forming a diseased human heart. The engineered diseased tissue contracted very weakly, as would the heart muscle seen in Barth syndrome patients. The investigators then used genome editinga technique pioneered by Harvard collaborator George Church, PhDto mutate TAZ in normal cells, confirming that this mutation is sufficient to cause weak contraction in the engineered tissue. On the other hand, delivering the TAZ gene product to diseased tissue in the laboratory corrected the contractile defect, creating the first tissue-based model of correction of a genetic heart disease. The release quotes Parker as saying, "You don't really understand the meaning of a single cell's genetic mutation until you build a huge chunk of organ and see how it functions or doesn't function. In the case of the cells grown out of patients with Barth syndrome, we saw much weaker contractions and irregular tissue assembly. Being able to model the disease from a single cell all the way up to heart tissue, I think that's a big advance."

Furthermore, the scientists discovered that the TAZ mutation works in such a way to disrupt the normal activity of mitochondria, often called the power plants of the cell for their role in making energy. However, the mutation didn't seem to affect overall energy supply of the cells. In what could be a newly identified function for mitochondria, the researchers describe a direct link between mitochondrial function and a heart cell's ability to build itself in a way that allows it to contract. "The TAZ mutation makes Barth syndrome cells produce an excess amount of reactive oxygen species or ROSa normal byproduct of cellular metabolism released by mitochondriawhich had not been recognized as an important part of this disease," said Pu, who cares for patients with the disorder. "We showed that, at least in the laboratory, if you quench the excessive ROS production then you can restore contractile function," Pu added. "Now, whether that can be achieved in an animal model or a patient is a different story, but if that could be done, it would suggest a new therapeutic angle." His team is now trying to translate this finding by doing ROS therapy and gene replacement therapy in animal models of Barth syndrome to see if anything could potentially help human patients. At the same time, the scientists are using their human 'heart disease-on-a-chip' as a testing platform for drugs that are potentially under trial or already approved that might be useful to treat the disorder.

"We tried to thread multiple needles at once and it certainly paid off," Parker said. "I feel that the technology that we've got arms industry and university-based researchers with the tools they need to go after this disease." Both Parker and Pu, who first talked about collaborating at a 2012 Stockholm conference, credit their partnership and scientific consilience for the success of this research. Parker asserted that the 'organs-on-chips' technology that has been a flagship of his lab only worked so fast and well because of the high quality of Pu's patient-derived cardiac cells. "When we first got those cells down on the chip, Megan, one of the joint first authors, texted me 'this is working,'" he recalled. "We thought we'd have a much harder fight." "When I'm asked what's unique about being at Harvard, I always bring up this story," Pu said. "The diverse set of people and cutting-edge technology available at Harvard certainly made this study possible." The researchers also involved in this work include: Joint first authors Gang Wang, MD, of Boston Children's Hospital, and Megan McCain, PhD, who earned her degree at the Harvard School of Engineering and Applied Sciences and is now an assistant professor at the University of Southern California. Amy Roberts, MD, of Boston Children's Hospital, and Richard Kelley, MD, PhD, at the Kennedy Krieger Institute provided patient data and samples, and Frdric Vaz, PhD, and his team at the Academic Medical Center in the Netherlands conducted additional analyses. Technical protocols were shared by Kenneth Chien, MD, PhD, at the Karolinska Institutet.

Kevin Kit Parker, PhD, is the Tarr Family Professor of Bioengineering and Applied Physics in Harvard's School of Engineering and Applied Sciences, a Core Faculty member of the Wyss Institute for Biologically Inspired Engineering, and a Principal Faculty member of the Harvard Stem Cell Institute. William Pu, MD, is an Associate Professor at Harvard Medical School, a member of the Department of Cardiology at Boston Children's Hospital, and an Affiliated Faculty member of the Harvard Stem Cell Institute. George Church, PhD, is a Professor of Genetics at Harvard Medical School and a Core Faculty member of the Wyss Institute of Biologically Inspired Engineering. The work was supported by the Barth Syndrome Foundation, Boston Children's Hospital, the National Institutes of Health, and charitable donations from Edward Marram, Karen Carpenter, and Gail Federici Smith.

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Stem Cells Make Heart Disease-on-a-Chip

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Newswise LA JOLLAUsing new stem cell technology, scientists at the Salk Institute have shown that neurons generated from the skin cells of people with schizophrenia behave strangely in early developmental stages, providing a hint as to ways to detect and potentially treat the disease early.

The findings of the study, published online in April's Molecular Psychiatry, support the theory that the neurological dysfunction that eventually causes schizophrenia may begin in the brains of babies still in the womb.

"This study aims to investigate the earliest detectable changes in the brain that lead to schizophrenia," says Fred H. Gage, Salk professor of genetics. "We were surprised at how early in the developmental process that defects in neural function could be detected."

Currently, over 1.1 percent of the world's population has schizophrenia, with an estimated three million cases in the United States alone. The economic cost is high: in 2002, Americans spent nearly $63 billion on treatment and managing disability. The emotional cost is higher still: 10 percent of those with schizophrenia are driven to commit suicide by the burden of coping with the disease.

Although schizophrenia is a devastating disease, scientists still know very little about its underlying causes, and it is still unknown which cells in the brain are affected and how. Previously, scientists had only been able to study schizophrenia by examining the brains of patients after death, but age, stress, medication or drug abuse had often altered or damaged the brains of these patients, making it difficult to pinpoint the disease's origins.

The Salk scientists were able to avoid this hurdle by using stem cell technologies. They took skin cells from patients, coaxed the cells to revert back to an earlier stem cell form and then prompted them to grow into very early-stage neurons (dubbed neural progenitor cells or NPCs). These NPCs are similar to the cells in the brain of a developing fetus.

The researchers generated NPCs from the skin cells of four patients with schizophrenia and six people without the disease. They tested the cells in two types of assays: in one test, they looked at how far the cells moved and interacted with particular surfaces; in the other test, they looked at stress in the cells by imaging mitochondria, which are tiny organelles that generate energy for the cells.

On both tests, the Salk team found that NPCs from people with schizophrenia differed in significant ways from those taken from unaffected people.

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New Stem Cell Research Points to Early Indicators of Schizophrenia

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May 14, 2014, 4 a.m.

STEM cell therapy is the great frontier of todays medical research.

STEM cell therapy is the great frontier of todays medical research.

While still in its infancy, stem cell technology has already moved from being a promising idea to delivering life-saving treatment for conditions such as leukaemia.

Last week about 70 people gathered at the Mid City Motel, Warrnambool, to hear about the advances from one of Australias leading researchers.

Stem cell researcher, Professor Graham Jenkin.

Professor Graham Jenkin, of the department of obstetrics and gynaecology at Monash University, is researching the use of stem cells harvested from umbilical cord blood to treat babies at risk of developing cerebral palsy as the result of oxygen deprivation during birth.

The event was hosted by the Warrnambool branch of the Inner Wheel Club as part of a national fund-raising program by the organisation.

Professor Jenkin, deputy director of The Ritchie Centre, said treating infants deprived of oxygen with cord blood stem cells was showing promising results in preventing the brain damage that leads to cerebral palsy.

We are looking at treating infants within a 24-hour window after birth, Professor Jenkin said. We would be aiming for treatment after about six hours if possible, which is about as soon as the stem cells can be harvested.

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Stem cell research offers new hope

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Newswise The axiom, growing like a weed, takes on new meaning in light of changes in gene expression that occur when weeds interact with the crops they infest, according to plant scientist Sharon Clay. Using sophisticated genetic-mapping techniques, the South Dakota State University professor and her research team are documenting how corn and weeds influence one another.

Weeds grow like weeds when they grow with corn, says Clay. They grow bigger and taller in corn than by themselves. And inversely, corn grows less among weeds.

Over the last 20 years, Clay has been studying weed management in range and cropping systems, weed physiology and interactions among herbicides, soil and crops. The weed scientist was the first woman to serve as president of the American Society of Agronomy.

She has received two awards from the Weed Science Society of America for outstanding papers published in Weed Science --one in 2007 and another in 2012. Both articles were written in collaboration with David Horvath, a research plant physiologist for the Agricultural Research Service at the U.S. Department of Agriculture in Fargo, N.D.

Growing better among corn To figure out how corn and weeds affect each others gene response, Clay and a team of two research associates and a soils expert, planted plots of velvetleaf alone, corn with velvetleaf and corn kept weed-free.

The researchers saw an entirely different response when velvetleaf was grown by itself versus among corn plants. The velvetleaf alone was shorter and stouter, Clay explains. In addition, specific genes that influenced photosynthesis and other important plant responses differed in expression.

Another study compared the corns growth and yield in response to weeds, lack of nitrogen, or shade. In all cases, Clay and Horvath found that genes were differentially expressed compared with nonstressed plants. However, each stress resulted in very different expression patterns.

Traditionally, weeds have been thought to reduce crop growth and yield due to competition for water, nutrients and light. This study, however, indicates that weed-crop interactions are much more complex than researchers have thought.

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Weeds Grow Bigger Among Corn

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ALAMEDA, Calif.--(BUSINESS WIRE)--BioTime, Inc. (NYSE MKT: BTX) and its subsidiary Asterias Biotherapeutics, Inc. today announced that Jane S. Lebkowski, PhD, President, Research & Development of Asterias, will present at the 17th Annual Meeting of the American Society of Gene & Cell Therapy taking place May 20-24, 2014 in Washington, DC.

Dr. Lebkowskis presentation will take place in the session titled The Next Generation in Stem Cell Therapies on Thursday May 22, 2014 at 10:15 AM EDT at the Marriot Wardman Park, Washington, DC. Dr. Lebkowskis presentation is titled Phase I Clinical Trial of Human Embryonic Stem Cell-Derived Oligodendrocyte Progenitors in Patients with Neurologically Complete Thoracic Spinal Cord Injury: Results and Next Steps. In her presentation, Dr. Lebkowski will disclose for the first time certain Phase I clinical trial results of OPC1. The presentation will be made available on BioTimes and Asterias websites at http://www.biotimeinc.com and http://www.biotimeinc.com/asterias-biotherapeutics/.

About Asterias

Asterias is a biotechnology company focused on the emerging field of regenerative medicine. Our core technologies center on stem cells capable of becoming all of the cell types in the human body, a property called pluripotency. We plan to develop therapies based on pluripotent stem cells to treat diseases or injuries in a variety of medical fields, with an initial focus on the therapeutic applications of oligodendrocyte progenitor cells (OPC1) and antigen-presenting dendritic cells (VAC1 and VAC2) for the fields of neurology and oncology respectively. OPC1 was tested for treatment of spinal cord injury in the worlds first Phase 1 clinical trial using human embryonic stem cell-derived cells. We plan to reinitiate clinical testing of OPC1 in spinal cord injury this year, and are also evaluating its function in nonclinical models of multiple sclerosis and stroke. VAC1 and VAC2 are dendritic cell-based vaccines designed to immunize cancer patients against the telomerase, a protein abnormally expressed in over 95% of human cancer types. VAC2 differs from VAC1 in that the dendritic cells presenting telomerase to the immune system are produced from human embryonic stem cells instead of being derived from human blood.

In October of 2013, Asterias acquired the cell therapy assets of Geron Corporation. These assets included INDs for the clinical stage OPC1 and VAC1 programs, banks of cGMP-manufactured OPC1 drug product, cGMP master and working cell banks of human embryonic stem cells, over 400 patents and patent applications filed worldwide, research cell banks, customized reagents and equipment, and various assets relating to preclinical programs in cardiology, orthopedics, and diabetes.

Asterias is a member of the BioTime family of companies.

About BioTime

BioTime is a biotechnology company engaged in research and product development in the field of regenerative medicine. Regenerative medicine refers to therapies based on stem cell technology that are designed to rebuild cell and tissue function lost due to degenerative disease or injury. BioTimes focus is on pluripotent stem cell technology based on human embryonic stem (hES) cells and induced pluripotent stem (iPS) cells. hES and iPS cells provide a means of manufacturing every cell type in the human body and therefore show considerable promise for the development of a number of new therapeutic products. BioTimes therapeutic and research products include a wide array of proprietary PureStem progenitors, HyStem hydrogels, culture media, and differentiation kits. BioTime is developing Renevia (a HyStem product) as a biocompatible, implantable hyaluronan and collagen-based matrix for cell delivery in human clinical applications. In addition, BioTime has developed Hextend, a blood plasma volume expander for use in surgery, emergency trauma treatment and other applications. Hextend is manufactured and distributed in the U.S. by Hospira, Inc. and in South Korea by CJ HealthCare Corporation under exclusive licensing agreements.

BioTime is also developing stem cell and other products for research, therapeutic, and diagnostic use through its subsidiaries:

Additional information about BioTime can be found on the web at http://www.biotimeinc.com.

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Asterias Biotherapeutics, Inc. to Present Phase I Clinical Data at the 17th Annual Meeting of the American Society of ...

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Scientists have identified a genetic marker that may be associated with the development of obsessive compulsive disorder (OCD).

OCD affects an estimated 2 percent of the population and is one of the least understood mental illnesses. The condition is marked by thoughts and images that chronically intrude in the mind and by repetitive behaviors aimed at reducing the associated anxiety. The standard treatments such as selective serotonin reuptake inhibitor (SSRI) medications and behavioral psychotherapy are about 60 to 70 percent effective, but they dont help all patients and only treat disease symptoms.

Identifying a genetic marker for OCD could help scientists develop more effective therapies for the condition.

Like most other medical and psychological conditions, we need to understand what causes conditions, so we can develop real and rational treatments for these conditions and/or prevention, lead study author Dr. Gerald Nestadt, a professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine, told FoxNews.com. Thats why its important to study or identify genetic causes, if there are any.

In collaboration with seven universities, Nestadt and his colleagues conducted a genome-wide association study of 1,400 people with OCD. For their control group, researchers studied the genomes of 1,000 parents of OCD patients. Researchers looked for an association between the condition and a particular genetic marker. They were able to identify a genetic marker located near a gene that encodes the protein tyrosine phosphokinase.In the study, more people in the OCD group had the genetic marker, compared to those in the control group.

A genetic marker typically is not the specific abnormality, but tells researchers something very close to the marker is the variant of interest, Nestadt said. Researchers note that, while they have a found a genetic marker, they have yet to discover the exact variant associated with OCD and therefore do not know the exact genetic cause of the disease.

That is the goal. The idea is that if we know what chemical or protein is affected in the condition, then we can work out what problem is in the brain that causes the condition and the next step is to find a pharmaceutical that changes that or affects that so as to improve the condition, said Nestadt, who is also director of Johns Hopkins Obsessive-Compulsive Disorder program.

While there has been significant genetic research into other physical diseases, such as diabetes and heart disease, OCD has been less studied. Nestadt believes its because there are fewer researchers in the field of OCD genetics, as well as less availability of funds and a lack of understanding of the disease.

We all have friends who say, Well, Im a little OCD. I think that has actually hurt the individuals who truly suffer from the condition everybody thinks of it as a joke or not serious or not disabling. If you seriously meet someone who has OCD and see what life is like, youll absolutely change your mind, he said.

The only known risk factor for OCD is having a family member with the disease. In previous research, Nestadt had found that 40 percent of people with OCD had a first-degree relative with the disease.

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Researchers identify genetic marker for OCD

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Spark Therapeutics, a gene therapy medical company, this week signed an agreement for a headquarters in West Philadelphia. Spark Therapeutics, spun out of Children's Hospital of Philadelphia in October with $50 million in capital, will build out a 28,000-square-foot facility at 3737 Market St. to house its business operations, clinical research and development, and manufacturing.

Jeffrey D. Marrazzo, cofounder and chief executive, said the new facility "will support the continued expansion of our team and expand our manufacturing capacity to support our clinical development and commercial plans."

Spark anticipates moving into its new headquarters and expanding to 50 full-time employees by the end of 2014. Spark is preparing to complete clinical development of its lead, Phase 3 clinical program to address inherited retinal dystrophies caused by mutations in the RPE65 gene.

- Erin Arvedlund

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Washington, May 12 : Researchers have merged stem cell and 'organ-on-a-chip' technologies to grow, for the first time, functioning human heart tissue carrying an inherited cardiovascular disease.

The research appears to be a big step forward for personalized medicine, as it is working proof that a chunk of tissue containing a patient's specific genetic disorder can be replicated in the laboratory.

Using their interdisciplinary approach, the investigators modeled the cardiovascular disease Barth syndrome, a rare X-linked cardiac disorder caused by mutation of a single gene called Tafazzin, or TAZ. The disorder, which is currently untreatable, primarily appears in boys, and is associated with a number of symptoms affecting heart and skeletal muscle function.

The researchers took skin cells from two Barth syndrome patients, and manipulated the cells to become stem cells that carried these patients' TAZ mutations. Instead of using the stem cells to generate single heart cells in a dish, the cells were grown on chips lined with human extracellular matrix proteins that mimic their natural environment, tricking the cells into joining together as they would if they were forming a diseased human heart.

The engineered diseased tissue contracted very weakly, as would the heart muscle seen in Barth syndrome patients.

The investigators then used genome editinga technique pioneered by Harvard collaborator George Church, PhDto mutate TAZ in normal cells, confirming that this mutation is sufficient to cause weak contraction in the engineered tissue.

On the other hand, delivering the TAZ gene product to diseased tissue in the laboratory corrected the contractile defect, creating the first tissue-based model of correction of a genetic heart disease.

Furthermore, the scientists discovered that the TAZ mutation works in such a way to disrupt the normal activity of mitochondria, often called the power plants of the cell for their role in making energy.

However, the mutation didn't seem to affect overall energy supply of the cells. In what could be a newly identified function for mitochondria, the researchers describe a direct link between mitochondrial function and a heart cell's ability to build itself in a way that allows it to contract.

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Stem cell and 'organ-on-a-chip' merger step forward for personalized meds

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Vancouver, British Columbia (PRWEB) May 12, 2014

STEMCELL Technologies Inc. has just released NEW MesenCult Proliferation Kit with MesenPure (Mouse), a novel cell culture medium to advance research on mouse mesenchymal stem and progenitor cells (MSCs).

When added to MesenCult medium, MesenPure supplement enriches mouse bone marrow- or compact bone-derived MSC cultures by reducing the number of hematopoietic cells. Culturing with MesenPure eliminates the time-intensive serial passaging steps and frequent cell culture medium changes normally required to decrease the unwanted hematopoietic cell population typically present in MSC cultures. Cultures treated with MesenPure appear homogeneous and mostly devoid of hematopoietic cells as early as passage zero and also contain increased numbers of mesenchymal stem cells that display more robust differentiation.

This easy-to-use and versatile kit, may save researchers from having to wait several weeks for homogeneous MSC cultures, explains Dr. Arthur Sampaio, Senior Scientist at STEMCELL Technologies. But, I think the greatest advantage to using MesenPure may be the ability to use lower-passage cultures. It has been shown that over time, extended passaging can bring about detrimental changes to MSCs, such as a loss of phenotype, senescence, and a decrease in the homing ability and differentiation potential of the cells. By using the MesenCult Proliferation Kit with MesenPure, researchers will be able to study lower passage mouse MSCs, increasing their ability to evaluate the true potential of these cells.

For more information or to request a free sample, please visit http://www.stemcell.com/freemesenpure.

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STEMCELL Technologies Inc. Launches Novel Cell Culture Medium to Advance Research on Mouse Mesenchymal Stem and ...

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Image Caption: Researchers use modified RNA transfection to correct genetic dysfunction in heart stem cells derived from Barth syndrome patients. The series of images show how inserting modified RNA into diseased cells causes the cells to produce functioning versions of the TAZ protein (first image: in green) that correctly localize in the mitochondria (second image: in red). When the images are merged to demonstrate this localization, green overlaps with red, giving the third image a yellow color. Credit: Gang Wang and William Pu/Boston Children's Hospital

[ Watch The Video: Cardiac Tissue Contractile Strength Differences Shown Using Heart-On-A-Chip ]

Harvard University

Harvard scientists have merged stem cell and organ-on-a-chip technologies to grow, for the first time, functioning human heart tissue carrying an inherited cardiovascular disease. The research appears to be a big step forward for personalized medicine, as it is working proof that a chunk of tissue containing a patients specific genetic disorder can be replicated in the laboratory.

The work, published in Nature Medicine, is the result of a collaborative effort bringing together scientists from the Harvard Stem Cell Institute, the Wyss Institute for Biologically Inspired Engineering, Boston Childrens Hospital, the Harvard School of Engineering and Applied Sciences, and Harvard Medical School. It combines the organs-on-chips expertise of Kevin Kit Parker, PhD, and stem cell and clinical insights by William Pu, MD.

Using their interdisciplinary approach, the investigators modeled the cardiovascular disease Barth syndrome, a rare X-linked cardiac disorder caused by mutation of a single gene called Tafazzin, or TAZ. The disorder, which is currently untreatable, primarily appears in boys, and is associated with a number of symptoms affecting heart and skeletal muscle function.

The researchers took skin cells from two Barth syndrome patients, and manipulated the cells to become stem cells that carried these patients TAZ mutations. Instead of using the stem cells to generate single heart cells in a dish, the cells were grown on chips lined with human extracellular matrix proteins that mimic their natural environment, tricking the cells into joining together as they would if they were forming a diseased human heart. The engineered diseased tissue contracted very weakly, as would the heart muscle seen in Barth syndrome patients.

The investigators then used genome editinga technique pioneered by Harvard collaborator George Church, PhDto mutate TAZ in normal cells, confirming that this mutation is sufficient to cause weak contraction in the engineered tissue. On the other hand, delivering the TAZ gene product to diseased tissue in the laboratory corrected the contractile defect, creating the first tissue-based model of correction of a genetic heart disease.

You dont really understand the meaning of a single cells genetic mutation until you build a huge chunk of organ and see how it functions or doesnt function, said Parker, who has spent over a decade working on organs-on-chips technology. In the case of the cells grown out of patients with Barth syndrome, we saw much weaker contractions and irregular tissue assembly. Being able to model the disease from a single cell all the way up to heart tissue, I think thats a big advance.

Furthermore, the scientists discovered that the TAZ mutation works in such a way to disrupt the normal activity of mitochondria, often called the power plants of the cell for their role in making energy. However, the mutation didnt seem to affect overall energy supply of the cells. In what could be a newly identified function for mitochondria, the researchers describe a direct link between mitochondrial function and a heart cells ability to build itself in a way that allows it to contract.

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'Heart Disease-On-A-Chip' Made From Patient Stem Cells

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