Archive for the ‘Gene Therapy Research’ Category

AS Guru Genetics part 2
The Cell Cycle 70:47From:Nicola BowkerViews:0 0ratingsTime:15:09More inEducation

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AS Guru Genetics part 3
Protein Synthesis 85:53 Gene technology 94:51From:Nicola BowkerViews:0 0ratingsTime:30:43More inEducation

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AS Guru Genetics part 3 - Video

Dr. Sheldon Peck (4 of 7)
Part 4: Main topic part one: "To find clues recorded long before the genetics revolution about abnormal conditions we would know now as familial" Dr. Sheldon Peck (DDS 1966): "The Modern Value of Early Writing in Medicine and Dentistry." Presented by the UNC Health Sciences Library and the Bullitt History of Medicine Club, November 13, 2012.From:hsluncViews:0 0ratingsTime:08:58More inEducation

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Fuchs Dystrophy - Mayo Clinic
Ophthalmologist Keith Baratz, MD, of Mayo Clinic in Rochester, Minnesota, discusses his work: Fuchs Dystrophy, endothelial keratoplasty and corresponding genetics research.From:mayoclinicViews:3 0ratingsTime:11:04More inScience Technology

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Fuchs Dystrophy - Mayo Clinic - Video

Gender Genetics
Learn how you inherited genes to determine if you were born a boy or girl. Men contain sex chromosomes XY and women have sex chromosomes XX.From:Mark DrollingerViews:0 0ratingsTime:03:00More inEducation

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Gender Genetics - Video

Reserva Privada #39;s Kandy Kush and OG Kush Seedlings
Just showing off the new strains the just got added to the garden, kandy kush and og kush. Both strains used the og kush reversal pollen to create the feminized seeds, I #39;ve had so much luck with strains created with those genetics that I wanted to check a few new strains for good pheno types. Like comment subscribe! By the way, I do not own the music playing in the background, fair use! 🙂 Song is Kid Cudi - I Be HighFrom:Theo M.Views:2 2ratingsTime:03:57More inEducation

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Reserva Privada's Kandy Kush and OG Kush Seedlings - Video

Fragile X at Boston Children #39;s Hospital: What should I expect?
A patient-friendly, behaviorally sensitive guide for children with Fragile X syndrome who are coming to Boston Children #39;s Hospital. It walks children through the entire experience, from arrival at the hospital to visiting Occupational Therapy, Genetics, a pediatrician and a psychologist.From:ChildrensHospitalViews:1 0ratingsTime:06:43More inNonprofits Activism

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Fragile X at Boston Children's Hospital: What should I expect? - Video

"Ask the Experts - Living with ALS" Seminar at Cedars-Sinai Medical Center
On Saturday, November 17, 2012, world-renowned researchers involved in the study of ALS participated in a this special event, "Ask the Experts -- Living with ALS" at Cedars-Sinai Medical Center in Los Angeles, California. The event, hosted by The ALS Association Golden West Chapter, offered people with ALS and their loved ones an opportunity to ask their questions directly to scientists and clinicians. Speakers include Catherine Lomen-Hoerth, MD, Ph.D., Director, The ALS Center at UCSF, who will discuss multidisciplinary care and ALS along with The ALS Association #39;s Chief Scientist, Lucie Bruijn, Ph.D., who will present an overview of ALS research. Following these discussions, Robert H. Baloh, MD, Ph.D., Director, Cedars-Sinai ALS Center, Don W. Cleveland, Ph.D, Department Chair, UCSD, and Clive Svendsen, Ph.D., Director, Cedars-Sinai RMI and Chair of the California ALS Research Network will speak about topics such as clinical trials, genetics, and stem cell research. To find out more, please visit: http://www.alsagoldenwest.org or httpFrom:Calabasas3Views:7 0ratingsTime:02:57:25More inEducation

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"Ask the Experts - Living with ALS" Seminar at Cedars-Sinai Medical Center - Video

Public release date: 4-Dec-2012 [ | E-mail | Share ]

Contact: Phyllis Edelman pedelman@genetics-gsa.org 301-634-7302 Genetics Society of America

Bethesda, MDDecember 4, 2012 Listed below are the selected highlights for the December 2012 issue of the Genetics Society of America's journal, Genetics. The December issue is available online at http://www.genetics.org/content/current. Please credit Genetics, Vol. 192, December 2012, Copyright 2012.

Please feel free to forward to colleagues who may be interested in these articles.

ISSUE HIGHLIGHTS

Genetic variation in Saccharomyces cerevisiae: Circuit diversification in a signal transduction network, pp. 1523-1532 Brian L. Chin, Owen Ryan, Fran Lewitter, Charles Boone, and Gerald R. Fink The plummeting cost of genome sequencing has revealed increasing amounts of genetic variation within a species. How much of that variation affects function, and how might it help us understand evolution? The authors addressed these questions by looking at how cell adhesion is controlled in two closely related yeast strains. Despite their similar genomic sequences, these two strains use different sets of genes to regulate adhesion. A signal transduction pathway has been rewired, partly because of polymorphisms in a transcription factor.

Gene functional trade-offs and the evolution of pleiotropy, pp. 1389-1409 Frdric Guillaume and Sarah P. Otto Pleiotropythe property of genes affecting multiple features of an organismis often considered to be an unavoidable by-product of a gene's evolutionary history. These authors explored how the pleiotropic degree of a gene may evolve, providing clues to why pleiotropy varies among genes. They found two common outcomes of the evolution of multifunctional genes: increased pleiotropy of genes more highly expressed, and specialization of all genes on the trait most important to fitness.

Receptors and other signaling proteins required for serotonin control of locomotion in Caenorhabditis elegans, pp. 1359-1371 Gliz Grel, Megan A. Gustafson, Judy S. Pepper, H. Robert Horvitz, and Michael R. Koelle This article offers insight into the mechanism of signaling by serotonin, a neurotransmitter involved in mood disorders in humans. The authors carried out screens for C. elegans mutants that fail to respond properly to this neurotransmitter, which worms use to control locomotion. They identified mutations in more than eight genes required for serotonin signaling. Two encode serotonin receptors, while the others encode proteins that in some cases are implicated for the first time in serotonin signaling by this work. There are similar human proteins that may mediate serotonin signaling in our brains. The two C. elegans serotonin receptors appear to act in parallel in different cells to coordinate behavioral responses to serotonin.

Long-term and short-term evolutionary impacts of transposable elements on Drosophila, pp. 1411-1432 Yuh Chwen G. Lee and Charles H. Langley Transposable elements are ubiquitous genomic parasites. Even though they are primarily vertically inherited as part of the genome, their interactions with the host are often likened to the coevolution of host genes and nongenomic, horizontally transferred pathogens. Here Lee and Langley show that genes involved in the interaction with transposable elements indeed show strong signals of positive selection similar to those of immunity genes in Drosophila, but with a fundamentally different mechanism from that of host-pathogen coevolution.

Unusual and typical features of a novel restorer-of-fertility gene of sugar beet (Beta vulgaris L.), pp. 1347-1358 Hiroaki Matsuhira, Hiroyo Kagami, Masayuki Kurata, Kazuyoshi Kitazaki, Muneyuki Matsunaga, Yuko Hamaguchi, Eiki Hagihara, Minoru Ueda, Michiyo Harada, Aki Muramatsu, Rika Yui-Kurino, Kazunori Taguchi, Hideto Tamagake, Tetsuo Mikami, and Tomohiko Kubo Plant pollen production is often impaired by incompatibility between the mitochondria and nucleus. A nuclear gene termed Rf can cancel this cytoplasmic male sterility. These authors report that sugar beet Rf encodes a metalloprotease-like gene, in contrast to other Rfs which encode proteins supposed to bind RNA. Interestingly, the sugar beet Rf locus exhibits the gene clustering often seen in plant Rf loci, suggesting a common evolutionary mechanism regardless of the Rf gene products.

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Genetics Society of America's Genetics journal highlights for December 2012

CHARLEROI, Belgium--(BUSINESS WIRE)--

During the inauguration of its new building, the Belgian Biotech Company Delphi Genetics SA announced that the first antibiotic-free DNA vaccine using the Staby technology was efficiently tested in vivo. Together with academic and Biotech key-players, Delphi Genetics is participating to the DNAVAC project funded by the Walloon Region (BioWin project). The aim of the project is to develop and produce antibiotic-free DNA vaccines targeting veterinary diseases. As a model, the consortium developed a DNA vaccine against the Aujezsky virus the causative agent of pseudo-rabies.

This virus was selected as it causes systematically an acute and lethal disease in susceptible species, thereby providing an excellent model to test the efficacy of a vaccine candidate. The results of the challenge performed by Dr Anca Reschner are very clear: all vaccinated animals using the Staby vectors were resistant to the lethal Aujeszky virus. said Prof. Alain Vanderplasschen from the University of Lige (Immunology-Vaccinology).

Cdric Szpirer PhD, Delphi Genetics co-Founder and CEO, explained: This is the first real DNA vaccine produced using the Staby technology. Several DNA vectors have been made in the past to generate production of antibodies, but this is the first time that in vivo tests were performed in order to evaluate efficiency against a disease. All production steps of the vaccine were performed efficiently avoiding completely the use of antibiotic-resistance genes as recommended by regulatory authorities (FDA, USDA, EMA). These results validate the use of Staby outside the field of protein production.

Indeed, a few weeks ago, on October, 8 Delphi Genetics announced a broad licensing agreement with a subsidiary of Merck & Co., Inc., known as MSD outside the United States and Canada, for the use of the StabyExpress technology to produce proteins in the areas of human and animal health. The same technology was licensed previously to Sanofi-Pasteur (2009) and GSK (2010) for production of proteins used in human vaccines.

As announced on January, 30, 2012, the DNAVAC project involves a consortium including Eurogentec SA, another Belgian Biotech company (part of Kaneka) in charge of large scale DNA production and purification, and two universities: the Catholic University of Louvain in charge of pharmaceutical and toxicity studies associated with the project and the University of Lige in charge of vaccinology and veterinary aspects.

About Delphi Genetics SA

Founded at the end of 2001, Delphi Genetics SA develops technologies for genetic engineering and protein expression using unique expertise in the domain of plasmid stabilisation systems. Since 2004, Delphi Genetics has been marketing innovative kits and services for researchers. Some of these kits contain the Staby technology that has since been licensed for industrial applications (see above). Indeed, the Staby technology can be applied to any industrial DNA or protein production process that involves bacterial fermentation. Delphi Genetics is involved in several research projects including adaptation of the technology to yeast and mammalian cells.

http://www.delphigenetics.com

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The Staby® Technology from Delphi Genetics Efficiently Applied To DNA-Vaccine

NEW YORK (AP) Shares of Myriad Genetics Inc. declined Monday after the U.S. Supreme Court agreed to hear a challenge to the practice of issuing patents on human genes.

THE SPARK: On Friday the Supreme Court said it will decide on a case on the patenting of genes. Myriad holds two genetic patents related to its BRACAnalysis test, which detects genetic mutations that are linked to increased risks of breast and ovarian cancer. The U.S. Patent and Trademark Office has been issuing DNA patents for almost 30 years, but the American Civil Liberties Union has challenged the practice.

THE BIG PICTURE: The Salt Lake City reported $405.5 million in revenue from BRACAnalysis testing in the fiscal year ended June 3, or 86 percent of its total revenue. Myriad and analysts say the test is protected by other patents, so Myriad would not immediately lose patent protection on the test if the Supreme Court rules that human genes can't be patented.

The ACLU and other groups have argued that the government shouldn't award patents on genes and that the patents prevent other groups for doing research. In March 2010 a New York district court ruled against Myriad, but the U.S. Court of Appeals for the Federal Circuit has ruled in Myriad's favor twice, most recently in August.

In March 2012 the Supreme Court threw out genetic patents held by Prometheus Laboratories that covered a test designed to help doctors set drug doses for autoimmune diseases like Crohn's disease. Some investors felt that decision was bad news for Myriad, but analysts have said the patents are not very similar to those held by Myriad.

THE ANALYSIS: Jefferies & Co. analyst Jon Wood said in a note Monday Myriad's patents should ultimately be upheld, and no matter what the court rules, the company's other patents should keep generic competition for BRACAnalysis from reaching the market until fiscal 2018. He rates the stock "Buy," with a $33 price target.

SHARE ACTION: Shares of Myriad Genetics lost 73 cents, or 2.5 percent, to $27.99 in midday trading. Earlier the stock fell as much as 6.4 percent. Myriad shares are up 37 percent in 2012.

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Myriad Genetics slips on Supreme Court review

SEATTLE, WA--(Marketwire - Dec 3, 2012) - Atossa Genetics, Inc. ( NASDAQ : ATOS ) announced today that it has been designated as the Expertise Partner to the 2nd Annual Cancer Genome Summit being held December 4-6, 2012 at the Revere Hotel Boston Common in Boston, Massachusetts.Dr. Steven C. Quay, M.D., Ph.D., FCAP, chairman, CEO and president of Atossa Genetics, will present on Thursday, December 6th, 2012, during the morning session.

Dr. Quay's presentation will focus on breast cancer prevention through the diagnosis and treatment of the abnormal cells that are the precursors of cancer, so-called reversible hyperplastic intraductal lesions. His presentation will include:

"Using Atossa Genetics' patented, FDA-cleared medical devices and our patented high-complexity laboratory developed tests to diagnose reversible, pre-cancerous breast changes and then treat them locally with intraductal therapy provides a platform that has the potential to realize our goal of preventing breast cancer," stated Dr. Steven Quay, MD, PhD, FCAP. "We look forward to identifying forward-looking pharma and biotech companies with novel treatment formulations to partner in this new paradigm for breast health, intraductal treatment of pre-cancerous lesions."

The Cancer Genome Summit is the only meeting that brings together thought leaders from pharmaceutical companies, academia and the clinic, to discuss harnessing the cancer genome to revolutionize drug development programs and patient treatment choices. The presentations will include the latest clinical data. Sharing these insights holds the key to understanding how genes cause cancer and how diagnostics and treatments can be improved. This year's meeting will show attendees how to identify new drug targets, combat resistance mechanisms, streamline clinical trials, and improve clinical management. More information about the meeting may be found at Cancer Genome Summit.

About Atossa Genetics, Inc.

Atossa Genetics, Inc. ( NASDAQ : ATOS ), The Breast Health Company, is based in Seattle, WA, and is focused on preventing breast cancer through the commercialization of patented, FDA-cleared diagnostic medical devices and patented, laboratory developed tests (LDT) that can detect precursors to breast cancer up to eight years before mammography, and through research and development that will permit it to commercialize treatments for pre-cancerous lesions.

The National Reference Laboratory for Breast Health (NRLBH), a wholly owned subsidiary of Atossa Genetics, Inc., is a CLIA-certified high-complexity molecular diagnostic laboratory located in Seattle, WA, that provides the patented ForeCYTE Breast Health Test, a risk assessment test for women 18 to 73 years of age akin to the Pap Smear, and the ArgusCYTE Breast Health Test, a blood test for recurrence in breast cancer survivors that provides a "liquid biopsy" for circulating cancer cells and a tailored treatment plan for patients and their caregivers.

Forward-Looking Statements

Except for the historical information contained herein, the matters set forth in this press release, including statements regarding Atossa's plans, expectations, projections, potential opportunities, goals and objectives are forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from the anticipated or estimated future results, including the risks and uncertainties associated with the efficacy of Atossa's products and services, the market demand for and acceptance of Atossa's products and services and other risks detailed from time to time in the Atossa's final prospectus, dated November 7, 2012, filed with the U.S. Securities and Exchange Commission.All forward-looking statements are qualified in their entirety by this cautionary statement, and Atossa undertakes no obligation to revise or update any forward-looking statement to reflect events or circumstances after the issuance of this press release.

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Atossa Genetics, Inc. Designated Expertise Partner to Cancer Genome Summit

Last month, a large team led by researchers at Boston hospitals reported a surprising result: a common variation in a gene was associated with being an early bird, and with the time of day people died.

Given how many things affect when we wake upnot to mention all the experiences accumulated over a lifetime that contribute to how and when we dieit seems a little crazy that a single gene could be meaningfully linked to those complicated traits.

But over the years, it has become increasingly clear that our bodies run on their own clocks, and that health is inextricably linked to those rhythms. Shift workers forced to adopt a schedule wildly out of rhythm with a typical day raise their risk of obesity and diabetes. Heart attacks have a propensity to strike in the morning and asthma attacks at night. A growing body of evidence suggests giving cancer drugs at specific times of day can make a therapys side effects less harsh.

The scientists who published the new findings in the Annals of Neurology said the research needs to be repeated in a larger group of people to see whether it holds up. They acknowledged that a complex trait such as being a night owl or dying at dusk rather than mid-day would likely have many contributions, not just one gene. But, given the obvious importance of our bodys natural rhythms, they and others argue, it is important to try and unravel the biology of the clock.

What youd like to do is youd like to see if theres some predictive value here, said Dr. Clifford Saper, chief of neurology at Beth Israel Deaconess Medical Center, and a coauthor. Could you predict who would be able to adjust to a job that requires that you start at 6 a.m.? ... Would you be able to pick your job based on knowing your genetic predisposition.

Researchers not involved in the study said it was a fascinating result, but just a first step in teasing out how the human body clock works, and what effect perturbing the clock can have.

The very significant association in their discovery data is on the one hand reassuring, but also suggests a massive effectreally atypical for complex traits like this, Jeffrey Barrett, a group leader at the Wellcome Trust Sanger Institute in England, wrote in an e-mail.

Dr. Louis Ptacek, a professor of neurology at the University of California, San Francisco, said that the study was interesting but that because the sleep-wake cycle is influenced by so many things, including things that range from genes to jobs, he has focused in his research on a different approach: studying true outliers, whose sleep schedules are radically shifted.

Studying rare, more extreme diseases to gain insight into more common conditions has become common in medicine. The connection between LDL cholesterol and heart disease, for example, was partly revealed by research into a rare genetic disorder that caused people to have heart attacks when they were young.

You and I have the biological tendency to wake up at a certain time, but you override that all the time because you have a deadline or you take coffee in the morning, or you have a glass of wine with dinner, Ptacek said. So instead of trying to unravel all the different reasons that people might tend to wake up a bit earlier or later, Ptacek has spent much of his career studying people who naturally wake up in the wee hours of the morning and go to bed before prime time.

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Researchers identify a gene that may predict what time of day people die

.Rejuvenare Stem Cell Therapy 888-988-5456
Rejuvenare Autologous Adult Stem Cell Therapy welcome video asks and answers questions on whether someone is a candidate for stem cell therapy. More can be found at http://www.rejuvenare.comFrom:rejuvenareViews:0 0ratingsTime:01:01More inPeople Blogs

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.Rejuvenare Stem Cell Therapy 888-988-5456 - Video

"Arthritis of ankle is being treated with cell therapy at the Center for Regenerative Medicin," according to A.J. Farshchian MD, a regenerative medicine practitioner at The Center for regenerative medicine.

(PRWEB) December 02, 2012

The ankle joint is known as a diarthrodial joint. Of all the joints in the body it is probably the joint most resistant to a degenerative condition. This immunity to arthrosis is primarily associated to the joints liberal distribution of forces throughout a series of interlinked compartments. The ankle joint and accompanying foot joints support the body as would a tri-pod supporting a camera. The supporting surfaces of the ankle and foot have a tri-pod structure to its form. The ankle joint represents the lateral (or outside) support column of the tri-pod supporting form. The heel bone represents the posterior column of the support form. The mid-foot and the forefoot represent the anterior support column. This tri-pod support form is not static but dynamic in its function. As the stresses change and the strains converge on points along the weight-bearing surfaces of the ankle foot adjustments are made to maintain the center of gravity within the supporting tri-pod columns.

Rarely would age related degenerative changes be seen in the ankle and foot. When degenerative changes develop in the ankle or the other support columns it is normally preceded by a history of trauma. This trauma is usually a fracture in one of the supporting hard tissues. Serious ligamental injury can also affect a degenerative condition. Following a ligamental or fracture injuries an uncoupling of the local traumatic region occurs. This uncoupling reduces the normal cellular metabolic response to weight-bearing forces of the local traumatized area. The traumatized area is isolated from the nutritious effect of tolerable strains and exposed to harmful stresses. These harmful stresses initiate cellular destruction which later becomes a degenerative condition.

The Center for Regenerative Medicine in Miami, Florida concentrates on helping arthritic and injured people to get back to a functional level of life and their activities using non-surgical techniques and Orthopedic medicine. The center's expertise is in treatment of conditions of spine, knees, shoulders and other cartilage damages. They have developed non-surgical and rehabilitation techniques focused on treatment and management of joint pain. Their team includes health professionals organized around a central theme. Their website is http://www.arthritisusa.net

Marty Eugene http://www.arthritisusa.net 305 8668384 Email Information

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Dr. Farshchian: Arthritis of the Ankle is Being Treated with Cell Therapy at the Center for Regenerative Medicine

Public release date: 2-Dec-2012 [ | E-mail | Share ]

Contact: Rachel Salis-Silverman Salis@email.chop.edu 267-426-6063 Children's Hospital of Philadelphia

Using powerful gene-analysis tools, researchers have discovered mutations in two related genes, ARID1A and ARID1B, that are involved in the most aggressive form of the childhood cancer neuroblastoma. While these findings do not immediately improve clinical treatments, they identify a novel pathway that is defective in these cancers, a pathway that scientists can now study to develop potential new therapies.

"These gene alterations were not previously known to be mutated in neuroblastoma, and they may significantly advance our knowledge of the underlying biological pathways that drive this disease," said study leader Michael D. Hogarty, M.D., a pediatric oncologist at The Children's Hospital of Philadelphia. "These two genes function in a group of genes that seems to play an important role in neural cell behavior, and we will now work to discover if this insight may open up new treatments for children with tumors having these mutations."

Hogarty, along with Victor Velculescu, M.D., Ph.D., of the Johns Hopkins Kimmel Cancer Center, co-led the study that appeared today in Nature Genetics.

The scientists received over $1 million in funding from the St. Baldrick's Foundation, a volunteer-driven and donor-centered charity dedicated to raising money for childhood cancer research.

The current study employed sophisticated next-generation sequencing technology that identified the entire DNA sequence for a set of neuroblastoma tumors. "When this project started, it was the first of its kind to focus on a childhood tumor," said Hogarty. "This is important, because cataloguing all the DNA mutations in neuroblastoma, or any tumor, will allow us to better understand the enemy, and ultimately to make better treatment decisions."

Striking the peripheral nervous system, neuroblastoma usually appears as a solid tumor in the chest or abdomen of young children. It accounts for 7 percent of all childhood cancers, but 10 to 15 percent of all childhood cancer-related deaths.

In the current study, Hogarty and colleagues identified alterations in two genes, ARID1A and ARID1B, neither of which had previously been reported to be involved in neuroblastoma. Both genes are thought to affect chromatin, a combination of DNA and protein that regulates the activities of genes and ultimately controls the behavior of a cell. During normal development, neural cells switch from a primitive, rapidly dividing state (neuroblasts) into a more differentiated, or mature state (neurons).

However, said Hogarty, mutations in ARID1A and ARID1B may prevent this orderly transition, keeping the neural cells in the uncontrolled stage of growth that becomes a cancerous tumor. "Unfortunately, children with these mutations have a particularly aggressive, treatment-resistant form of neuroblastoma," he added. The current study found that ARID1A and ARID1B mutations occur in 5 to 15 percent of high-risk neuroblastomas, but the pathway these genes affect may have a broader role in the diseasea possibility that Hogarty and colleagues plan to investigate further. It is possible that children having tumors with these mutations will receive more aggressive or more experimental treatments in the future.

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New gene-sequencing tools offer clues to highest-risk form of a childhood cancer

Researchers have discovered a new gene they say helps explain how humans evolved from chimpanzees.

The gene, called miR-941, appears to have played a crucial role in human brain development and could shed light on how we learned to use tools and language, according to scientists.

A team at the University of Edinburgh compared it to 11 other species of mammals, including chimpanzees, gorillas, mice and rats.

The results, published in Nature Communications, showed that the gene is unique to humans.

The team believe it emerged between six and one million years ago, after humans evolved from apes.

Researchers said it is the first time a new gene carried by humans and not by apes has been shown to have a specific function in the human body.

Martin Taylor, who led the study at the Institute of Genetics and Molecular Medicine at the University of Edinburgh, said: 'As a species, humans are wonderfully inventive - we are socially and technologically evolving all the time.

'But this research shows that we are innovating at a genetic level too.

'This new molecule sprang from nowhere at a time when our species was undergoing dramatic changes: living longer, walking upright, learning how to use tools and how to communicate.

'We're now hopeful that we will find more new genes that help show what makes us human.'

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'Unique' evolution gene find hailed

(MENAFN - ProactiveInvestors - Australia) Benitec Biopharma (ASX:BLT) research on muscular dystrophy shows encouraging in-vitro results via gene silencing.

The research targets the silencing of a gene (PABPN1), the mutant form of which causes the disease.

Data collected supports the development of a vector for combined silencing of the mutant gene by ddRNAi and replacement with a normal gene.

The data confirms that the delivery of a unique multi-shRNA cassette, Pabparna, to cells expressing the target gene is highly effective at silencing the target gene in those cells, reducing the expression levels to around 10%.

If achieved in vivo, this level of silencing by the clinical candidate is likely to result in significant improvement of the muscle disease, currently untreatable.

The researchers expect the optimal therapeutic to be based on both suppression of the target mutant gene and the replacement with a healthy gene.

Successful results at the stage of in vivo testing will be crucial to committing to advance the program into the clinic.

The program is being collaborated with Professor George Dickson from the Royal Holloway, University of London, and Dr Capucine Trollet from the Institut de Myologie.

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Benitec Biopharma makes breakthrough in gene silencing to treat muscular dystrophy

Washington, December 3 (ANI): A large, international consortium of scientists has identified fifteen new genetic regions associated with coronary artery disease- taking a significant step forward in understanding the root causes of this deadly disease.

The new research brings the total number of validated genetic links with heart disease discovered through genome-wide association studies to 46.

Coronary artery disease is the process by which plaque builds up in the wall of heart vessels, eventually leading to chest pain and potentially lethal heart attacks. It is the leading cause of death worldwide.

The study, which includes researchers at the Stanford University School of Medicine, provides insights into the molecular pathways causing coronary artery disease, which is also known as coronary atherosclerosis.

"Perhaps the most interesting results of this study show that some people may be born with a predisposition to the development of coronary atherosclerosis because they have inherited mutations in some key genes related to inflammation," said Themistocles (Tim) Assimes, MD, PhD, a Stanford assistant professor of medicine and one of the study's lead authors.

"There has been much debate as to whether inflammation seen in plaque buildup in heart vessels is a cause or a consequence of the plaques themselves. Our network analysis of the top approximately 240 genetic signals in this study seems to provide evidence that genetic defects in some pathways related to inflammation are a cause," Assimes noted.

More than 170 researchers were involved in this massive meta-analysis combining genetic data from more than 190,000 research participants. Interestingly, about a quarter of the genetic regions associated with coronary disease or heart attack were also found to be strongly associated with cholesterol, especially high levels of the so-called bad cholesterol known as LDL. Another 10 percent were associated with high blood pressure. Both of these conditions are known risk factors for coronary artery disease.

"The signals that do not point to known risk factors may be pointing to novel mechanisms of disease. It is imperative that we quickly gain a better understanding of how these regions are linked to heart disease, as such understanding will greatly facilitate the development of new drugs to prevent heart disease," Assimes said.

"Studies like this one help provide new pathways for scientists to investigate in more detail. The promise is in providing better insights into the pathophysiology of this disease," added co-author Thomas Quertermous, MD, a Stanford professor of medicine.

The study is being published online Dec. 2 in Nature Genetics. (ANI)

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15 new genes associated with heart disease identified

ScienceDaily (Dec. 2, 2012) Fifteen new genetic regions associated with coronary artery disease have been identified by a large, international consortium of scientists -- including researchers at the Stanford University School of Medicine -- taking a significant step forward in understanding the root causes of this deadly disease. The new research brings the total number of validated genetic links with heart disease discovered through genome-wide association studies to 46.

Coronary artery disease is the process by which plaque builds up in the wall of heart vessels, eventually leading to chest pain and potentially lethal heart attacks. It is the leading cause of death worldwide.

The study, published online Dec. 2 in Nature Genetics, provides insights into the molecular pathways causing coronary artery disease, which is also known as coronary atherosclerosis.

"Perhaps the most interesting results of this study show that some people may be born with a predisposition to the development of coronary atherosclerosis because they have inherited mutations in some key genes related to inflammation," said Themistocles (Tim) Assimes, MD, PhD, a Stanford assistant professor of medicine and one of the study's lead authors. "There has been much debate as to whether inflammation seen in plaque buildup in heart vessels is a cause or a consequence of the plaques themselves. Our network analysis of the top approximately 240 genetic signals in this study seems to provide evidence that genetic defects in some pathways related to inflammation are a cause."

More than 170 researchers were involved in this massive meta-analysis combining genetic data from more than 190,000 research participants. Interestingly, about a quarter of the genetic regions associated with coronary disease or heart attack were also found to be strongly associated with cholesterol, especially high levels of the so-called bad cholesterol known as LDL. Another 10 percent were associated with high blood pressure. Both of these conditions are known risk factors for coronary artery disease.

"The signals that do not point to known risk factors may be pointing to novel mechanisms of disease," Assimes said. "It is imperative that we quickly gain a better understanding of how these regions are linked to heart disease, as such understanding will greatly facilitate the development of new drugs to prevent heart disease."

Genome-wide association studies, or GWAS, were first introduced in 2005 as a way of quickly scanning the entire genome to identify differences in the DNA code, or "polymporphisms," that predispose people to various common but genetically complex diseases. Results of these studies have shown that conditions such as heart disease involve the combined, subtle effects of far more polymorphisms than initially expected, requiring multiple massive meta-analyses such as this one to reliably uncover all of these genetic signals. The hope of scientists is that by working together in ongoing worldwide collaborations, the entire genetic contribution to the cause of heart disease will eventually be identified.

"Studies like this one help provide new pathways for scientists to investigate in more detail," said co-author Thomas Quertermous, MD, a Stanford professor of medicine. "The promise is in providing better insights into the pathophysiology of this disease."

This meta-analysis study built upon previous research published last year in Nature Genetics. In that study, investigators examined 2.5 million SNPs (genetic variants at specific locations on individual chromosomes) from 14 GWA studies, which led to the discovery of 13 new gene regions associated with heart disease. Investigators looked at data from the complete genetic profiles of more than 22,000 people of European descent with heart disease and more than 64,000 healthy people.

In the new study, scientists used all information from last year's study then added to it, reaching 41,513 patients with heart disease and 65,919 control patients. To genetically fingerprint a large number of subjects in a very cost-effective manner, the researchers used a specialized genetic chip that incorporated only the top signals from the original meta-analysis of the initial 14 GWA studies.

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Inflammation may be a cause of plaque buildup in heart vessels

Public release date: 2-Dec-2012 [ | E-mail | Share ]

Contact: Tracie White traciew@stanford.edu 650-723-7628 Stanford University Medical Center

STANFORD, Calif. Fifteen new genetic regions associated with coronary artery disease have been identified by a large, international consortium of scientists including researchers at the Stanford University School of Medicine taking a significant step forward in understanding the root causes of this deadly disease. The new research brings the total number of validated genetic links with heart disease discovered through genome-wide association studies to 46.

Coronary artery disease is the process by which plaque builds up in the wall of heart vessels, eventually leading to chest pain and potentially lethal heart attacks. It is the leading cause of death worldwide.

The study, which will be published online Dec. 2 in Nature Genetics, provides insights into the molecular pathways causing coronary artery disease, which is also known as coronary atherosclerosis.

"Perhaps the most interesting results of this study show that some people may be born with a predisposition to the development of coronary atherosclerosis because they have inherited mutations in some key genes related to inflammation," said Themistocles (Tim) Assimes, MD, PhD, a Stanford assistant professor of medicine and one of the study's lead authors. "There has been much debate as to whether inflammation seen in plaque buildup in heart vessels is a cause or a consequence of the plaques themselves. Our network analysis of the top approximately 240 genetic signals in this study seems to provide evidence that genetic defects in some pathways related to inflammation are a cause."

More than 170 researchers were involved in this massive meta-analysis combining genetic data from more than 190,000 research participants. Interestingly, about a quarter of the genetic regions associated with coronary disease or heart attack were also found to be strongly associated with cholesterol, especially high levels of the so-called bad cholesterol known as LDL. Another 10 percent were associated with high blood pressure. Both of these conditions are known risk factors for coronary artery disease.

"The signals that do not point to known risk factors may be pointing to novel mechanisms of disease," Assimes said. "It is imperative that we quickly gain a better understanding of how these regions are linked to heart disease, as such understanding will greatly facilitate the development of new drugs to prevent heart disease."

Genome-wide association studies, or GWAS, were first introduced in 2005 as a way of quickly scanning the entire genome to identify differences in the DNA code, or "polymporphisms," that predispose people to various common but genetically complex diseases. Results of these studies have shown that conditions such as heart disease involve the combined, subtle effects of far more polymorphisms than initially expected, requiring multiple massive meta-analyses such as this one to reliably uncover all of these genetic signals. The hope of scientists is that by working together in ongoing worldwide collaborations, the entire genetic contribution to the cause of heart disease will eventually be identified.

"Studies like this one help provide new pathways for scientists to investigate in more detail," said co-author Thomas Quertermous, MD, a Stanford professor of medicine. "The promise is in providing better insights into the pathophysiology of this disease."

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International study points to inflammation as a cause of plaque buildup in heart vessels

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