Part 2 Stem Cell Therapy – Video
Part 2 Stem Cell Therapy
By: Tiffany Vinson
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Part 2 Stem Cell Therapy - Video
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Be happy – your genes will thank you for it: Doing good leads to strong immune cells
American scientists said individuals who derive their happiness from a sense of purpose showed favourable gene-expression profiles in their immune cells UCLA research found people with high levels of the type of happiness that comes from consuming goods showed weak antiviral genes Doing good and feeling good have very different effects on the human genome, even though they generate similar levels of positive emotion
By Sarah Griffiths
PUBLISHED: 11:39 EST, 30 July 2013 | UPDATED: 11:41 EST, 30 July 2013
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People who derive their happiness from helping others, like Mother Teresa, have strong antibody genes, UCLA scientists claim
American scientists have found different types of happiness have surprisingly contrary effects on our genes.
UCLA research found that people who derive their happiness from helping others have strong antibody genes, while people who get their kicks from self-gratification can suffer from low antiviral and anitbody gene expression.
The study, which also involved the University of North Carolina, is the first of its kind to examine how positive psychology impacts human gene expression.
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Be happy - your genes will thank you for it: Doing good leads to strong immune cells
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Free NGS Report Demo – Bypass the Data Bottleneck with Genefficiency Services
Rapidly identify meaningful results with OGT's Genefficiency NGS Report
Oxford, UK Oxford Gene Technology (OGT), provider of innovative genetics research and biomarker solutions to advance molecular medicine, is offering the research community a snapshot of its user-friendly Genefficiency NGS Variant Analysis Report software, with the release of a free-to-download demo version. The interactive report efficiently manages the complete data analysis process for NGS workflows and delivers fully annotated data, allowing the identification of meaningful results in just a few simple mouse clicks.
The demo allows researchers to explore the easy-to-use features of the software with publicly-available sequence data from Tariq et al (2011)1, which identified a novel candidate gene (SHROOM3) for heterotaxy, a severe form of congenital heart disease. It provides researchers with a unique opportunity to experience the interactive report format, discovering what's possible with OGT's Genefficiency NGS Services. The report offers rapid filtering options, built-in quality control metrics and the ability to retrospectively analyse the data with additional or new selection criteria.
On completion of all OGT Genefficiency NGS exome and targeted panel projects, customers receive their results pre-loaded into the Genefficiency NGS Variant Analysis Report, so that they can quickly and easily identify relevant data. OGT's services cover the complete NGS pipeline, from project conception through to the delivery of high-quality, meaningful results via the software, bypassing the bottleneck of complex data analysis.
The Genefficiency NGS Variant Analysis Report is an intuitive solution to NGS data analysis and reporting. Thousands of variations can be filtered within minutes to just a handful requiring further validation with no requirement for additional bioinformatics resources. Bespoke analysis is easily integrated into the reporting software, allowing variants to be filtered based on biological function or other tailored criteria, for the easy identification of the most significant regions of genetic variation relevant to each individual study. Furthermore, the readily accessible in-depth quality metrics provide maximum confidence that the results are of the highest quality.
To download the demo, register here. For more information on OGT's Genefficiency services contact OGT or visit the website. References: 1. Tariq M, et al (2011). SHROOM3 is a novel candidate for heterotaxy identified by whole exome sequencing. Genome Biol. Sep 21;12(9):R91. doi: 10.1186/gb-2011-12-9-r91.
For further information, please contact: Oxford Gene Technology Begbroke Science Park Begbroke Hill Woodstock Road Begbroke, Oxfordshire, OX5 1PF, U.K T: +44 (0) 1865 856826 F: +44 (0) 1865 848684 E: contact@ogt.com W: http://www.ogt.com Twitter: @OxfordGeneTech
About Oxford Gene Technology Founded by Professor Ed Southern, Oxford Gene Technology (OGT) provides innovative genetics research and biomarker solutions to advance molecular medicine. The company has two trading businesses: Genomics comprises of CytoSure cytogenetics array, labelling and interpretation software products and services for the detection of chromosomal abnormalities, and Genefficiency Genomic Services, a unique combination of platforms, expertise and processing capabilities to deliver rapid, relevant genomic data. The Biomarkers business utilises proprietary next generation technologies to build a rich patent-protected portfolio of promising biomarkers for early stage cancer detection including advanced programmes in colorectal and prostate cancer plus the autoimmune disease systemic lupus erythematosus.
CytoSure and Genefficiency NGS browser/report: For Research Use Only; Not for Use in Diagnostic Procedures
CytoSure: This product is provided under an agreement between Agilent Technologies, Inc., and OGT. The manufacture, use, sale or import of this product may be subject to one or more of U.S. patents, pending applications, and corresponding international equivalents, owned by Agilent Technologies, Inc. The purchaser has the non-transferable right to use and consume the product for RESEARCH USE ONLY AND NOT for DIAGNOSTICS PROCEDURES. It is not intended for use, and should not be used, for the diagnosis, prevention, monitoring, treatment or alleviation of any disease or condition, or for the investigation of any physiological process, in any identifiable human, or for any other medical purpose.
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Free NGS Report Demo - Bypass the Data Bottleneck with Genefficiency Services
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Rare Genetic Mutation Linked To Congenital Heart Defects
July 30, 2013
April Flowers for redOrbit.com Your Universe Online
A team of scientists from The Research Institute at Nationwide ChildrensHospital has found a mutation in a gene crucial to normal heart development could play a role in some types of congenital heart defects the most common birth defect in the US. The findings were published in the journal Human Mutation and could help narrow the search for genes that contribute to this genetic defect, which affects as many as 40,000 newborns a year.
So far, several hundred genes have been implicated in the formation of the heart. Mutation in any one of those genes could potentially contribute to a cardiac defect. Vidu Garg, MD, is the principal investigator in the Center for Cardiovascular and Pulmonary Research and director of Translational Research in The Heart Center at Nationwide Childrens. He says identifying which of these genes is responsible for human congenital heart disease has been a challenge for researchers.
We have to ask ourselves, what subset of the more than 20,000 genes that make up the human genome are contributing to congenital heart disease? he says. Right now, we dont know enough about a lot of those genes, so this study provides another piece of the puzzle.
That puzzle piece is the so-called FOXP1 gene, a member of a large gene family that helps regulate tissues throughout the body, including in the heart, lungs and brain. Previous studies of FOXP1 have described its function and role in the development of the heart in animal models, but it took a former colleague calling up Dr. Garg to report the results of particularly interesting case to make him take a closer look at the gene.
Linda Baker, MD, from the University of Texas Southwestern Medical Center, found a rare genetic abnormality while analyzing a DNA sample from an 8-month-old infant who died from complications of complex congenital heart disease. The abnormality was a small chromosomal deletion in the FOXP1 gene.
Dr. Gargs team performed a search of DNA samples from patients with congenital heart disease in a repository at Nationwide Childrens one of the largest in the nation which revealed two additional patients with a similar heart defect who also had a rare mutation in the same gene.
The team analyzed the gene and found this mutation affected the genes ability to express a transcription factor called Nkx2.5, which has been implicated in congenital heart disease.
If you have three unrelated people with an abnormality in the same gene, and they also have an extremely rare type of congenital heart disease, theres a high likelihood that the gene is contributing to the condition, says Dr. Garg, who also is an associate professor of pediatrics at The Ohio State University College of Medicine. Understanding how either deletion or loss of FOXP1 affects normal heart development could help contribute to our understanding of congenital heart disease.
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Yes on Proposition 37 to Label Genetically Engineered Food? – Video
Yes on Proposition 37 to Label Genetically Engineered Food?
In this video Myles discusses an advert promoting proposition 37. Yes on Proposition 37 to Label Genetically Engineered Food? http://mylespower.co.uk/2012/10...
By: Myles Power (powerm1985)
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Yes on Proposition 37 to Label Genetically Engineered Food? - Video
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Genetic engineering may the only thing that can save the world’s oranges
Genetic engineering may save the orange tree from becoming an endangered speciesThere's a virulent disease destroying orange trees around the world, and growers are facing a hard choice genetically engineer the orange to survive this plague, or possibly see the fruit, and their livelihood, disappear.
The effects of Citrus GreeningThe disease, called Citrus Greening (or Huanglongbing or yellow dragon disease), is a bacteria that was first reported in China in the early 20th century, and it's spread by tiny insects called Asian citrus psyllids. Orange trees infected by this bacteria drop their leaves, and their fruit becomes stunted. There's no pesticide that can control the psyllids that carry the disease (they quickly adapted to the ones we have), and there's no treatment for the disease itself. The only way to 'treat' an infection is to quarantine the area and burn the infected trees. However, even those efforts aren't helping much. This disease has spread throughout the southern United States, Mexico and Central America, Brazil, southeast Asia and western Africa, threatening crops from the largest orange producers in the world.
[ Related: GMO companies launch website to fight anti-biotech movement ]
One source of hope, it seems, is genetic engineering.
According to a New York Times article from this past weekend (which I highly recommend reading), growers in Florida have been looking into genetic engineering since 2005, but despite some promising results so far, they are understandably worried about public reaction.
Genetically-modified organisms 'GMOs' have a very bad reputation with the public these days. It's hard to even mention them without someone speaking of the evils of Monsanto, or hearing the word 'frankenfood', or about how genetically-modified foods cause any number of illnesses and diseases. Given that it's our health and our lives that we're talking about, being concerned about what we're being given to eat is understandable.
However, historically, we've been genetically modifying our crops and livestock for centuries, if not millennia. It's been done through cross-breeding and cross-pollination, with mixed results. The point is, though, that it's very unlikely that anything we eat these days has gone without some kind of human manipulation at some point. New techniques of directly changing the DNA of the plant or animal cause more concerns, though, with talk of splicing in animal DNA into plants.
Take it from a self-proclaimed hippy who thinks Monsanto is evil, though, that's not what scientists are doing. They create artificial genes based on what they see in animal genes, rather than splicing animal genes directly into plant DNA. That may not help someone's perception of what's going on, since it still impacts how 'natural' a food is, but in that case, I'll simply point back to the start of the previous paragraph. Also, another point this 'hippy' makes is that the more 'natural' cross-breeding methods are no safer than directly altering DNA (in fact, the more direct method is the safer of the two).
The science speaks on behalf of GMOs as well. The American Association for the Advancement of Science wrote last October that "the World Health Organization, the American Medical Association, the U.S. National Academy of Sciences, the British Royal Society, and 'every other respected organization that has examined the evidence has come to the same conclusion: consuming foods containing ingredients derived from GM crops is no riskier than consuming the same foods containing ingredients from crop plants modified by conventional plant improvement techniques.'"
[ More Geekquinox: U.S. supercomputer now doubles power for hurricane forecasts ]
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Genetic engineering may the only thing that can save the world’s oranges
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Diverse sex-determining mechanisms revealed
Unstable genetic "capacitor" can "discharge" to accelerate the pace of evolutionary change.
Scientists historically have argued that evolution proceeds through gradual development of traits. But how can incremental changes apply to the binary switch between two sexes, male or female? Researchers at Case Western Reserve University's School of Medicine have found that a genetic process among the many species of rodents could have significant implications regarding our assumptions about sex determination and the pace of evolution.
"What we addressed is a long-standing puzzle in natural history: why different types of rodents can exhibit profound differences in how male sex is determined in the embryo," said Michael Weiss, MD, PhD, chairman of the Department of Biochemistry, the Cowan-Blum Professor of Cancer Research and a professor of biochemistry and medicine. "Some rodent populations have both XY males and XY females, and in other populations the Y chromosome has disappeared entirely."
In a study published in Proceedings of the National Academy of Sciences, Weiss and his research team analyzed the Sry gene, which is part of the Y chromosome. This mammalian gene, which steers differentiation in the embryonic gonad toward the development of testes, begins the process leading to the birth of males. For most mammals, including primates, Sry is a conserved feature of the Y chromosome, ultimately giving rise to male anatomy; females generally have two X chromosomes and no Y.
But within anomalous families of rodents, common in South America, activation of the Sry gene may have uncertain consequences. Some of these groups have both XY males and XY females as normal components of the population. Other related species have even lost their Y chromosomes altogether. Without the emergence of compensating ways of specifying sex, the species could not produce malesand would become extinct. For such rodents, therefore, evolution meant inventing entirely different methods of sex determination. These mammals have in essence evolved other ways to play nature's mating game.
The CWRU team attributed the rapid evolvability of sex determination in rodents to a novel protein domain added to the SRY protein. Scientists knew that this domain existed, but Weiss and his team wanted to understand more about its function in gene regulation and its role in evolution. The team determined that the new protein domain acts as a "genetic capacitor," providing a protective buffer to the Sry gene. This buffer allowed male development even when a mutation occurs elsewhere in the gene that might otherwise cause sex reversalbut the buffer is unstable over generations. Slippage of DNA during the production of sperm can lead to sudden changes in the length of the buffer and the degree of protection. By analogy to a capacitor in an electric circuit, the team suggested that this domain can "discharge" to accelerate the pace of evolutionary change. The idea of a genetic capacitor was pioneered by MIT Professor Susan Lindquist in studies of heat-shock proteins in fruit flies in (Nature, "Hsp90 as a capacitor for morphological evolution") and the present paper extended this idea to the pace of mammalian evolution.
How did the Sry buffer arise? "We discovered that a genetic accident 20 million years ago in an ancestral rodent holds the key to solving this puzzle. A simple DNA repeat sequence (called a 'micro-satellite') invaded the Y chromosome and was incorporated into the Sry gene. This invasion accelerated the evolvability of Sry and probably the Y chromosome in general, enabling this subgroup of rodents to explore new molecular mechanisms of sex determination," Weiss said.
Weiss and his team will continue this research, but believe these initial results may have additional implications for our understanding of human evolution and genetics. Because rodents have higher mutation rates and shorter life spans, they also evolve more rapidly and so provide a natural laboratory for studies of mammalian evolution.
Research last year at MIT has shown that in humans and other primates the Y chromosome has been stable for at least the past 25 million years (Nature, Strict evolutionary conservation followed rapid gene loss on human and rhesus Y chromosomes), which Weiss suggests may reflect the absence of micro-satellite-related slippage in the Sry gene. Yet the transcriptional strengths of the murine and human Sry factors are similar. The research suggests that human SRY and its specification of male development has evolved to be just above a genetic threshold of activity, which may in turn enable human communities to benefit from a diversity of male characteristics and behaviors.
"A key lesson of this 20 million-year history is that maleness is a 'close call' as the Sry protein functions near the edge of ambiguity," Weiss explained. "We think that the 'genetic decision' in an embryo to create a testis (instead of an ovary) is tenuous in all social mammals, including us. The critical next question is why?"
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Diverse sex-determining mechanisms revealed
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Dr. Bogdanka Militescu, Director General Personal Genetics invitata la matinalul Digi 24 – Video
Dr. Bogdanka Militescu, Director General Personal Genetics invitata la matinalul Digi 24
Testele genetice, preventia si tratamentele personalizate.
By: Personal Genetics
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TIGEM (Telethon Institute of Genetics and Medicine), Napoli – Video
TIGEM (Telethon Institute of Genetics and Medicine), Napoli
L #39;Istituto Telethon di Genetica e Medicina (TIGEM) è stato creato nel 1994 dalla Fondazione Telethon per promuovere l #39;avanzamento della ricerca finalizzata a...
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TIGEM (Telethon Institute of Genetics and Medicine), Napoli - Video
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Myriad Genetics Announces Date of Full-Year and Fourth-Quarter Fiscal 2013 Financial Results Conference Call
SALT LAKE CITY, July 30, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced it will hold its fourth-quarter 2013 sales and earnings conference call with institutional investors and analysts at 4:30 p.m. ET on Tuesday, Aug. 13. During the call, Peter D. Meldrum, president and chief executive officer; James Evans, chief financial officer; and Mark Capone, president, Myriad Genetics will provide an overview of Myriad's financial performance for the quarter and full year.
To listen to the call, interested parties in the United States may dial 800-404-5245 or +1- 303-223-2688 for international callers. All callers will be asked to reference reservation number 21668391. The conference call also will be available through a live webcast at http://www.myriad.com. A replay of the call will be available two hours after the end of the call for seven days and may be accessed by dialing 800-633-8284 within the United States or +1-402-977-9140 for international callers, and entering reservation number 21668391.
About Myriad Genetics
Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.
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Myriad Genetics Announces Date of Full-Year and Fourth-Quarter Fiscal 2013 Financial Results Conference Call
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Let’s Play Metal Gear Solid – Part 11 – Video
Let #39;s Play Metal Gear Solid - Part 11
During a training mission on Shadow Moses Island in February 2005, at a nuclear weapons facility on a remote island off the coast of Alaska, FOXHOUND and the...
By: Pro Starr
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Let's Play Metal Gear Solid - Part 11 - Video
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Inhalable gene therapy may help pulmonary arterial hypertension patients
Public release date: 30-Jul-2013 [ | E-mail | Share ]
Contact: Lauren Woods lauren.woods@mountsinai.org 212-241-2836 The Mount Sinai Hospital / Mount Sinai School of Medicine
The deadly condition known as pulmonary arterial hypertension (PAH), which afflicts up to 150,000 Americans each year, may be reversible by using an inhalable gene therapy, report an international team of researchers led by investigators at the Cardiovascular Research Center at Icahn School of Medicine at Mount Sinai.
In their new study, reported in the July 30 issue of the journal Circulation, scientists demonstrated that gene therapy administered through a nebulizer-like inhalation device can completely reverse PAH in rat models of the disease. In the lab, researchers also showed in pulmonary artery PAH patient tissue samples reduced expression of the SERCA2a, an enzyme critical for proper pumping of calcium in calcium compartments within the cells. SERCA2a gene therapy could be sought as a promising therapeutic intervention in PAH.
"The gene therapy could be delivered very easily to patients through simple inhalation -- just like the way nebulizers work to treat asthma," says study co-senior investigator Roger J. Hajjar, MD, Director of the Cardiovascular Research Center and the Arthur & Janet C. Ross Professor of Medicine and Professor of Gene & Cell at Icahn School of Medicine at Mount Sinai. "We are excited about testing this therapy in PAH patients who are in critical need of intervention."
This same SERCA2a dysfunction also occurs in heart failure. This new study utilizes the same gene therapy currently being tested in patients to reverse congestive heart failure in a large phase III clinical trial in the United States and Europe.
"What we have shown is that gene therapy restores function of this crucial enzyme in diseased lungs," says Dr. Hajjar. "We are delighted with these new findings because it suggests that a gene therapy that is already showing great benefit in congestive heart failure patients may be able to help PAH patients who currently have no good treatment options and are in critical need of a life sustaining therapy."
When SERCA2a is down-regulated, calcium stays longer in the cells than it should, and it induces pathways that lead to overgrowth of new and enlarged cells. According to researchers, the delivery of the SERCA2a gene produces SERCA2a enzymes, which helps both heart and lung cells restore their proper use of calcium.
"We are now on a path toward PAH patient clinical trials in the near future," says Dr. Hajjar, who developed the gene therapy approach. Studies in large animal models are now underway. SERCA2a gene therapy has already been approved by the National Institutes of Health for human study.
A Simple Inhalation Corrects Deadly Dysfunction
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Inhalable gene therapy may help pulmonary arterial hypertension patients
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uniQure to Build 55,000 Square Foot State-of-the-Art Gene Therapy Production Plant in US to Leverage AAV-Manufacturing …
AMSTERDAM, THE NETHERLANDS--(Marketwired - Jul 30, 2013) - uniQure B.V., a leader in human gene therapy, today announced it has commenced build-out of a state-of-the-art 55,000 square foot US manufacturing plant in Lexington, Massachusetts for the production of commercial grade Adeno Associated Virus (AAV)-based gene therapy products to complement its current EMA-approved site in Amsterdam, the Netherlands. The Company expects the facility to be operational by early 2015.
The US site will significantly expand the Company's current production capacity. Once completed, it is expected to allow uniQure to capitalize on its modular manufacturing platform and leverage its process leadership in commercial grade AAV manufacturing. With two validated manufacturing sites on stream, the Company will be able to ensure it can supply commercial grade material for its pipeline of products as they advance into pivotal studies and will be positioned as the partner of choice for the manufacturing, development and commercialization of AAV-based gene therapies.
In connection with uniQure's US expansion, the Company has appointed Lance Weed as VP US Operations. Mr. Weed was previously Executive Director, Site Operations at Amgen, and prior to that VP of Operations at BioVex Inc. Mr. Weed has extensive experience with the manufacturing of viral-based pharmaceuticals and oversaw the construction of Amgen's (BioVex's) launch grade viral vector manufacturing facility in Woburn, MA from scratch. He will join the Company on September 1.
In addition, uniQure raised USD 10 million in venture debt from Hercules Technology Growth Capital, Inc. (NYSE: HTGC) ("Hercules") to finance the build-out of the US plant, and for general working capital purposes.
"The construction of this facility represents our commitment to establishing a global, fully integrated gene therapy company as we continue to build on our leadership position in the field of AAV-based gene therapy products," said Jrn Aldag, CEO of uniQure.
About uniQure uniQure is delivering on the promise of gene therapy, single treatments with potentially curative results. We have developed a modular platform to rapidly bring new disease modifying therapies to patients with severe disorders. Our approach is validated by multiple partnerships and the regulatory approval of our lead product Glybera. http://www.uniqure.com.
About Hercules Technology Growth Capital, Inc.Hercules Technology Growth Capital, Inc. (NYSE: HTGC) ("Hercules") is the leading specialty finance company focused on providing senior secured loans to venture capital-backed companies in technology-related markets, including technology, biotechnology, life science and energy technology (aka cleantech) industries at all stages of development. Since inception (December 2003), Hercules has committed more than $3.8 billion to over 240 companies and is the lender of choice for entrepreneurs and venture capital firms seeking growth capital financing.
DisclaimerThis press release contains forward-looking statements based on uniQure's current expectations. These forward-looking statements include statements regarding the completion of the build-out of our new manufacturing facility, receipt of regulatory approval of our manufacturing facility, and the development of additional gene therapies. Actual results may differ materially from these forward-looking statements due to a number of factors, including uncertainties regarding further regulatory requirements, the success of further clinical trials, and competitive pressures. uniQure assumes no responsibility to update such forward-looking statements.
Press release (PDF): http://hugin.info/157414/R/1719581/572296.pdf
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uniQure to Build 55,000 Square Foot State-of-the-Art Gene Therapy Production Plant in US to Leverage AAV-Manufacturing ...
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Project Walk Carlsbad – Jose R. Spinal Cord Injury Milestone – Video
Project Walk Carlsbad - Jose R. Spinal Cord Injury Milestone
Jose R. suffered a C5/6 complete spinal cord injury in September of 2012. In his first visit to our Carlsbad location, he is showing that initial prognosis d...
By: Project Walk
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Project Walk Carlsbad - Jose R. Spinal Cord Injury Milestone - Video
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Discussing: My intro Stem Cell Therapy – Video
Discussing: My intro Stem Cell Therapy
This video explains my intro into the World of MS.
By: Tiffany Vinson
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Discussing: My intro Stem Cell Therapy - Video
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BrainStorm's NurOwn Cell Therapy Receives Orphan Drug Designation in the European Union for ALS
NEW YORK, NY and PETAH TIKVA, ISRAEL--(Marketwired - Jul 29, 2013) - BrainStorm Cell Therapeutics (OTCQB: BCLI), a leading developer of adult stem cell technologies for neurodegenerative diseases, today announced that the European Commission has granted Orphan Drug Designation for NurOwn, the Company's stem cell therapy consisting of autologous bone marrow-derived mesenchymal stromal cells secreting neurotrophic factors, for the treatment of Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig's Disease.NurOwn received Orphan Drug Designation from the Food and Drug Administration (FDA) in 2011.
Orphan drugs benefit from 10 years market exclusivity in the European Union (EU) after marketing approval. Additional benefits for sponsor companies include reduced fees for various centralized activities including applications for marketing authorization, inspections and protocol assistance, as well as possible eligibility for EU grants and other R&D-supporting initiatives.
BrainStorm is currently conducting a Phase IIa dose-escalating trial with 12 ALS patients at the Hadassah Medical Center in Jerusalem, Israel. The company anticipates launching a Phase II multi-center trial at three leading institutions in the United States towards the end of 2013, pending FDA approval.
About BrainStorm Cell Therapeutics, Inc.BrainStorm Cell Therapeutics Inc. is a biotechnology company engaged in the development of first-of-its-kind adult stem cell therapies derived from autologous bone marrow cells for the treatment of neurodegenerative diseases. The Company holds the rights to develop and commercialize its NurOwn technology through an exclusive, worldwide licensing agreement with Ramot, the technology transfer company of Tel Aviv University. For more information, visit the company's website at http://www.brainstorm-cell.com.
Safe Harbor Statement - Statements in this announcement other than historical data and information constitute "forward-looking statements" and involve risks and uncertainties that could cause BrainStorm Cell Therapeutics Inc.'s actual results to differ materially from those stated or implied by such forward-looking statements. Terms and phrases such as "may", "should", "would", "could", "will", "expect", "likely", "believe", "plan", "estimate", "predict", "potential", and similar terms and phrases are intended to identify these forward-looking statements.The potential risks and uncertainties include, without limitation, risks associated with BrainStorm's limited operating history, history of losses; minimal working capital, dependence on its license to Ramot's technology; ability to adequately protect the technology; dependence on key executives and on its scientific consultants; ability to obtain required regulatory approvals; and other factors detailed in BrainStorm's annual report on Form 10-K and quarterly reports on Form 10-Q available at http://www.sec.gov.These factors should be considered carefully, and readers should not place undue reliance on BrainStorm's forward-looking statements.The forward-looking statements contained in this press release are based on the beliefs, expectations and opinions of management as of the date of this press release. We do not assume any obligation to update forward-looking statements to reflect actual results or assumptions if circumstances or management's beliefs, expectations or opinions should change, unless otherwise required by law. Although we believe that the expectations reflected in the forward-looking statements are reasonable, we cannot guarantee future results, levels of activity, performance or achievements.
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BrainStorm's NurOwn Cell Therapy Receives Orphan Drug Designation in the European Union for ALS
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Nuvilex Is Ready to Lead the Medical Marijuana Research Arena
BALTIMORE, MD--(Marketwired - Jul 29, 2013) - Goldman Small Cap Research, a stock market research firm focused on the small cap and microcap sectors, notes in a recent article on its website that Nuvilex Inc.'s (OTCQB: NVLX) recent acquisition of all of the oncology-related assets and licenses for the use of a live-cell encapsulation therapy serves as a catalyst to accelerate the research engaged by its subsidiary, Medical Marijuana Sciences, Inc.
With exclusive worldwide rights in the entire oncology space, and with broad access to encapsulated live cells, management may elect to study the effects of multiple cannabidiol (CBD)-based cancer treatments. These studies would seek to combine the Company's highly efficacious live-cell encapsulation-based therapies used for oncology therapy, with therapies based on cannabidiol.CBD is one of about 70 constituents of Cannabis that are collectively known as cannabinoids. The medical marijuana arena is enjoying a great deal of attention and a growing cadre of investors and entrepreneurs as many prognosticatorsforecast huge revenue growth over the next 3 years as more states pass medical marijuana legislation. For example, independent financial news and data firm See Change Strategy estimates that the U.S. medical marijuana market is worth $1.7 billion and could reach $8.9 billion by 2016.
In a landmark announcement in mid-July of this year, a large-scale medical marijuana research study was just commissioned by the National Institutes of Health. This is significant due to the negative approach the federal government has previously taken towards medical marijuana. Observers may view this news as a potential softening of its position on marijuana which still classifies it as a Schedule I controlled substance.
According to Drexel University's website, Drexel has received a grant for a five-year study of medical marijuana and its impact on drug use and physical and psychological health among young adults in Los Angeles. It is the first large-scale NIH project funded to directly investigate medical marijuana use among young adults aged 18 to 26.
If these kinds of dollars are going to be provided by NIH, Nuvilex appears well positioned to be eligible to receive research lucrative grants or funding from other partner firms seeking to study the efficacy of live-cell encapsulation-based therapies used for oncology therapy, with those based on cannabidiol or other cannabinoids.Given that virtually no other firm in the space can match its clinical trials and oncology R&D experience, Nuvilex is primed to be a high-profile, go-to medical marijuana research force.
To view Nuvilex reports and articles and to view our disclaimer, please visit http://www.goldmanresearch.com.
About Goldman Small Cap Research: Led by former Piper Jaffray analyst and mutual fund manager Rob Goldman, Goldman Small Cap Research produces small cap and micro cap stock research reports, daily stock market blogs, and popular investment newsletters.For more information, visit http://www.goldmanresearch.com.
A Goldman Small Cap Research report is not intended as an offering, recommendation, or a solicitation of an offer to buy or sell the securities mentioned or discussed.Please read the report's full disclosures and analyst background on our website before investing. Neither Goldman Small Cap Research nor its parent is a registered investment adviser or broker-dealer with FINRA or any other agency. To download our research, view our disclosures, or for more information, visit http://www.goldmanresearch.com.
About Nuvilex, Inc. (OTCQB: NVLX): Nuvilex, Inc. has been a provider of all-natural products for many years, has expanded its company to increase its natural product-based footprint through medical marijuana studies and is becoming an international biotechnology provider of live, therapeutically valuable, encapsulated cells and services for treatments, research and medicine. The Company's offerings will ultimately include cancer, diabetes and other clinical treatments using the company's natural product knowledge, product base, cell and gene therapy expertise, and live-cell encapsulation technology in addition to other new products currently under development. For more information, visit http://www.nuvilex.com.
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Nuvilex Is Ready to Lead the Medical Marijuana Research Arena
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Bel Marra Health Reports on New Research Discovering an Obesity Gene That Increases One’s Risk of Obesity
Toronto, ON (PRWEB) July 29, 2013
Bel Marra Health, who offers high-quality, specially formulated vitamins and nutritional supplements, reports on a new study revealing a gene directly linking ones predisposal to obesity.
As Bel Marra Health reports in its article, (http://www.belmarrahealth.com/weight-management/the-fat-gene-is-real-what-to-do-if-you-have-it) approximately one-third of American adults are obese, putting them at an increased risk for a number of diseases including diabetes and heart disease. Obesity is not caused by any singular factor. Instead there are multiple factors at play, one of which is genetics. Researchers are beginning to understand the genetic factors involved in obesity, and more recently, they have pinpointed how a specific genetic variation vastly increases an individuals risk of the disease.
British researchers recently conducted a set of studies to examine why people who have two copies of a variant in the FTO gene are more likely to be obese. For the study, they asked 20 men (10 with the double FTO variant genes and 10 without) to rate how hungry they were before and after eating a meal. The researchers also took blood samples of the participants in order to assess levels of the hunger producing hormoneghrelin. Since ghrelin is meant to regulate the appetite, levels of ghrelin typically rise before meals and fall after meals. Although this pattern occurred in the men without the double FTO variant, those who had the variant experienced high ghrelin levels even after eating a meal, and the elevated ghrelin levels caused them to feel hungrier sooner than the other men.
Real-time brain imaging scans also revealed that having the two copies of the variant FTO gene changes the way that a persons brain responds to ghrelin. The scans revealed that neural responses in the brain region that regulate appetite were different in the group of men who had the double variation of the gene, causing them to be more sensitive to the presence of ghrelin. The brains of the men with the FTO variant also reacted differently to images of food, and these men rated pictures of high-calorie food as more appealing than the participants without the genetic variant. "Not only do these people have higher ghrelin levels and therefore feel hungrier, their brains respond differently to ghrelin and to pictures of food -- it's a double hit," said lead author Dr. Rachel Batterham.
According to the study, approximately 17 percent of the population carries this specific genetic variation, and these unfortunate individuals have a 70 percent greater likelihood of struggling with obesity, than people who do not have it. Batterham believes that this gene may have actually served an evolutionary purpose. "For the majority of the time that humans have existed, food has been scarce. Having this genetic variant would have conferred a survival advantage," she explains.
The researchers also used human and mice cells to pinpoint how the double FTO variant causes an increase in ghrelin levels. They discovered that the increased expression of the FTO gene, caused by having the double variant, unlocks the genetic template that produces ghrelin. Consequently, causes an increased production of the hunger producing hormone. "We've known for a while that variations in the FTO gene are strongly linked with obesity, but until now we didn't know why," says Batterham. "What this study shows us is that individuals with two copies of the obesity-risk FTO variant are biologically programmed to eat more."
Previous studies have found that ghrelin (and therefore persistent hunger) can be reduced by eating a high-protein diet. Moreover, a high-protein diet has long been recommended for those with weight loss goals in mind. High-protein foods include chicken, fish, and egg whites, among others. It is important to remember, however, that genes are just one of the many contributing factors to obesity, and obesity can be overcome with dietary and lifestyle modifications even if one does carry the obesity genes.
(SOURCE: Reuters. "Scientists Find How "obesity Gene" Makes People Fat." NewsDaily. N.p., 15 July 2013.)
Bel Marra Health is the maker of LipoLose, a high-quality nutritional supplement that helps suppress appetite and promotes fast weight loss. All ingredients are backed with scientific evidence. Every product is tested for safety, quality, and purity at every stage of the manufacturing process. Furthermore, Bel Marra Health products are produced only in Health Canada approved facilities, going the extra mile to ensure that our health-conscious customers are getting top quality products. For more information on Bel Marra Health visit belmarrahealth.com or call 1-866-531-0466.
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Bel Marra Health Reports on New Research Discovering an Obesity Gene That Increases One’s Risk of Obesity
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Researchers identify genetic mutation linked to congenital heart disease
Public release date: 29-Jul-2013 [ | E-mail | Share ]
Contact: Gina Bericchia Gina.Bericchia@NationwideChildrens.org 614-355-0495 Nationwide Children's Hospital
A mutation in a gene crucial to normal heart development could play a role in some types of congenital heart diseasethe most common birth defect in the U.S. The finding, from a team in The Research Institute at Nationwide Children's Hospital, could help narrow the search for genes that contribute to this defect, which affects as many as 40,000 newborns a year. The findings were published in a recent issue of in Human Mutation.
Several hundred genes have been implicated in the formation of the heart, and a mutation in any of them could potentially contribute to a cardiac defect. Identifying which of these genes is involved in human congenital heart disease has been a challenge for scientists in the field, says Vidu Garg, MD, senior author of the new study, principal investigator in the Center for Cardiovascular and Pulmonary Research and director of Translational Research in The Heart Center at Nationwide Children's.
"We have to ask ourselves, what subset of the more than 20,000 genes that make up the human genome are contributing to congenital heart disease?" he says. "Right now, we don't know enough about a lot of those genes, so this study provides another piece of the puzzle."
That piece is FOXP1, a member of a large gene family that helps regulate tissues throughout the body, including in the heart, lungs and brain. A few studies on FOXP1 had described its function and role in cardiac development in animal models, but it wasn't until a former colleague called with an interesting case that Dr. Garg decided the gene was worth a closer look.
While analyzing a DNA sample from an 8-month-old infant who died from complications of complex congenital heart disease, Linda Baker, MD, at the University of Texas Southwestern Medical Center, had found a rare genetic abnormalitya small chromosomal deletionin the patient's FOXP1 gene.
A search of DNA samples from patients with congenital heart disease in a repository at Nationwide Children'sone of the largest in the nationrevealed two additional patients with a similar complex heart defect who had a rare mutation in the same gene. On further analysis, Dr. Garg's team found that this mutation affected the gene's ability to express a transcription factor called Nkx2.5, which has been implicated in congenital heart disease.
"If you have three unrelated people with an abnormality in the same gene, and they also have an extremely rare type of congenital heart disease, there's a high likelihood that the gene is contributing to the condition," says Dr. Garg, who also is an associate professor of pediatrics at The Ohio State University College of Medicine. "Understanding how either deletion or loss of FOXP1 affects normal heart development could help contribute to our understanding of congenital heart disease."
The next step in the research is to see if they can find the FOXP1 mutation in patients with different types of congenital heart disease. From there, they will begin to look at how the gene interacts with others involved in the formation of a normal heart. Given that congenital heart disease is probably the result of mutations in many genes, Dr. Garg says, it's quite possible that by studying this gene and its potential partners, we can uncover other potential candidate genes for heart malformations.
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Researchers identify genetic mutation linked to congenital heart disease
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The PMO is talking the GMO language but people will fight it out
India, July 29 -- Four major committees of the Government of India, including the Parliamentary Standing Committee on Agriculture, have called for a moratorium on testing Genetically Modified (GM) food. Now, we also have the Technical Expert Committee (TEC) report submitted to the Supreme Court which is strong in its recommendations. Both democracy and science support a ban on GMOs.
Earlier, Jairam Ramesh as environment minister had decided to stop the testing of Bt Brinjal. Ramesh was compelled, after the series of public hearings which he thankfully attended. Why? It was because he realised that the government's position was not backed by science; instead, science was on the side of those who called for it to not be introduced.
What we know from science is that the complexity of the DNA and gene has not been completely understood. Genetic engineering is based on the orthodox genetic reductionism, genetic determinism and the false assumption that one gene contributes to one trait. Science teaches us that a trait has contributions from many genes and the context in which the organism is. Disciplines like gene ecology and epigenetics have made genetic reductionism obsolete. Yet, the GM industry and pseudo-scientists are pushing ahead with genetic modification.
Every claim that the GMO industry made in the last 20 years has proved to be false. The first was that GM foods will be a solution to hunger and give us food security. Nothing could be farther from the truth. Vidarbha's Bt Cotton story proves this. Monsanto had promised 1500 kg per acre when it started trials; the yield today is 400 kg per acre. The second was that pesticide use will reduce; there has been a 13-fold rise, the bollworm became resistant to pesticides and new pests emerged.
Even in the US, the use of herbicides has gone up by 15 per cent with GM crops. Pests have become super-pests, weeds have become super-weeds. There's evidence that GMOs are killing beneficial species both in the soil and our gut. Finally, it's seed monopoly. GMOs mean patents, patents mean royalties. That's why GMOs are being pushed. It's a fact that 95 per cent of cotton seed in India is now owned by Monsanto.
On purely scientific basis, India should not have GMOs or GM foods but there seem to be extraneous reasons.
I would say that the PMO is bulldozing us, as a nation, into doing what's not backed by evidence and what should never be done. The PMO is pushing the GMO agenda, especially GM foods, because it's a commitment he made, under the Indo-US Agriculture Knowledge Initiative, to the US government. So, the PMO is talking the language of the GMO industry.
There are others like Sharad Pawar who pushes for GMO even though he has been totally countered by data. He is too close to the GM lobby, to Monsanto, to take an independent view. There are industry-led lobby groups who are paid to peddle the industry's version. And, the government does not listen to independent voices and look at scientific evidence.
On no count is genetic engineering delivering on its promises. GMO technology has proved to be inefficient compared to all available alternatives. If we allow this technology to wipe out our biodiversity, farmers, food security, society, it would be a crime.
Now that Monsanto and Blackwater, a private military, have joined forces it's even more dangerous. They will use all undemocratic means to mobilise the market here. The BRAI Bill is an example. They have made seed their weapon of control.
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The PMO is talking the GMO language but people will fight it out
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Genetic Engineering: A New Use for Algae in Biofuel Production
Lawrence, KS (PRWEB) July 29, 2013
Phycologia In recent years major companies from all over the globe, including Exxon Mobile and Itochu Corporation, have merged with research facilities to research algae as a renewable energy source. However, it has been determined that far more research is needed before movement to the commercial production phase of algae biofuel can truly take place. A recent research study took up this challenge and examined a promising freshwater algal strain for possible genetic engineering applications that could make it a viable biofuel.
An article in the journal Phycologia takes an in-depth look at the genetic structure of a unicellular green alga, Botryococcus braunii, and explores its unique ability to be utilized in the genetic engineering of biofuel development. Botryococcus braunii was initially selected for large-scale biofuel production because of its extraordinary ability to synthesize large amounts of hydrocarbon oils. Several difficulties were encountered in the initial production and harvesting processes, leaving it by the wayside. However, this latest research reintroduces B. braunii as the perfect vehicle for genetic engineering applications when compared with three other species of green algae, five species of land plants, and eight other phyla species, including bacteria, archaea, fungi, and mammals.
The research focused on the codon usage, or DNA compatibility, of B. braunii with the other organisms. Codon usage for this particular alga is one of the fundamental genetic markers that had not been explored. Codons are greatly affected by the vast amount of guanines (G) and cytosines (C), two of the four nucleotides that make up a DNA molecule. Many green algal species having high GC content, which causes codon usage bias, or poor compatibility, with other organisms. Surprisingly, B. braunii had comparatively low GC content and its codon usage was similar to that of bacteria, mammals, and land plants.
Although further study is necessary, the ability of B. braunii to synthesize hydrocarbons, combined with the newly discovered codon usage and GC content data, could lead to new genetic engineering techniques that could hasten biofuel development and production.
Full text of the article, Codon usage of Botryococcus braunii (Trebouxiophyceae, Chlorophyta): implications for genetic engineering applications, Phycologia, Vol. 52, No. 4, 2013, is available at http://www.phycologia.org/doi/full/10.2216/12-041.1
About Phycologia Phycologia is the official publication of the International Phycological Society and publishes papers on any aspect of algal research. For more information, visit http://www.intphycsoc.org.
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Genetic Engineering: A New Use for Algae in Biofuel Production
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We’re Crazy Close To A Cure For Allergies – Video
We #39;re Crazy Close To A Cure For Allergies
Allergies are perhaps the most unpleasant part of spring and summer... but they could all be coming to an end! Anthony explains. Read More: Johns Hopkins res...
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We're Crazy Close To A Cure For Allergies - Video
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Unraveling genetic networks
Public release date: 29-Jul-2013 [ | E-mail | Share ]
Contact: Jason Socrates Bardi jbardi@aip.org 240-535-4954 American Institute of Physics
WASHINGTON D.C., July 29, 2013 -- If genes are the currency of life, then the whole economies are genetic networks, which include genes as well as the complex webs of interactions and interconnections between them. Genetic networks are integrally important to the proper development and functioning of an organism, just as genes are, but they tend to be far more complex and difficult to understand.
Because of their complexity, the field has been slow to unravel genetic networks, said Leon Glass, the Isadore Rosenfeld Chair in Cardiology and a professor of physiology at McGill University.
Now a special issue of the journal CHAOS, produced by AIP Publishing, explores new experimental and theoretical techniques for unraveling genetic networks.
"Most emphasis has been on the properties of individual genes, and mutations in individual genes have been identified that lead to diseases, such as the cystic fibrosis gene," said Glass. But the proper expression of individual genes is regulated by both environmental factors, metabolic factors and the expression of other genes in the body, he added.
"To understand these interactions," Glass said, "it is essential to consider genetic networks."
Because of the convoluted interconnectedness of gene networks, researchers have realized that they might best be understood using nonlinear dynamics -- an analytical method to understand systems (such as the weather) in which simple changes can have complex, cascading and even chaotic effects.
Just such methods are the subject of the special issue of CHAOS. Included among the collection of articles are two papers describing powerful new methods to understand very large genetic networks and a paper combining experimental and theoretical work to unravel the genetic networks controlling development in fruit flies.
"The rapid expansion of biologic data concerning structure and dynamics of genetic networks makes it essential to develop appropriate computer and analytical methods to deal with these problems," said Glass, who was an early pioneer in the development of theoretical methods for understanding gene network models. Glass is the author of the introduction to the new issue along with James Collins, an HHMI Investigator and a bioengineering professor at Boston University and Harvard's Wyss Institute, and Rka Albert, a professor of physics and biology at Pennsylvania State University.
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Unraveling genetic networks
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Evolution of diverse sex-determining mechanisms in mammals
Public release date: 29-Jul-2013 [ | E-mail | Share ]
Contact: Amanda Petrak amanda.petrak@case.edu 216-368-0345 Case Western Reserve University
Scientists historically have argued that evolution proceeds through gradual development of traits. But how can incremental changes apply to the binary switch between two sexes, male or female? Researchers at Case Western Reserve University's School of Medicine have found that a genetic process among the many species of rodents could have significant implications regarding our assumptions about sex determination and the pace of evolution.
"What we addressed is a long-standing puzzle in natural history: why different types of rodents can exhibit profound differences in how male sex is determined in the embryo," said Michael Weiss, MD, PhD, chairman of the Department of Biochemistry, the Cowan-Blum Professor of Cancer Research and a professor of biochemistry and medicine. "Some rodent populations have both XY males and XY females, and in other populations the Y chromosome has disappeared entirely."
In a study published in Proceedings of the National Academy of Sciences, Weiss and his research team analyzed the Sry gene, which is part of the Y chromosome. This mammalian gene, which steers differentiation in the embryonic gonad toward the development of testes, begins the process leading to the birth of males. For most mammals, including primates, Sry is a conserved feature of the Y chromosome, ultimately giving rise to male anatomy; females generally have two X chromosomes and no Y.
But within anomalous families of rodents, common in South America, activation of the Sry gene may have uncertain consequences. Some of these groups have both XY males and XY females as normal components of the population. Other related species have even lost their Y chromosomes altogether. Without the emergence of compensating ways of specifying sex, the species could not produce malesand would become extinct. For such rodents, therefore, evolution meant inventing entirely different methods of sex determination. These mammals have in essence evolved other ways to play nature's mating game.
The CWRU team attributed the rapid evolvability of sex determination in rodents to a novel protein domain added to the SRY protein. Scientists knew that this domain existed, but Weiss and his team wanted to understand more about its function in gene regulation and its role in evolution. The team determined that the new protein domain acts as a "genetic capacitor," providing a protective buffer to the Sry gene. This buffer allowed male development even when a mutation occurs elsewhere in the gene that might otherwise cause sex reversalbut the buffer is unstable over generations. Slippage of DNA during the production of sperm can lead to sudden changes in the length of the buffer and the degree of protection. By analogy to a capacitor in an electric circuit, the team suggested that this domain can "discharge" to accelerate the pace of evolutionary change. The idea of a genetic capacitor was pioneered by MIT Professor Susan Lindquist in studies of heat-shock proteins in fruit flies in (Nature, "Hsp90 as a capacitor for morphological evolution") and the present paper extended this idea to the pace of mammalian evolution.
How did the Sry buffer arise? "We discovered that a genetic accident 20 million years ago in an ancestral rodent holds the key to solving this puzzle. A simple DNA repeat sequence (called a 'micro-satellite') invaded the Y chromosome and was incorporated into the Sry gene. This invasion accelerated the evolvability of Sry and probably the Y chromosome in general, enabling this subgroup of rodents to explore new molecular mechanisms of sex determination," Weiss said.
Weiss and his team will continue this research, but believe these initial results may have additional implications for our understanding of human evolution and genetics. Because rodents have higher mutation rates and shorter life spans, they also evolve more rapidly and so provide a natural laboratory for studies of mammalian evolution.
Research last year at MIT has shown that in humans and other primates the Y chromosome has been stable for at least the past 25 million years (Nature, Strict evolutionary conservation followed rapid gene loss on human and rhesus Y chromosomes), which Weiss suggests may reflect the absence of micro-satellite-related slippage in the Sry gene. Yet the transcriptional strengths of the murine and human Sry factors are similar. The research suggests that human SRY and its specification of male development has evolved to be just above a genetic threshold of activity, which may in turn enable human communities to benefit from a diversity of male characteristics and behaviors.
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Evolution of diverse sex-determining mechanisms in mammals
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Parents don't fully understand biobank research, study finds
Public release date: 29-Jul-2013 [ | E-mail | Share ]
Contact: Gina Bericchia Gina.Bericchia@NationwideChildrens.org 614-355-0495 Nationwide Children's Hospital
Researchers who collect genetic samples from children for medical research need to explain the process more clearly to parents, according to a new study that suggests many parents don't fully understand the finer details about how these samples will be used and stored. The study was published in June in Genetics in Medicine.
Kim McBride, MD, MS, principal investigator in the Center for Cardiovascular and Pulmonary Research in The Research Institute at Nationwide Children's Hospital, and colleagues followed up with families enrolled in a genetic biobanka storage facility for DNA, genetic data, and tissue samplesafter their initial consent, to find out whether they were fully aware of the nature of their agreement. The results were alarming: more than half of all parents misunderstood key concepts of the study.
Ensuring parental understanding of the consent process is a crucial element of ethical genetics research, says Dr. McBride. For the study, he and his colleagues collected anonymous questionnaires from families that had consented between 2004 and 2008 to the storage and analysis of their children's DNA samples in a genetic biobank. The biobank was created to study the genetics of congenital malformations of the heart's left ventricular outflow tract.
The researchers found that, while parents had a good grasp of some consent concepts, other important information was poorly understood. For example, parents understood that their consent was voluntary and the samples would be used for research on the causes of heart defects. However, they overestimated how the research might benefit their child and undervalued the risks of enrolling in the study.
"Although the primary purpose of the study was to obtain biologic samples for future testing, parents did not understand that their child's samples would be stored indefinitely," Dr. McBride says. When both parents were involved in the decision, they displayed a better overall understanding of the true nature of the consent agreement than parents making the decision alone.
Most families participating in research are involved with clinical trials, which involve a different set of expectations and agreements during the consent process than genetic sampling. "Participants in a clinical trial are enrolled in a treatment and are followed over time with the expectation that they may receive a new and better therapy," Dr. McBride says. In a biobank study, however, participants cannot typically expect any personal benefit or even any follow-up.
This is starting to change, however. Some new models for biobank studies are more inclusive of the research subject, offering on-going contact and return of results that may impact their health, says Dr. McBride, who also is an assistant professor in pediatrics at The Ohio State University College of Medicine. "To provide individuals and families with adequate knowledge to participate in genetic research, informed consent delivery must evolve, especially as the demand for genomic data increases."
Interventions to improve understandingoften incorporating visual aids and video consentingprovide promising results, but few studies demonstrate their effectiveness for biobanking consent. Furthermore, there is currently no movement to adopt these techniques widely, something Dr. McBride says warrants consideration. "The focus of researchers should shift to how to improve the informed consent process through alternative methods of consent delivery, so that consenting families are truly informed partners in genetic research."
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Parents don't fully understand biobank research, study finds
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