Healthier men, one moustache at a time - Adam Garone
View full lesson: http://ed.ted.com/lessons/healthier-men-one-moustache-at-a-time-adam-garone Adam Garone has an impressive moustache, and it #39;s for a good ca...

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Hello, Deneb! #9 -- Ramps and self.DNA() -- JET Plays Minecraft
I #39;ve finally returned to construction on my island tower fortress citadel castle city, as yet unnamed. I begin this two-part section wherein all I accomplish...

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#1B

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#39;Errors of the Human Body #39; Trailer
http://www.hollywood.com #39;Errors of the Human Body #39; Trailer Director: Eron Sheean Starring: Michael Eklund, Karoline Herfurth, Tómas Lemarquis Following divo...

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BOSTON and BIRMINGHAM,England, April 9, 2013 /PRNewswire/ --Cartagenia, the world leader in providing genetic labs and clinicians software-based workflow support for variant assessment, lab reporting, and integration of diagnostic knowledge-bases, announced today that it has signed a license agreement for its cloud-based BENCHlab CNV solution for genetic variant storage and analysis with West Midlands Regional Genetics Laboratory (WMRGL) at Birmingham Women's Hospital NHS Foundation Trust (BWHFT).

WMRGL is the first UK-based lab to license the Cartagenia BENCHlab CNV platform, a software and database solution created in collaboration with genetics labs and clinical experts to automate and speed up testing practices and develop high-quality lab reports. For WMRGL, the Cartagenia solution will support the storage, filtration, analysis and interpretation of CNV data produced by the laboratories' pre- and post-natal testing services. The BENCHlab solutions can also handle NGS data generated as gene panels, exomes and whole genomes and can automatically generate clinical reports specific to a laboratory's needs.

The Cartagenia BENCHlab platform will also help link clinical and phenotypic data from the Fetal Medicine Centre at BWHFT with genetic data generated at WMRGL for submission into the UK EACH (Evaluation of Array Comparative Genomic Hybridisation in Prenatal Diagnosis of Fetal Anomalies) research project, a three-year national, multi-center study designed to assess how array CGH testing (also known as chromosomal microarray analysis) compares to traditional karyotyping in prenatal diagnosis in terms of detecting chromosomal imbalances in fetuses. The EACH project is built on another Cartagenia product, BENCHlab Consortium, a solution for multi-center genotype and phenotype data aggregation projects.

Additionally, Cartagenia is working with WMRGL and several other centres in the UK's National Health Service (NHS) to create a pilot national CNV database in which UK-based diagnostic labs can optimally pool and share their genetic information. As envisioned, that database will ultimately be linked to the International Collaboration of Clinical Genetics (formerly ISCA), an even larger pool of research consortia.

"We are a very large lab with a Regional Genetics Service serving a population of nearly 6 million people, and the Cartagenia BENCHlab product is the perfect tool for us to add quality and consistency to our data collection and analytical needs," said Dom McMullan, Principal Clinical Scientist at WMRGL. "BENCHlab is an attractive option because it's platform neutral, with very robust and adaptable filtering options, allowing us to more easily manage, collect and store various types of microarray data. BENCHlab will provide us a more consistent output and aid us in bringing consistency to our analyses."

Cartagenia CEO Herman Verrelst noted that working with BWHFT and WMRGL provides Cartagenia an important entrance to the UK market as well as the UK EACH research project.

"We are very pleased to have our BENCHlab tool serving such a respected and important lab as the WMRGL," Verrelst said. "We believe partnering with WMRGL in the piloting of a national UK-based CNV database will prove that our BENCHlab platform is the perfect collaborative tool that allows labs to pool and share information and improve the quality of the data and diagnostic yield of their efforts. Furthermore, this database could serve as a cornerstone in our effort to market to other genetics labs in the UK and in Europe as well as help create a network to provide and promote better patient care."

About BWHFT and WMRGL

BWHFT provides a range of healthcare services to women and men across the West Midlands and beyond. Services include maternity, gynecology, fetal medicine, neonatal intensive care, genetics, radiology, specialist pathology and fertility medicine. WMRGL provides fully comprehensive germline and cancer genetic diagnostic programme services with a strong research and development component to a population of nearly 6 million and is the largest NHS diagnostic laboratory in the UK.

About Cartagenia

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Apr. 9, 2013 Scientists at The University of Manchester have found evidence of the genetic basis of the evolutionary arms-race between parasitoids and their aphid hosts.

The researchers studied the reaction of aphids when a parasitic wasp with genetic variation laid eggs in them. They found that different genotypes of the wasp affected where the aphids went to die, including whether they left the plant host entirely. The team also found an example of the emergence of a shared phenotype that was partly wasp and partly aphid.

Dr Mouhammad Shadi Khudr, a visiting scientist at the Faculty of Life Sciences, led the research: Natural selection on the aphid prey depends not only on aphid genes, but also on the genetics of the parasitic wasp. The indirect genetic effects underlying the relationship between natural enemies have been rarely shown, especially when they arise between species. Parasite-manipulation is endlessly fascinating, albeit with a somewhat ghoulish quality! This study sheds light on how genetic variation can influence that manipulation.

The researchers began the study by breeding 13 males with 3 females of the wasp Aphidius ervi, through which a quantitative genetic design was created. The resulting offspring of full and half siblings provided a basis of genetic variation in the parasitic wasp to test how different individuals of the latter are associated with variation in the aphids behaviour when aphids are prone to the wasps manipulation. One genotype of the pea aphid Acyrthosiphon pisum was chosen. Since this species reproduces asexually by parthenogenesis, the resulting genetically identical individuals make up a specific type of colony known as clone.

The team then introduced the wasps into 156 cages that contained a broad bean plant and an aphid colony. They then compared the behaviour of aphids in the presence and absence of the wasp by monitoring what the aphids did over the next ten days. Successful parasitism ends with the death of the aphid host which becomes a pale brownish remainder called a mummy. Once the aphids had mummified, the location of each mummy was recorded according to its position on the plant and at other locations within the cage.

Dr Khudr says: Our results confirm that parasitism by a parasitoid wasp can lead to behavioural modifications in an aphid host. The effect of the wasp fathers was significant on the distribution of the parasitised and non-parasitised aphids. There was also a notable effect of mothers indicating a maternal influence on the distribution of parasitised vs. non-parasitised aphids. This can reflect a fitness-difference between father families.

As well as monitoring their behaviour whilst they were alive, the positions of the aphids bodies once the new wasp has hatched also varied both on and off the plants. This variation was dependent on the wasp genotype. Its this relationship between the wasp and its host which starts with parasitism and ends with predation that fascinates Dr Khudr.

What were witnessing on the broad bean plants is an evolutionary arms-race between two enemies where each one strives to cap each others fitness. This can be observed through varying manipulative strategies applied by the parasitic wasps in order to subdue their hosts. The wasp has to ensure the aphid can be kept alive long enough to ensure it can mature. The parasitised aphid will on occasion commit suicide if it realises it has the wasp growing within it and by doing so it can save the rest of the colony from a subsequent attack. What weve been able to do in this study is to open the window on how the genetics of one species influence the behaviour and manipulation of another host species.

The findings have been published in the Royal Societys Biology Letters. Discussing the findings Dr Khudr says he was surprised by what the team recorded: We had expected some variation in the aphids movement and behaviour but not to the extent that we witnessed. An organisms phenotype (behaviour) can be the product of the genes expressed in another organism

The next step is to carry out further research to establish if specific genes in the wasps can be linked to particular behaviours in the aphids. Dr Khudr hopes this type of information could increase our understanding of the importance of genetic diversity in ecosystem services, and lead to the development of better biological controls for aphid populations.

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Genetics of life and death in an evolutionary arms-race

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ADAPTED FROM: PETER DAZELEY/GETTY

When Sharlayne Tracy showed up at the clinical suite in the University of Texas (UT) Southwestern Medical Center in Dallas last January, the bandage wrapped around her left wrist was the only sign of anything medically amiss. The bandage covered a minor injury from a cheerleading practice led by Tracy, a 40-year-old African American who is an aerobics instructor, a mother of two and a college student pursuing a degree in business. I feel like I'm healthy as a horse, she said.

Indeed, Tracy's well-being has been inspiring to doctors, geneticists and now pharmaceutical companies precisely because she is so normal. Using every tool in the modern diagnostic arsenal from brain scans and kidney sonograms to 24-hour blood-pressure monitors and cognitive tests researchers at the Texas medical centre have diagnostically sliced and diced Tracy to make sure that the two highly unusual genetic mutations she has carried for her entire life have produced nothing more startling than an incredibly low level of cholesterol in her blood. At a time when the target for low-density lipoprotein (LDL) cholesterol, more commonly called 'bad cholesterol', in Americans' blood is less than 100 milligrams per decilitre (a level many people fail to achieve), Tracy's level is just 14.

A compact woman with wide-eyed energy, Tracy (not her real name) is one of a handful of African Americans whose genetics have enabled scientists to uncover one of the most promising compounds for controlling cholesterol since the first statin drug was approved by the US Food and Drug Administration in 1987. Seven years ago, researchers Helen Hobbs and Jonathan Cohen at UT-Southwestern reported1 that Tracy had inherited two mutations, one from her father and the other from her mother, in a gene called PCSK9, effectively eliminating a protein in the blood that has a fundamental role in controlling the levels of LDL cholesterol. African Americans with similar mutations have a nearly 90% reduced risk of heart disease. She's our girl, our main girl, says Barbara Gilbert, a nurse who has drawn some 8,000 blood samples as part of Cohen and Hobbs' project to find genes important to cholesterol metabolism.

Of all the intriguing DNA sequences spat out by the Human Genome Project and its ancillary studies, perhaps none is a more promising candidate to have a rapid, large-scale impact on human health than PCSK9. Elias Zerhouni, former director of the US National Institutes of Health (NIH) in Bethesda, Maryland, calls PCSK9 an iconic example of translational medicine in the genomics era. Preliminary clinical trials have already shown that drugs that inhibit the PCSK9 protein used with or without statins produce dramatic reductions in LDL cholesterol (more than 70% in some patients). Half-a-dozen pharmaceutical companies all aiming for a share of the global market for cholesterol-reducing drugs that could reach US$25 billion in the next five years according to some estimates are racing to the market with drugs that mimic the effect of Tracy's paired mutations.

Stephen Hall talks about Sharlaynes unusual condition and whether similar cases might lead to a new line of drugs.

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Zerhouni, now an in-house champion of this class of drug as an executive at drug firm Sanofi, headquartered in Paris, calls the discovery and development of PCSK9 a beautiful story in which researchers combined detailed physical information about patients with shrewd genetics to identify a medically important gene that has made super-fast progress to the clinic. Once you have it, boy, everything just lines up, he says. And although the end of the PCSK9 story has yet to be written the advanced clinical trials now under way could still be derailed by unexpected side effects it holds a valuable lesson for genomic research. The key discovery about PCSK9's medical potential was made by researchers working not only apart from the prevailing scientific strategy of genome research over the past decade, but with an almost entirely different approach.

As for Tracy, who lives in the southern part of Dallas County, the implications of her special genetic status have become clear. I really didn't understand at first, she admits. But now I'm watching ads on TV [for cholesterol-lowering drugs], and it's like, 'Wow, I don't have that problem'.

Cardiovascular disease is and will be for the foreseeable future, according to the World Health Organization the leading cause of death in the world, and its development is intimately linked to elevated levels of cholesterol in the blood. Since their introduction, statin drugs have been widely used to lower cholesterol levels. But Jan Breslow, a physician and geneticist at Rockefeller University in New York, points out that up to 20% of patients cannot tolerate statins' side effects, which include muscle pain and even forgetfulness. And in many others, the drugs simply don't control cholesterol levels well enough.

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Genetics: A gene of rare effect

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BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today announced that research related to its antibody-drug conjugate (ADC) technology was presented in multiple sessions at the 104th Annual Meeting of the American Association for Cancer Research (AACR) being held in Washington, D.C. Three data presentations highlight the rapid progress being made in ADC technology and testing. This includes preclinical data evaluating ADCs using a potent and newly developed cytotoxic agent, pyrrolobenzodiazepine (PBD) dimer, against two targets, CD33 and CD70. The former, SGN-CD33A, is expected to be advanced into a phase 1 clinical trial in 2013 for patients with acute myeloid leukemia (AML). In addition, preclinical data demonstrate activity of a new ADC for metastatic breast cancer, SGN-LIV1A, utilizing the same proprietary ADC technology as ADCETRIS (brentuximab vedotin). The company also presented research on a novel method for making highly stable linkers, an advance that is being evaluated for potential future ADCs. In addition, many of the companys collaborators, including Genentech, Pfizer, Progenics and Genmab, are reporting preclinical and clinical data from multiple ADC programs utilizing Seattle Genetics proprietary ADC technology.

As the leader in developing ADCs for the treatment of cancer, we are focused on both the current and future technology of this important class of therapeutics. More than half of the ADCs currently in clinical development utilize our technology, and we continue to advance additional candidates, such as SGN-CD33A and SGN-LIV1A, at a rapid pace. We are also looking at ways to enhance the next generation of ADCs, and believe that new potent cytotoxic agents such as PBD dimers, advances in antibody technology such as engineered cysteine antibodies (EC-mAbs), and highly stable linkers are part of that future, said Jonathan Drachman, M.D., Senior Vice President, Research and Translational Medicine at Seattle Genetics. We are driven to test these ADC advances quickly because cancer patients need new options to fight this relentless disease.

ADCs are designed to harness the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. This approach is intended to spare non-targeted cells and thus reduce many of the toxic effects of traditional chemotherapy while enhancing antitumor activity. Seattle Genetics and its collaborators have ten data presentations at AACR that highlight the widespread evaluation of its ADC technology to potentially impact the way cancer is treated in a meaningful way.

Seattle Genetics presentations at AACR highlight the following ADC findings:

Multiple presentations by Seattle Genetics ADC collaborators highlight strong preclinical and clinical progress.

About Seattle Genetics

Seattle Genetics is a biotechnology company focused on the development and commercialization of monoclonal antibody-based therapies for the treatment of cancer. The companys lead program, ADCETRIS (brentuximab vedotin), received accelerated approval from the U.S. Food and Drug Administration in August 2011 and approval with conditions from Health Canada in February 2013 for two indications. In addition, under a collaboration with Millennium: The Takeda Oncology Company, ADCETRIS received conditional approval from the European Commission in October 2012. Seattle Genetics also has four other clinical-stage ADC programs: SGN-75, ASG-5ME, ASG-22ME and SGN-CD19A. Seattle Genetics has collaborations for its ADC technology with a number of leading biotechnology and pharmaceutical companies, including AbbVie (formerly Abbott), Agensys (an affiliate of Astellas), Bayer, Celldex Therapeutics, Daiichi Sankyo, Genentech, GlaxoSmithKline, Millennium, Pfizer and Progenics, as well as ADC co-development agreements with Agensys and Genmab. More information can be found at http://www.seattlegenetics.com.

Certain of the statements made in this press release are forward looking, such as those, among others, relating to the therapeutic potential of our preclinical product candidates and collaborator ADCs. Factors that may cause such a difference include the risk of adverse events as these ADCs advance in clinical trials. More information about the risks and uncertainties faced by Seattle Genetics is contained in the companys Annual Report on Form 10-K for the year ended December 31, 2012 filed with the Securities and Exchange Commission. Seattle Genetics disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.

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Daily Biology! Gene Therapy

By: John Abbott

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Daily Biology! Gene Therapy - Video

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PROJECT WALK -SPINAL CORD INJURY
REVIEW APRIL 6.

By: Narayan Savithri

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TakoBar Cell Therapy Featuring J-Blev and Southside Eaze E
late night freestyle session with @JBlev and @Southsideeazee at TakeBar (818 Juniper St. Atlanta,Ga). Just a friendly PSA to let yu know that we really do tu...

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Performance After Adipose Stem Cell Therapy for Horse - Cash Fuez and Flaxey
Performance After Adipose Stem Cell Therapy for Horse - Cash Fuez and Flaxey http://wichitaequinevet.com "This is the video of Flaxey after he and Cash won t...

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Apr. 8, 2013 Normal functioning of the eye depends on a proper supply of blood to the retina. Light entering the eye passes through the cornea, the lens, and the vitreous body before reaching the retina, where it stimulates the nerves. If the retina contains too few or too many blood vessels -- i.e., if it is under- or oversupplied with blood -- a number of severe, often blinding eye diseases can develop.

An international group of researchers led by Professor Alfred Nordheim at the University of Tbingen's Interfaculty Institute for Cell Biology has found, using experiments on mice, that genes for blood vessel growth in the retina are "switched on" by a known factor -- a protein called SRF. The scientists showed that by eliminating this factor, they could artificially induce a certain disease profile in newborn mice and a different one in adult mice. Their results, which are published now in The Journal of Clinical Investigation, offer important clues on the diseases afflicting human eyes and provide starting-points for the development of treatments for defective retinae and vitreous bodies.

Professor Alfred Nordheim's team has been examining the serum response factor (SRF) and its various functions for several years. SRF regulates the function of many genes in the genome of mice and men -- thereby setting in motion distinct growth processes for organs. Experimenting on mice in the laboratory, the Tbingen researchers have developed sophisticated mechanisms to influence the activity of SRF and its co-factors in distinct types of cells and at defined time points when the organism reaches a certain developmental stage.

In the current study, the researchers switched off SRF in the blood vessels of mouse embryos, as well as in newborn and adult mice. As a result, the blood vessels in the retinae of the newborns were not fully developed. Their eye problems were very similar to certain hereditary forms of a disease affecting the retina and vitreous body in the human eye (vitreoretinopathy and Norrie disease). Children affected by it often go blind at an early age. In mice of adult ages, however, switching off SRF had the opposite effect -- too many new blood vessels were formed in the retina, oversupplying it with blood. Doctors have made corresponding observations in elderly patients with a certain form of age-related macular degeneration (AMD), a disease which increasingly damages the retina and leads to vision loss. It is characterized by dilated blood vessels and the formation of excess blood vessels.

"I expected that SRF would play a role in the development of the vessel system, because it generally works to ensure the formation of cellular protrusions and new branched cellular structures in many organs, for instance in the nervous system and the vascular system," says Alfred Nordheim. But, he added, it was astonishing how closely the pathology of mice with switched-off SRF resembled that of human patients with particular eye diseases. "I think we have established a very good model with which we can investigate these diseases much more precisely," Nordheim says. It represents an important step for research into possible treatments, he adds.

The study was carried out in collaboration with researchers at the Max Planck Institute for Molecular Biomedicine in Mnster (Prof. Adams), the Institute for Ophthalmic Research Tbingen (Prof. Seeliger), the Pathology Department at the Tbingen University Hospital (Prof. Wolburg) and the University of Texas, Dallas, USA (Prof. Olson).

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Gene switch steers blood supply to the retina

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Apr. 8, 2013 Research from Western University and Lawson Health Research Institute sheds new light on a gene called ATRX and its function in the brain and pituitary.

Children born with ATRX syndrome have cognitive defects and developmental abnormalities. ATRX mutations have also been linked to brain tumors. Dr. Nathalie Brub, PhD, and her colleagues found mice developed without the ATRX gene had problems in in the forebrain, the part of the brain associated with learning and memory, and in the anterior pituitary which has a direct effect on body growth and metabolism. The mice, unexpectedly, also displayed shortened lifespan, cataracts, heart enlargement, reduced bone density, hypoglycemia; in short, many of the symptoms associated with aging.

The research is published in the Journal of Clinical Investigation.

Ashley Watson, a PhD candidate working in the Brub lab and the first author on the paper, discovered the loss of ATRX caused DNA damage especially at the ends of chromosomes which are called telomeres. She investigated further and discovered the damage is due to problems during DNA replication, which is required before the onset of cell division. Basically, the ATRX protein was needed to help replicate the telomere.

Working with Frank Beier of the Department of Physiology and Pharmacology at Western's Schulich School of Medicine & Dentistry, the researchers made another discovery. "Mice that developed without ATRX were small at birth and failed to thrive, and when we looked at the skeleton of these mice, we found very low bone mineralization. This is another feature found in mouse models of premature aging," says Brub, an associate professor in the Departments of Biochemistry and Paediatrics at Schulich Medicine & Dentistry, and a scientist in the Molecular Genetics Program at the Children's Health Research Institute within Lawson. "We found the loss of ATRX increases DNA damage locally in the forebrain and anterior pituitary, resulting in systemic defects similar to those seen in aging."

The researchers say the lack of ATRX in the anterior pituitary caused problems with the thyroid, resulting in low levels of a hormone called insulin-like growth factor-one (IGF-1) in the blood. There are theories that low IGF-1 can deplete stores of stem cells in the body, and Brub says that's one of the explanations for the premature aging. This research was funded by the Canadian Institutes of Health Research.

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Shedding light on a gene mutation that causes signs of premature aging

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A faulty gene normally associated with breast cancer can lead to aggressive and deadly prostate cancer in men, research has shown.

Prostate cancer spreads more quickly and is more likely to be fatal in men with a defective BRCA2 gene, a study found.

The researchers argue that men with the gene who are diagnosed with the disease should be given more radical treatment than non-carriers. They need immediate surgery or radiotherapy, it is claimed.

Currently many men with early-stage prostate cancer are advised to wait and see if the disease starts to progress.

This "active surveillance" approach suits men with slow-growing, non aggressive tumours, but not those with the BRCA2 mutant, say the scientists.

The new study, published in the Journal of Clinical Oncology, involved analysing the medical records of 61 BRCA2 mutation carriers, 18 carriers of a sister faulty gene, BRCA1, and 1,940 non-carriers.

Men with either of the defective genes were more likely to be diagnosed with advanced stage prostate cancers, or tumours that had already spread.

Those with BRCA2 mutations were also significantly less likely to survive. They lived an average of 6.5 years after diagnosis compared with 12.9 years for non-carriers.

Study co-leader Professor Ros Eeles, from the Institute of Cancer Research in London, said: "It is clear from our study that prostate cancers linked to inheritance of the BRCA2 cancer gene are more deadly than other types.

"It must make sense to start offering affected men immediate surgery or radiotherapy, even for early-stage cases that would otherwise be classified as low-risk. We won't be able to tell for certain that earlier treatment can benefit men with inherited cancer genes until we've tested it in a clinical trial, but the hope is that our study will ultimately save lives by directing treatment at those who most need it."

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Mutant gene cancer link probed

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8 April 2013 Last updated at 20:31 ET By Michelle Roberts Health editor, BBC News online

Men with prostate cancer and an inherited gene mutation have the worst form of the disease, research reveals.

The BRCA2 gene is linked to hereditary breast cancer, as well as prostate and ovarian cancer.

Now scientists say that as well as being more likely to get prostate cancer, men with BRCA2 are also more likely to develop aggressive tumours and have the poorest survival rates.

They say these men should be treated quickly to save lives.

This study shows that doctors need to consider treating men with prostate cancer and a faulty BRCA2 gene much sooner than they currently do, rather than waiting to see how the disease develops

Around one in every 100 men with prostate cancer will have the BRCA2 mutation.

These men might benefit from immediate surgery or radiotherapy, even if their disease is at an early stage and would normally be classified as low risk, according to the latest work in the Journal of Clinical Oncology.

Prostate cancer can grow extremely slowly or very quickly, and this is something that is hard to predict early on.

Some men may live symptom-free for a lifetime, despite having this cancer.

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'Deadly' prostate cancer gene find

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Bref. Nous sommes Technico-Commerciaux en Instrumentation Biotechnologique et Biomédicale!
Présentation de la licence pro TCIBB, réalisée par la promo TCIBB 2012-2013. Pour tout renseignement : caroline.norez@univ-poitiers.fr.

By: Caroline Norez

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The Reptilian Illuminati Watchers Bloodlines In The Real World (HD)
The connections between the Reptilian Illuminatus Watchers Bloodlines and our political leaders in the real world. What do we know about the true origins of ...

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THOMAS SHERIDAN EXCLUSIVE INTERVIEW UN-PENNED SHOW APRIL 2ND 2013
special guest THOMAS SHERIDAN-THE ANVIL OF THE PSYCHE, PSYCHOPATHY. The Un-penned Show with Paul Andy. Decoding Oceania. http://thomassheridanarts.com/view...

By: MrPaulVickers

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THOMAS SHERIDAN EXCLUSIVE INTERVIEW UN-PENNED SHOW APRIL 2ND 2013 - Video

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Gigantic Fallen Angels Seen? Winged Beings With Human Faces Witnessed In Space!
link http://mysteriousuniverse.org/2012/04/space-angels-aliens-or-sign-of-the-apocalypse/

By: hyungs

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Gigantic Fallen Angels Seen? Winged Beings With Human Faces Witnessed In Space! - Video

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Take action against GM foods!

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Public release date: 8-Apr-2013 [ | E-mail | Share ]

Contact: Bill Ferguson bferguson@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, April 8, 2013New Space (http://www.liebertpub.com/space), the groundbreaking, peer-reviewed Journal published by Mary Ann Liebert, Inc., publishers (http://www.liebertpub.com), launched its inaugural issue (http://online.liebertpub.com/toc/space/1/1) at the 29th National Space Symposium being held April 8-11 at the Broadmoor Hotel in Colorado Springs, CO. Spearheaded by Editor-in-Chief Professor Scott Hubbard from the Department of Aeronautics and Astronautics at Stanford University, the Journal facilitates the emerging multidisciplinary and entrepreneurial opportunities for space-based collaborations of industry, academia, and government. New Space (http://www.liebertpub.com/space) is published quarterly online with Open Access (http://www.liebertpub.com/openaccess/new-space/610/) options and in print.

The inaugural issue includes premium content from leading experts in the field, including an editorial by Scott Hubbard, a cogent opinion statement by Space Foundation CEO Elliot Holokauahi Pulham, and a roundtable discussion titled "Growing the Future of Commercial Space" hosted by Dr. Hubbard with timely, valuable perspectives from participants Ken Davidian, Steve Isakowitz, John Logsdon, James R. (Russ) McMurry, George Nield, and Marcia Smith. Additionally, the issue includes new peer-reviewed original articles "Industry Structural Analysis of the Commercial Suborbital Research Market" by Ken Davidian and Cindy Conrad; "The State of Space Economical Analyses: Real Questions, Questionable Answers" by Henry R. Hertzfeld; "Commercial On-Orbit Satellite Servicing" by Alanna Krolikowski and Emmanuelle David; "The B612 Foundation Sentinel Space Telescope" by Edward T. Lu, Harold Reitsema, John Troeltzsch, and Scott Hubbard; and "Certification Versus Licensing for Human Spaceflight in Commercial Space Transportation" by George C. Nield, Mahamane Toure', John Sloan, and David Gerlach.

"This new Journal provides a much-needed forum for the rapidly advancing knowledge, engineering, and technological developments in this important fieldwith great potential for benefit to humanity and our world," says Editor-in-Chief Hubbard.

In addition to peer-reviewed manuscripts, New Space publishes interviews with leading innovators, roundtable discussions with experts in a variety of fields, point-counterpoint discussions, and briefs describing lab demonstrations and field trials.

###

About the Journal

New Space (http://www.liebertpub.com/space) facilitates and supports the efforts of researchers, engineers, analysts, investors, business leaders, and policymakers to capitalize on the opportunities of commercial space ventures. Spanning a broad array of topics including technological advancements, global policies, and innovative applications, the journal will bring the new space community together to address the challenges and discover new breakthroughs and trends in this epoch of private and public/private space discovery. The Journal is published quarterly online with Open Access options (http://www.liebertpub.com/openaccess/new-space/610/) and in print. Complete table of contents are available on the New Space (http://www.liebertpub.com/space) website.

About the Publisher

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Premier issue of New Space journal launched at 29th National Space Symposium in Colorado Springs

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April 8, 2013

Brett Smith for redOrbit.com Your Universe Online

Despite the frequently encountered that scientists are playing God with nature, the pros of genetic engineering are numerous and significant.

When discussing genetically modified organisms (GMO), it is important to note that the FDA and the World Health Organization have both deemed that the food products created with the technology are considered safe.

GMO produce has several genetically altered advantages over non-GMO fruits and vegetables, including increased resistance to pests, disease and drought.

These benefits of genetic engineering translate directly into cheaper prices. A recent Iowa State University study found that prices would be at least 10 percent higher for soybeans and 6 percent higher for corn worldwide without biotechnical modifications.

Some GMOs have even been found to taste better than their conventional counterparts. In a study published in the journal Nature Biotechnology, researchers found that as many as 60 percent of the people they surveyed actually preferred the taste of a genetically modified tomato.

The study focused on a particular modified tomato that had the genetically engineered advantage of a rose-scented compound that was coded into the tomato genome. The researchers said their study proves that food products can not only be made more resilient through biotechnology, but that they can also be made more flavorful.

The pros of genetic engineering can also be seen in fields besides agriculture. Scientists at the Department of Energy revealed that they have created a modified virus capable of generating electrochemical energy. Using the genetically modified viruses, they were able to create a device that is powered simply by applying pressure.

Cancer researchers and patients are also constantly reaping the benefits of genetic engineering. Many experimental treatments use genetically modified viruses to target and destroy cancer cells. A recent study showed that oncologists from Memorial Sloan-Kettering Cancer Center in New York were able to effectively treat a specific form of acute leukemia using genetically engineered viruses.

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The Pros of Genetic Engineering: Why ‘Playing God’ Could Help The Human Race

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COLUMBIA, Mo. A Mizzou researcher has found genes that may predispose laziness in rats. The findings may translate to humans.

Frank Booth, professor with the College of Veterinary Medicine, said, We have shown that it is possible to be genetically predisposed to being lazy, Booth said. This could be an important step in identifying additional causes for obesity in humans, especially considering dramatic increases in childhood obesity in the United States."

Booth's team was able to breed rats that exhibited traits of either extreme activity or extreme laziness. They wrote in an academic paper that these rats indicate that genetics could play a role in exercise motivation, even in humans.

"It would be very useful to know if a person is genetically predisposed to having a lack of motivation to exercise, because that could potentially make them more likely to grow obese, Booth said.

Studies show 80 to 97 percent of American adults get less than 30 minutes of exercise a day, which is the minimum recommended by federal guidelines.

Roberts' team put rats in cages with running wheels and measured how much each rat willingly ran on its wheel over six days. They then bred the top 26 runners with each other and bred the 26 rats that ran the least with each other.

They repeated this process through 10 generations and found that the line of running rats chose to run 10 times more than the line of lazy rats.

Once the researchers created their super runner and couch potato rats, they studied the levels ofmitochondriamitochondria in muscle cells, compared body composition and conducted genetic evaluations.

While we found minor differences in the body composition and levels of mitocondriain muscle cells of the rats, the most important thing we identified were the genetic differences between the two lines of rats, Roberts said. Out of more than 17,000 different genes in one part of the brain, we identified 36 genes that may play a role in predisposition to physical activity motivation.

The study is in the April 3 edition of the American Journal of Physiology: Regulatory, Integrative and Comparative Physiology.

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Researcher finds genetic link to couch potato-itis in rats, maybe humans

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