Starting rare Wonder genetics
Popping some of the rarest and best cannabis seeds.

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How-To: Genetics Worksheet
How-To: Genetics Worksheet.

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AAV-Mediated Inclusion Formation as a Novel Gene Therapy Strategy for ALS
Ole Isacson, Ph.D., McLean Hospital. Dr. Isacson is a CDMRP-funded investigator supported by the DoD Amyotrophic Lateral Sclerosis Research Program (ALSRP).

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Tilting Wheelchair For Spinal Cord Injury -CRP
Tilting Wheelchair, Made in CRP, Savar, Bangladesh - first time ever made in Bangladesh. Very useful for Tetraplegic patients.

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NewsLife Interview: Dr. Theresa Deischer, Founder, SCPI- benefits and effects of stem cell therapy
NewsLife Interview: Dr. Theresa Deischer, Founder, Sound Choice Pharmaceutical Institute - benefits and effects of stem cell therapy - [May 7, 2013] For more...

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Milwaukee, WI (PRWEB) May 10, 2013

The American Society of Gene & Cell Therapy (ASGCT) is honored to recognize Dr. Sonia Skarlatos, PhD, and Dr. Catherine McKeon, PhD as the recipients of the Distinguished Service Award at the Societys 16th Annual Meeting. This award recognizes an ASGCT member or group that has consistently fostered and enhanced the field of genetic and cellular therapy. The award presentation will begin on Friday, May 17th, at 8:00am in Ballroom E-J at the Salt Palace Convention Center.

Dr. Skarlatos, the Deputy Director of the Division of Cardiovascular Sciences with National Heart, Lung, and Blood Institute is credited for her development in various educational programming designed to support gene and cell therapy investigators as well as ensuring certified good manufacturing practices (GMP) grade vectors are available to researchers. Dr. Skarlatos was also instrumental in the conception and implementation of gene therapy programming within the NHLBI.

Dr. McKeon serves as the Senior Advisor for Genetic Research at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Dr. McKeon organized one of the first Requests for Application of research centered on gene transfer and gene therapy. Her participation in gene therapy symposia during the 1990s would help to form ASGCT. Dr. McKeon has also been significantly involved in educational speaking events focused on assisting young investigators in obtaining funding to continue their research.

"Both Sonia Skarlatos and Catherine McKeon have played vital roles in catalyzing the difficult but eventually successful evolution of gene therapy from interesting new science with great potential to a remarkably successful field of clinical medicine. They have become the two most essential intermediaries in the scientific and translation conversation between the ASGCT and the NIH. With one foot at the NIH and another in the ASGCT, Drs. Skarlatos and McKeon have coalesced the programs in the two institutions and have worked enthusiastically and tirelessly to bring the dream of gene therapy to reality, said Dr. Theodore M. Friedmann, past President of ASGCT and professor at the University of San Diego School of Medicine.

The American Society of Gene & Cell Therapy (ASGCT) is a professional nonprofit medical and scientific organization dedicated to the understanding, development and application of genetic and cellular therapies and the promotion of professional and public education in the field. For more information on ASGCT, visit its website, http://www.asgct.org.

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Pioneering Researchers Recognized for Scientific Achievements in Gene and Cell Therapy

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Javascript is currently disabled in your web browser. For full site functionality, it is necessary to enable Javascript. In order to enable it, please see these instructions. May 10, 2013 The shifting structure of US patents referring to and claiming nucleotide sequences. Credit: Nature Biotechnology 31, 404410 (2013) doi:10.1038/nbt.2568

(Phys.org) As the U.S. Supreme Court moves closer to a decision this summer in the landmark gene patent case against Myriad Genetics, a study, led by Colorado State University, is shedding light on what may be at stake.

Gregory Graff, associate professor of Agricultural and Resource Economics at CSU, and a team of researchers at University of Minnesota and Pennsylvania State University analyzed U.S. patents to find that the case may not have the dramatic impact that some in the biotechnology industry fear it will. However, they caution, the Supreme Court's decision may have unanticipated impacts on patents that claim sequences from species other than just humans.

Graff's paper ,"Not Quite a Myriad of Gene Patents: Assessing the potential impact of the U.S. Supreme Court on the changing landscape of U.S. patents that claim nucleic acids," will be published in Nature Biotechnology this month.

The plaintiffs in the Myriad Genetics case are seeking resolution as to whether of not an isolated DNA molecule with a natural genetic sequence from the human genome should be considered eligible to be patented. According to recent commentary, there is good reason to expect the Supreme Court may decide to ban gene patents.

As the case was winding its way up through the courts, Graff and his team of collaborators began a comprehensive, in-depth review of how many and what sorts of U.S. patents make the kind of claims to DNA that were being challenged in the Myriad Genetics case.

The study analyzes the different types of claims that constitute a "gene patent" and then determines the number and nature of U.S. patents that could be invalidated by a Supreme Court ban.

"Our intention was to give some sort of measure to the potential legal and commercial implications of what is squaring up to become a landmark patent case, one of the most significant Supreme Court cases in the biological sciences for decades," said Graff.

This is the first study of several to draw upon a new and massive worldwide compilation of patents related to genetics and genomics, put together by Graff and collaborators at the International Science and Technology Practice and Policy (InSTePP) Center at the University of Minnesota over the past three years with funding from the National Institutes of Health (NIH).

What distinguishes the study from previous research is the way in which patents were counted and "read" by computer algorithms. Graff worked with other collaborators at Pennsylvania State University to train computer programs to pick out just those patents with precisely the same kind of legal language being challenged in the case. The research also goes beyond just considering human genes to analyze genes patented from all types of organisms, leading the study to raise questions about the full implications of the case.

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Study assesses impact of pending landmark US Supreme Court case on gene patents

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By Barbara Bronson Gray HealthDay Reporter

THURSDAY, May 9 (HealthDay News) -- In the war against cancer, it looks like matchmaking -- between genes and drugs -- could be an important tool, according to new research into the genetic underpinnings of two rare forms of leukemia.

By matching a patient's genetic mutation responsible for a rare, rapidly progressing form of leukemia with a drug that specifically targets the problem the mutation creates, researchers report that one patient is experiencing fast, marked improvement.

The new findings shed light on how many forms of cancer may be tackled in the near future. Scientists are discovering how to differentiate between mutations that are driving the proliferation of cancer cells and those that are merely passengers in the process.

"If your car breaks down, you have to open up the hood to see what part has broken," said study author Jeffrey Tyner, an assistant professor at the Knight Cancer Institute at Oregon Health & Science University. "Here we have to open up the tumor cells to see what part is broken to understand what to do."

After first identifying the genetic drivers of a specific type of cancer, scientists then match those mutant genes to drugs that will specifically target them.

According to Julia Maxson, study first author and a postdoctoral fellow at the Knight Cancer Institute, "The move in the field is to take the individual broken genes and say which of these really promote cell growth. Then, you can find the right drugs."

The research, published May 9 in the New England Journal of Medicine, identified "driver" gene mutations related to two rare forms of blood cancers: chronic neutrophilic leukemia (CNL) and chronic myeloid leukemia (CML). The scientists identified particular mutations in the gene responsible for what is called "colony-stimulating factor 3," which signals kinases, a type of cell enzyme.

A patient with CNL who carries that gene mutation was given ruxolitinib, a drug that specifically inhibits that mutation (and is known as a kinase inhibitor). Ruxolitinib is already on the market, used to treat a different blood cancer, called myelofibrosis. But up until now, although it has been widely available, the drug hasn't been tried with CNL, Tyner said.

Because CNL is rare, most patients with the disease have the same mutant gene, which somewhat simplifies the process, Tyner explained. Other more common cancers will be more complicated to tackle because they are more genetically diverse, he pointed out.

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Gene Discovery May Offer Breakthrough for Rare Leukemia

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But scientists now hope that identifying the genetic cause it will help them develop drugs that can block activity in the mutant gene, thus treating SWS and port wine stains far more effectively than at present.

Researchers at the Kennedy Krieger Institute in Baltimore uncovered the mutation by sequencing the genomes of affected and unaffected tissue and blood samples from three people with SWS.

They were able to identify one mutation shared by all three affected samples, in gene GNAQ on chromosome 9q21.

Study author Dr Anne Comi, whose findings are published in the New England Journal of Medicine said: "This is a complete game changer for those with Sturge-Weber syndrome and the millions born with port-wine birthmarks.

"Now that we know the underlying genetic mutation responsible for both conditions, we're hopeful that we can move quickly towards targeted therapies, offering families the promise of new treatments for the first time."

Co-author Dr Jonathan Pevsner said: "This study presents a turning point for research on Sturge-Weber syndrome and port-wine birthmarks.

"While we suspected that a somatic mutation was the cause for decades now, the technology to test the theory didn't exist.

"The advancements in whole genome sequencing and the development of next-generation sequencing tools finally allowed my lab to test and prove the hypothesis."

The team also discovered a link between the mutant gene and a type of melanoma that occurs in the eye, raising hopes that a new method of treating it could also be uncovered.

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Genetic mutation causing port wine stain birthmarks discovered

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Dr. Christian de Duve, a Belgian biochemist whose discoveries about the internal workings of cells shed light on genetic disorders such as Tay-Sachs disease and earned him a Nobel Prize in 1974, died at his home in Nethen, Belgium, on May 4. He was 95.

The cause was euthanasia, legal in Belgium, and administered by two doctors at Dr. de Duves request, his son Thierry said.

He was suffering from a number of health problems, including cancer and arrhythmia, Dr. Gunter Blobel, a colleague of Dr. de Duves at the Rockefeller University in Manhattan, said, and decided to end his life after falling a few weeks ago. He wanted to make the decision while he was still able to do it and not be a burden.

Dr. de Duve spent the last month writing letters to friends and colleagues telling them of his decision, and he put off his death until Thierry, who lives in Los Angeles, could be with him, along with his three other children, he told the Belgian newspaper Le Soir in an interview published after his death.

Beginning in the late 1940s, Dr. de Duve used a centrifuge and other techniques to separate and examine the inner components of cells. He discovered the lysosome, a tiny sack filled with enzymes that functions like a garbage disposal, destroying bacteria or parts of the cell that are old or worn out.

His discoveries helped unravel the biology of Tay-Sachs disease and more than two dozen other genetic diseases in which a shortage of lysosomal enzymes causes waste to accumulate in cells, eventually destroying them. In Tay-Sachs, a buildup of fatty substances in the brain and other tissues leads to blindness, paralysis, mental retardation and death.

After learning he had been awarded a Nobel, Dr. de Duve said that although his discoveries brought great intellectual satisfaction, his goal was to use them to conquer disease. Its now time to give mankind some practical benefit, he said.

He shared the 1974 Nobel Prize in Physiology or Medicine with Dr. Albert Claude, who first used centrifugal techniques to glance inside cells, and Dr. George E. Palade, who pioneered using the electron microscope to better understand cell structures. Claude died in 1983; Palade died in 2008.

Before the scientists embarked on their research, the cell was perceived as a workbasket containing indeterminate parts. The scientists, working separately, transformed that view with discoveries of important cell components.

Claude discovered mitochondria, which store energy, and Palade discovered ribosomes, the protein factories within cells. The Karolinska Institute, in awarding the Nobel, credited the three scientists with giving birth to the field of modern cell biology.

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Genetic research earned biologist Christian de Duve a Nobel Prize

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By Duke Medicine News and Communications

DURHAM, N.C. A non-inherited genetic mutation that arises during fetal development has been shown to be the cause of port-wine stains, one of the most common birth defects, as well as a related, but rare disorder called Sturge-Weber Syndrome (SWS). In a study published May 8, 2013, in the New England Journal of Medicine, Duke Medicine scientists, in collaboration with researchers at Kennedy Krieger Institute, Johns Hopkins School of Medicine, and the Medical College of Wisconsin, have identified a variant of the gene GNAQ as the mutation that causes the defects. Sturge-Weber Syndrome occurs in approximately 1 in 20,000-50,000 live births, and is characterized by seizures, developmental delays and glaucoma, among other health problems. Researchers believe that the earlier the mutation in GNAQ happens during fetal development, the more likely it will lead to the more severe SWS outcome. The findings confirms a hypothesis posited by German dermatologist Rudolf Happle in 1987, who observed that the conditions did not appear to be inherited, suggesting they resulted from a somatic mutation a mutation that happens during development. What was really exciting was that Happle was right, said co-senior author Douglas Marchuk, Ph.D., professor and vice chair of the Department of Molecular Genetics and Microbiology at Duke. If he was right, people with Sturge-Weber and people with port-wine stains would have a mutation in the same gene, because theyre really the same thing, with the difference being when the mutation happens during development. Sure enough, we found the same mutation in both affected tissues, and not only was it the same gene, it was exactly the same mutation. The researchers performed whole genome sequencing on both affected and non-affected tissue samples from individuals with SWS and port-wine stains, and from normal subjects. Advanced sequencing technology and bioinformatics were critical to identifying the gene, the mutation, and the protein involved in the disease process, which is called G-alpha(q) (Gq). The Gq protein is a highly studied compound associated with G-protein-coupled receptors, the family of signaling receptors involved in a wide variety of physiological processes. The receptors are the subject of research that led to Dukes Robert Lefkowitz winning the 2012 Nobel Prize in Chemistry. Marchuk said the association may bode well for development of new therapies for SWS and port-wine stains. Gq is an important protein in a lot of processes, so people are already studying drugs that might inhibit the receptor, he said. Although the research team has not yet isolated which specific cell type is involved, they suspect the mutation occurs in endothelial cells in the blood vessels in the region of the eye and nearby brain. Now that the gene and the mutation have been identified, the next step will be to develop an animal model to characterize the tissue and cell types. Marchuk and his colleagues worked closely with the patient advocacy group Sturge-Weber Foundation. Karen Bell, Sturge-Weber Foundation president and CEO, said identifying the gene and mutation is a major milestone toward eradicating the condition. I think the first emotional wave is to just be dumbstruck and then the wow moment will come and theyll be giddy, she said. Then I hope individuals affected by Sturge-Weber will be even more united to drive home therapies that can help their loved ones. Its an opportunity to educate the public and the members, and to have a rallying point for more significant change, personally and medically. The study was funded by Hunters Dream for a Cure Foundation and the Brain Vascular Malformation Consortium (U54NS065705). The Brain Vascular Malformation Consortium is part of the National Institutes of Health Rare Disease Clinical Research Network, supported through the NIH Office of Rare Diseases Research at the National Center for Advancing Translational Science and the National Institute of Neurological Disorders and Stroke. In addition to Marchuk, study authors at Duke include Hao Tang and Carol Gallione; along with Jonathan Pevsner, Anne Comi, Matthew D. Shirley, Joseph D. Baugher and Laurence Frelin of Kennedy Krieger Institute; Bernard Cohen of the Johns Hopkins; and Paula E. North of the Medical College of Wisconsin. # # #

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Genetic Mutation During Development Causes Port Wine Stains and Sturge-Weber Syndrome

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Public release date: 10-May-2013 [ | E-mail | Share ]

Contact: Shaun Mason smason@mednet.ucla.edu 310-206-2805 University of California - Los Angeles

Led by Dr. Peiyee Lee and Dr. Richard Gatti, researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA have used induced pluripotent stem (iPS) cells to advance disease-in-a-dish modeling of a rare genetic disorder, ataxia telangiectasia (A-T).

Their discovery shows the positive effects of drugs that may lead to effective new treatments for the neurodegenerative disease. iPS cells are made from patients' skin cells, rather than from embryos, and they can become any type of cells, including brain cells, in the laboratory. The study appears online ahead of print in the journal Nature Communications.

People with A-T begin life with neurological deficits that become devastating through progressive loss of function in a part of the brain called the cerebellum, which leads to severe difficulty with movement and coordination. A-T patients also suffer frequent infections due to their weakened immune systems and have an increased risk for cancer. The disease is caused by lost function in a gene, ATM, that normally repairs damaged DNA in the cells and preserves normal function.

Developing a human neural cell model to understand A-T's neurodegenerative process and create a platform for testing new treatments was critical because the disease presents differently in humans and laboratory animals. Scientists commonly use mouse models to study A-T, but mice with the disease do not experience the more debilitating effects that humans do. In mice with A-T, the cerebellum appears normal and they do not exhibit the obvious degeneration seen in the human brain.

Lee and colleagues used iPS cellderived neural cells developed from skin cells of A-T patients with a specific type of genetic mutation to create a disease-in-a-dish model. In the laboratory, researchers were able to model the characteristics of A-T, such as the cell's lack of ATM protein and its inability to repair DNA damage. The model also allowed the researchers to identify potential new therapeutic drugs, called small molecule read-through (SMRT) compounds, that increase ATM protein activity and improve the model cells' ability to repair damaged DNA.

"A-T patients with no ATM activity have severe disease but patients with some ATM activity do much better," Lee said. "This makes our discovery promising, because even a small increase in the ATM activity induced by the SMRT drug can potentially translate to positive effects for patients, slowing disease progression and hopefully improving their quality of life."

These studies suggest that SMRT compounds may have positive effects on all other cell types in the body, potentially improving A-T patients' immune function and decreasing their susceptibility to cancer.

Additionally, the patient-specific iPS cellderived neural cells in this study combined with the SMRT compounds can be an invaluable tool for understanding the development and progression of A-T. This iPS cellneural cell A-T disease model also can be a platform to identify more potent SMRT drugs. The SMRT drugs identified using this model can potentially be applied to most other genetic diseases with the same type of mutations.

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UCLA stem cell researchers move toward treatment for rare genetic nerve disease

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge - Episode 3
This is a POSSIBLE LP that I am starting - I have recorded 3 episodes and will look at the responses (comments and likes) to determine if I will add this cha...

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Immunology Lecture 11 Part 6 Genetics of Immunoglobulin Diversity
Immunoglobulins are important part of immune systems. These molecules are instrumental for defending against viruses, bacteria, and helminths etc. These mole...

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Immunology Lecture 11 Part 6 Genetics of Immunoglobulin Diversity - Video

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Let #39;s Play The Sims 3 - Perfect Genetics Challenge - Episode 4 - The First Born
Life moves fast in Riverview for Stefan and Heather. A new addition to the house in anticipation of their first child finds new purposes before being handed ...

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Let's Play The Sims 3 - Perfect Genetics Challenge - Episode 4 - The First Born - Video

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RUTHERFORD, N.J.--(BUSINESS WIRE)--

Cancer Genetics, Inc. (CGIX) ("CGI" or the "Company"), a leader in oncology-focused personalized medicine, will hold a conference call on Thursday, May 16, 2013, at 9:00 a.m. Eastern time to discuss its results for the first quarter ended March 31, 2013.

Cancer Genetics president and chief executive officer, Panna Sharma, and chief financial officer, Elizabeth Czerepak, will host the call and be available during the question-and-answer session.

To participate in the call, please dial (877) 941-1428, or (480) 629-9665 for international calls, approximately 10 minutes prior to the scheduled start time. Interested parties can also listen via a live Internet webcast, which can be found via the Companys website at http://ir.stockpr.com/cancergenetics/events, or alternately at http://ViaVid.net.

A replay of the call will be available for two weeks from 5:00 p.m. ET on May 16, 2013, until 11:59 p.m. ET on May 30, 2013. The number for the replay is (877) 870-5176, or (858) 384-5517 for international calls; the passcode for the replay is 4619856. In addition, a recording of the call will be available via the Companys website at http://www.cancergenetics.com.

About Cancer Genetics, Inc.

Cancer Genetics, Inc. (CGI) is an emerging leader in DNA-based cancer diagnostics and servicessome of the most prestigious medical institutions in the world. Our tests target cancers that are difficult to diagnose and predict treatment outcomes. These cancers include hematological, urogenital and HPV-associated cancers. We also provide a comprehensive range of non-proprietary oncology-focused tests and laboratory services.

CGIs cutting-edge proprietary tests and state-of-the-art reference laboratory provide critical genomic information to healthcare professionals as well as biopharma and biotech. Our state-of-the-art reference lab is focused entirely on maintaining clinical excellence and is both CLIA certified and CAP accredited and has licensure from several states including New York State.

Founded in 1999 by world-renowned cytogeneticist Dr. R.S.K. Chaganti, the Company has been built on a foundation of world-class scientific knowledge and IP in solid and blood-borne cancers, and has established strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic and the National Cancer Institute. For further information, please seewww.cancergenetics.com.

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Cancer Genetics Announces Conference Call to Discuss First Quarter Results

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Stem Cell Therapy for Knees, Osteoarthritis and Autoimmune Disorders: King Goff Discusses Treatment
King Goff received three applications of his own adipose tissue-derived stem cells over the course of 3 days for a knee injury and autoimmune issues at the S...

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Bharat Book Presents: Cell Therapy Technologies, Markets and Companies
For More Information Kindly Visit On : http://www.bharatbook.com/market-research-reports/healthcare-market-research-report/cell-therapy-technologies-markets-and-companies.html Summary This...

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/bvsbx5/cell_therapy) has announced the addition of the "Cell Therapy Partnering Yearbook 2013" report to their offering.

The Cell Therapy Partnering Yearbook 2013 report series provides comprehensive understanding and unprecedented access to the partnering deals and agreements entered into by the worlds leading healthcare companies during 2012.

Using these reports, dealmakers will effectively and efficiently gain insight into the partnering activities of the past year. The report series allows you to view all the partnering and alliances deals announced worldwide.

The initial chapters of this report provide an orientation of 2012's dealmaking and business activities.

The chapter is organized by company A-Z, stage of development at signing, deal type (collaborative R&D, co-promotion, licensing etc), therapy area and technology type. Each deal title links via Weblink to an online version of the deal record and where available, the contract document, providing easy access to each contract document on demand.

The report series also includes numerous tables and figures that illustrate the trends and activities in bigpharma partnering and dealmaking during 2012.

In conclusion, this report provides everything a prospective dealmaker needs to know about partnering in the research, development and commercialization of technologies and products during 2012.

Key benefits

- In-depth understanding of recent dealmaking trends during 2012

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Research and Markets: Cell Therapy Partnering Yearbook 2013

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STOCKHOLM, Sweden--(BUSINESS WIRE)--

Regulatory News:

Elekta (NSE:EKTAB.ST) and Royal Philips Electronics (NYSE: PHG, AEX: PHIA) announced today that Sunnybrook Health Sciences Centre (Toronto, Canada) will join their growing consortium to validate the clinical potential of MRI-guided radiation therapy.

Sunnybrook Health Sciences Centre, the sixth largest cancer center in North America, is the fourth member to sign the research agreement to evaluate the new technology, which merges radiation therapy and magnetic resonance imaging (MRI) in a single system. Current clinical members of the group include the University Medical Center Utrecht, The University of Texas MD Anderson Cancer Center, and The Netherlands Cancer Institute-Antoni van Leeuwenhoek Hospital.

Integrating an advanced 1.5 Tesla MRI machine with a sophisticated radiation therapy system will provide physicians with exceptional depictions of a patients soft tissues and tumor and allow them to dynamically track their motion. This breakthrough innovation is designed to permit doctors to deliver radiation in real time under MR guidance for the most precise cancer treatments possible.

Sunnybrook Health Sciences Centre distinguishes itself in the world of science and medicine by its longstanding dedication of integrating research into clinical domain for the benefit of patients, says Tomas Puusepp, Elekta President and CEO. With their international strength in the physical sciences particularly in imaging technology and its worldwide repute as a top flight cancer center, Sunnybrook is an ideal partner to help us advance this new technology.

According to Michael Julius, Vice President, Research at Sunnybrook Health Sciences Centre, Sunnybrooks participation in the research consortium will bring a unique team of physicists, engineers and clinicians to focus on validating the advantages of MRI-guided radiation therapy through technology development and clinical trials.

We have identified a number of areas to study the value of this technology for patients, he says. The ultimate goal acquiring high resolution MRI images of pathology in real time as the radiation is being delivered could have a dramatic impact on patient health and clinical outcomes.

Today, the safety margin of normal tissue around the tumor absorbs a large portion of the radiation beam, adds Jean-Philippe Pignol, Professor of Radiation Oncology and a key leader on the Elekta partnership at Sunnybrooks Odette Cancer Centre. The expectation is that MR-guided radiation therapy will enable us to treat more cancer tissue than normal tissue. In doing so, we could apply, in a single fraction, a huge dose to the tumor while avoiding side effects to normal tissues, he says.

The development of advanced imaging solutions for oncology therapy planning and delivery is a key focus area for Philips, says Gene Saragnese, CEO Imaging Systems at Philips Healthcare. Philips is already closely working together with Sunnybrook Health Sciences Centre in this field, and we welcome their expertise to the research consortium for MR guided radiotherapy. The members will jointly work on the design and implementation of the clinical studies with the objective of bringing image-guided oncology therapy to the next level, and ultimately creating the future of healthcare.

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Canada’s Sunnybrook Health Sciences Centre Joins Elekta and Philips Research Consortium on MRI-Guided Radiation Therapy

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Washington, May 10 (ANI): A new study has found that dads' genome is more ready for fertilization than of mothers'.

Researchers from Huntsman Cancer Institute (HCI) at the University of Utah have discovered that while the genes provided by the father arrive at fertilization pre-programmed to the state needed by the embryo, the genes provided by the mother are in a different state and must be reprogrammed to match.

The findings have important implications for both developmental biology and cancer biology.

In the earliest stages, embryo cells have the potential to develop into any type of cell, a state called totipotency.

Later, this potency becomes restricted through a process called differentiation. As a result, as cells continue to differentiate, they give rise to only a subset of the possible cell types.

"In cancer, normal processes of cell differentiation and growth go wrong, and cells either become arrested at an early state of differentiation, or instead go backwards and are 'reprogrammed' to become more like early embryo cells," Bradley R. Cairns, co-author of the article and Senior Director of Basic Science at HCI said.

"By understanding how cells are normally programmed to the totipotent state, and how they develop from that totipotent state into specific cell types, we hope to better understand how cancer cells misregulate this process, and to use that knowledge to help us devise strategies to reverse this process," he said.

Cairns said that the work added another interesting finding.

"We found that the mother's genome takes care of that remodeling on its own, without using the father's genome as a template," he said.

Cairns' experiments showed that when the father's genetic contribution was removed, the mother's genome still remodeled itself to the correct state.

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Male gene more ready at fertilization than female's

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May 9, 2013 Researchers from the RIKEN Center for Integrative Medical Sciences have identified a gene that when mutated is responsible for a spectrum of disorders affecting the bones and connective tissue. This finding opens new avenues for research into a diagnosis and treatment for these until now incurable diseases.

The study is published today in the American Journal of Human Genetics.

Spondyloepimetaphyseal dysplasia with joint laxity, type I or SEMD-JL1 is a disorder of the skeleton resulting in short stature and spinal problems starting from birth, and worsening with age. The disease is also known as SEMD Beighton type.

In order to find the gene responsible for the disorder, and Dr Ikegawa and his team examined the entire coding sequence of the genome of 7 individuals suffering from SEMD-JL1 using next-generation sequencing technology.

The researchers found that the study subjects all had mutations that resulted in significant loss of function of the gene B3GALT6, known to be involved in the biosynthesis of an important component of connective tissue.

To the reseachers' surprise, mutations in B3GALT6 were also found in patients suffering from a disorder of the connective tissue called Ehlers-Danlos syndrome progeroid type.The researchers show that a deficiency in the B3GALT6 enzyme results in a spectrum of disorders affecting various tissues, including the skin, bones, cartilage, tendons and ligaments. Their results indicate that B3GALT6 is essential for the development and the maintenance of these tissues.

B3GALT6 is known to encode for an enzyme involved in the biosynthesis of the glucosaminoglycan (GAG) linker region.

"The GAG linker region is key for GAG biosynthesis and proteoglycan metabolism," explains Dr Ikegawa "and proteoglycans are important because they are a major component of the matrix of connective tissue in animals."

"Our findings show that mutations in B3GALT6 cause a spectrum of disorders that were previously thought to belong to different families of diseases - some were thought to be skeletal dysplasia and others connective tissue disorders," explain the authors.

"More clinical, genetic and biological studies are needed to understand the pathological mechanism of the diseases and the role of GAG metabolism and function," they conclude.

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Gene identified, responsible for a spectrum of disorders affecting the bones and connective tissue

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May 9, 2013 A novel gene associated with canine atopic dermatitis has been identified by a team of researchers led by professors Kerstin Lindblad-Toh, Uppsala university and ke Hedhammar, SLU, Sweden. The gene encodes a protein called plakophilin 2, which is crucial for the formation and proper functioning of the skin structure, suggesting an aberrant skin barrier as a potential risk factor for atopic dermatitis.

Details appear today in the open-access journal PLoS Genetics.

Atopic dermatitis (or eczema) is an inflammatory, relapsing non-contagious skin disease affecting about 10-30 percent of the human population. It is not only humans that suffer from the disease: about 3-10 percent of dogs are also affected. The skin of a patient with atopic dermatitis becomes easily irritated by various allergens such as certain types of food, pollens or house mites. Such irritation causes very strong itching which leads to scratching, redness and flaky skin that becomes vulnerable to bacterial and yeast infections.

To-date, despite many scientific efforts, little has been known about the genetics of the disease. In their study, researchers from Uppsala University, SLU and Broad Institute, compared DNA samples from a large group of German shepherd dogs affected by atopic dermatitis with DNA coming from healthy dogs to reveal the specific DNA segment associated with the disease.

"With the help of pet owners, we have managed to collect a unique set of DNA samples from sick and healthy dogs which allowed us to gain insight into atopic dermatitis genetics," said first author Katarina Tengvall, Uppsala University.

Purebred dogs such as German shepherds have been selected for specific physical features for several generations. Selection led to an inadvertent enrichment for disease-risk genes in certain breeds. Moreover, the resulting architecture of canine DNA makes it easier to pinpoint segments that carry these disease risk-genes. This helped the researchers to reveal the genetics of atopic dermatitis. They found a region associated with the atopic dermatitis containing the gene PKP-2, which encodes Plakophilin-2, a protein involved in the formation and maintaining of the proper skin structure.

"The finding that certain variants of the PKP-2 gene may increase the risk of developing the disease opens new possibilities in understanding the disease mechanism leading to atopic dermatitis," continues Katarina Tengvall.

These findings will not only lead to better understanding of the disease, which may lead to better treatment strategies long term. It also opens up the possibilities of development of a genetic test for the disease.

"Our study suggests that plakophilin-2 and an intact skin barrier is important to avoid atopic dermatitis," says senior author, Kerstin Lindblad-Toh, professor at Uppsala University and Director of SciLifeLab Uppsala. "Another gene involved in the skin barrier has recently been linked to human atopic dermatitis emphasizing the similarity between canine and human atopic dermatitis" continues Kerstin Lindblad-Toh.

The study was supported by the European Commission (FP7-LUPA, GA-201370) and the Swedish Research Council Formas. KT was supported by the Uppsala University, MK was supported by the Swedish Foundation for Strategic Research (SSF) grant and C and KLT were supported by independent EURYI-Awards. FF was supported by the Swedish Institute Scholarship.

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Gene associated with eczema in dogs identified

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By Amy Norton HealthDay Reporter

WEDNESDAY, May 8 (HealthDay News) -- Mutations in a gene involved in bone development appear to cause certain severe forms of bone loss, a finding that could lead to new therapies for the common bone-thinning disorder osteoporosis, researchers report.

The mutations were found in a Swedish family with 10 members affected by a severe, early onset form of osteoporosis, as well as a Hmong family from Laos in which two sisters suffered from osteogenesis imperfecta.

Osteogenesis imperfecta, which is also known as brittle bone disease, affects six to seven out of every 100,000 people worldwide. The disease causes the bones to break easily, often from little or no trauma. There are four main forms, the most severe of which is fatal before or soon after birth.

The most common -- and mildest -- form is Type 1, in which most of a child's bone fractures happen before puberty. Some other problems, such as weak muscles and brittle teeth, are also possible.

Researchers have long known that about 90 percent of osteogenesis imperfecta cases are caused by a single mutation in one of two genes involved in making collagen, a fibrous protein in bone, skin and connective tissue.

It is only in the past decade, though, that the mystery behind the other 10 percent has become clearer, said Dr. Francis Glorieux, chairman of the Osteogenesis Imperfecta Foundation's medical advisory council.

The latest findings, published in the May 9 issue of the New England Journal of Medicine, underscore the role of a gene family known as WNT, said Glorieux, who was not involved in the research.

WNT genes make proteins called ligands, which means they latch onto receptors on the surface of body cells. Scientists have known that WNT is important in bone development and the upkeep of bone mass.

"But we haven't known which protein is key, which WNT ligand is actually doing the work. This study addresses that," said lead researcher Dr. Brendan Lee, a professor of molecular and human genetics at Baylor College of Medicine in Houston.

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Gene Discoveries Give Hope Against 'Brittle Bone' Disease

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Genetic Engineering PSA Final
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By: Melissa Salinas

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Genetic Engineering PSA Final - Video

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