PHILADELPHIA A newly developed, more specific approach to classifying tumors by molecular type can help cancer researchers to determine tumor characteristics and guide treatment strategies. A team of researchers from the Perelman School of Medicine at the University of Pennsylvania and the Wistar Institute have created the first isoform-level assay for stratifying tumors at a molecular level, in patients with glioblastoma, the most common and most aggressive type of malignant primary brain tumor. This new classifier is more efficient and replicable in a laboratory setting than existing diagnostic tools, and can provide more accurate predictions for survival and how glioblastoma patients may respond to different treatments.

"Current tests can help classify tumor types to a lesser degree. This new classifying system improves both the diagnostic accuracy and the efficiency of the testing process," said Donald O'Rourke, MD, associate professor of Neurosurgery with Penn's Abramson Cancer Center and director of the Penn Brain Tumor Tissue Bank. "The more detailed information we have about the tumor, at a molecular level, the better we can target new immunotherapies and other treatments for our patients with glioblastoma."

Penn Medicine's Center for Personalized Diagnostics (CPD) currently analyzes all brain tumors to determine the best treatment approach for a given tumor type. This new approach would be complementary to the work of the CPD on brain tumor specimens and enhance the overall effort of molecular sub typing of GBM tumors.

This new isoform-based classifier, which looks at variations within cellular RNA, improves prediction accuracy and requires half the variables for the analysis than the genetic-based analysis. The isoform classifier glioblastoma tumor noted the correct subtype with 92 percent accuracy, according to the study, published in Nucleic Acids Research.

The study was completed in collaboration with Ramana Davuluri, PhD, formerly at The Wistar Institute and now at Northwestern University and colleagues. For more details on the study, please see the Wistar Institute press release.

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Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of theRaymond and Ruth Perelman School of Medicine at the University of Pennsylvania(founded in 1765 as the nation's first medical school) and theUniversity of Pennsylvania Health System, which together form a $4.3 billion enterprise.

The Perelman School of Medicine has been ranked among the top five medical schools in the United States for the past 16 years, according toU.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $398 million awarded in the 2012 fiscal year.

The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania -- recognized as one of the nation's top "Honor Roll" hospitals byU.S. News & World Report; Penn Presbyterian Medical Center; Chester County Hospital; Penn Wissahickon Hospice; and Pennsylvania Hospital -- the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Chestnut Hill Hospital and Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine.

Penn Medicine is committed to improving lives and health through a variety of community-based programs and activities. In fiscal year 2012, Penn Medicine provided$827million to benefit our community.

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New Genetics Dank Fire!
Fire Genetics coming soon! I would highly recommend any of these genetics!! Cheers hg.

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NEW YORK(CBSNewYork) It has been called the cancer breakthrough of the year by a major scientific journal.

Therapy that eradicates cancer using a patients own cells has already saved a number of terminal leukemia patients, CBS 2s Dr. Max Gomez reported.

It has been the Holy Grail of cancer therapy and it harnesses the patients own immune system to attack cancer.

Now, a major new study has shown how to do that when treating leukemia. It involves using gene therapy to convert a patients white blood cells into killers.

Ive had several doctors tell me there is nothing else that can be done, leukemia patient Paolo Cavalli said, It is difficult with a new family to think about those things.

After six years of chemotherapy, stem cell transplants, and multiple relapses Cavalli was out of options for his leukemia.

I dont think I had many days left, he said.

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Injections of a normally silent gene sparked recovery in pigs induced to have heart attacks

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When a heart attack brings blood flow to a screeching halt, thats only the first assault on our fist-size organ. Among survivors, the recovery itself fuels more permanent damage to the heart. Scar tissue can harden once-flexible heart muscle, making it less elastic. And as tentacles of this tissue creep over the aorta the heart muscle can no longer fully contract. This long-term damage can minimize the amount of oxygen-rich blood sent throughout the body, which can send patients spiraling into heart failure. Heart transplants are one way to circumvent these scar tissue issues, but donor hearts are always in short supply. Devising other truly effective solutions has long eluded researchers. A form of gene therapy, however, is now showing promise in pigs. It turns out that a normally silent gene called Cyclin A2, or CCNA2, can be coaxed into action to combat the formation of scar tissue in pigs that suffer a heart attack. This treatment sparked regeneration of heart muscle cells in pigs as well as improvements in the volume of blood pushed out with every beat. The finding is published in the February 19 issue of Science Translational Medicine. Gene therapy, the authors hope, may one day join stem cell treatments as a contender for transforming the way doctors treat heart failure. Stem cellbased therapies have already resulted in more healthy tissue and decreased scar mass in human clinical trials as well as small improvements in how much blood the heart can pump from one chamber to another. But as Scientific American reported in April 2013, many questions remain about which stem cells to use and how to prepare them. For this study, researchers randomly assigned 18 pigs recovering from heart attacks to either receive injections of the gene expressed under a promoter (which would force it to be expressed) or the same solution without the gene. Pigs treated with the gene had greater success pushing out blood with each heartbeat, but also produced a greater number of heart muscle cells. These findings echo the teams earlier heart regeneration successes in mice and rats. The researchers replicated their findings in a petri dish and watched adult porcine heart muscle cells treated with the same regimen of gene therapy undergo complete cell division in the dishdemonstrating under a microscope how the heart cells were dividing and thriving with the gene therapy. This new approach mimics the kind of regeneration we see in the newt and zebra fish, says lead author Hina Chaudhry, the director of cardiovascular regenerative medicine at The Mount Sinai Hospital in New York City. If the technique proves successful in humans, it could boost patient recovery rates by helping strengthen heart muscles and improving blood flow, all while giving a needed lift to gene therapy research, which has been slow to gain momentum in the U.S. In 1999 Jesse Gelsinger, 18, died after a gene therapy experiment cost him his life. The virus used to deliver a gene that would potentially control his rare digestive disorder fueled a massive and fatal immune reaction. That highly publicized case, along with other gene therapy missteps, put a pall on the field. Chaudhry says that her team is proceeding with caution and plans to be careful when administering this treatment to patient populations. For patients who have a large heart attack who are at risk of heart failure, I think the therapy is going to be very beneficial, she says. If you have a small heart attack, it probably wont make as much of a difference in overall survival because of advances with todays medicines. As more researchers look to gene therapy for previously intractable human conditions, a success with heart attack treatments could send ripples throughout the field.

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A new study describes the complexity of the new T cell repertoire following immune-depleting therapy to treat multiple sclerosis, improving our understanding of immune tolerance and clinical outcomes.

In the Immune Tolerance Network's (ITN) HALT-MS study, 24 patients with relapsing, remitting multiple sclerosis received high-dose immunosuppression followed by a transplant of their own stem cells, called an autologous stem cell transplant, to potentially reprogram the immune system so that it stops attacking the brain and spinal cord. Data published in the Journal of Clinical Investigation quantified and characterized T cell populations following this aggressive regimen to understand how the reconstituting immune system is related to patient outcomes.

ITN investigators used a high-throughput, deep-sequencing technology (Adaptive Biotechnologies, ImmunoSEQTM Platform) to analyze the T cell receptor (TCR) sequences in CD4+ and CD8+ cells to compare the repertoire at baseline pre-transplant, two months post-transplant and 12 months post-transplant.

Using this approach, alongside conventional flow cytometry, the investigators found that CD4+ and CD8+ lymphocytes exhibit different reconstitution patterns following transplantation. The scientists observed that the dominant CD8+ T cell clones present at baseline were expanded at 12 months post-transplant, suggesting these clones were not effectively eradicated during treatment. In contrast, the dominant CD4+ T cell clones present at baseline were undetectable at 12 months, and the reconstituted CD4+ T cell repertoire was predominantly composed of new clones.

The results also suggest the possibility that differences in repertoire diversity early in the reconstitution process might be associated with clinical outcomes. Nineteen patients who responded to treatment had a more diverse repertoire two months following transplant compared to four patients who did not respond. Despite the low number of non-responders, these comparisons approached statistical significance and point to the possibility that complexity in the T cell compartment may be important for establishing immune tolerance.

This is one of the first studies to quantitatively compare the baseline T cell repertoire with the reconstituted repertoire following autologous stem cell transplant, and provides a previously unseen in-depth analysis of how the immune system reconstitutes itself following immune-depleting therapy.

About The Immune Tolerance Network

The Immune Tolerance Network (ITN) is a research consortium sponsored by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health. The ITN develops and conducts clinical and mechanistic studies of immune tolerance therapies designed to prevent disease-causing immune responses, without compromising the natural protective properties of the immune system. Visit http://www.immunetolerance.org for more information.

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The above story is based on materials provided by Immune Tolerance Network. Note: Materials may be edited for content and length.

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A study published in the journal Biomaterials finds that the rhythmic pulsation of cardiac muscle cells is a driving force in the initial formation of heart valves.

The heart forms as a simple U-shaped tube of tissue, comprised of three layers.

A layer of cardiac muscle cells begin to pulse even before blood vessels are formed. Beneath the muscle is a layer of "cardiac jelly," and below that is a layer of endothelial cells that will transform into valvular interstitial cells (VICs).

Where the heart valves form, endothelial cells embed themselves into cushions of cardiac jelly.

The endothelial cells transform into VICs, and these cells co-ordinate the transformation of the cardiac jelly into the two or three flaps (called "leaflets") that comprise the valve and control the flow of blood to the heart by opening and closing.

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Newswise NASHVILLE, Tenn. To develop correctly, baby hearts need rhythm...even before they have blood to pump.

We have discovered that mechanical forces are important when making baby hearts, said Mary Kathryn Sewell-Loftin, a Vanderbilt graduate student working with a team of Vanderbilt engineers, scientists and clinicians attempting to grow replacement heart valves from a patients own cells.

In an article published last month in the journal Biomaterials the team reported that they have taken an important step toward this goal by determining that the mechanical forces generated by the rhythmic expansion and contraction of cardiac muscle cells play an active role in the initial stage of heart valve formation.

A heart valve is a marvelous device. It consists of two or three flaps, called leaflets, which open and close to control the flow of blood through the heart. It is designed well enough to cycle two to three billion times in a persons lifetime. (Humans and chickens are outliers: Most other animals, large and small, have hearts that beat about one billion times in their lives.) However, heart valves can be damaged by diseases such as rheumatic fever and cancer, aging, heart attacks and birth defects.

For the last 15 years, people have been trying to create a heart valve out of artificial tissue using brute-force engineering methods without any success, said Assistant Professor of Biomedical Engineering W. David Merryman. We decided to take a step back and study how heart valves develop naturally so we can figure out how to duplicate the process. To do so, they designed a series of experiments with chickens, whose hearts develop in a fashion similar to the human heart.

The discovery that the deformations produced by the beating cardiac muscle cells are important provides an entirely new perspective on the process, said Merryman, who directed the three-year study.

The Vanderbilt effort is part of a broader program to develop artificial organs named the Systems-based Consortium for Organ Design and Engineering (SysCODE). It is a National Institutes of Health Roadmap initiative to speed the movement of scientific discoveries from the bench to the bedside.

This is the second major advance that weve made, said Professor of Pharmacology Joey Barnett, co-principal investigator of the heart valve project.

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A MOTHER whose son successfully battled a brain tumour but was later diagnosed with leukaemia is starting a campaign to encourage people to donate their stem cells.

Andrea Poyser's son Laughlin known as Lockey Whiteley, 7, had a brain tumour removed in 2011. But he was then diagnosed with treatment-related acute myeloid leukaemia (AML) last November.

Since then, the Burnham family has spent countless hours travelling to and from London's Great Ormond Street Hospital for Lockey's treatment.

Now Andrea, 42, with the help of friends, has set up "Unlock a Life for LocKEY", which aims to help raise awareness about stem cell donations.

"The general public think that stem cells come from the bone marrow and that's just not true," said the former drama teacher and actress Andrea.

"It's such a simple and easy procedure that costs nothing you can really make a difference to the lives of children. If you can, then why not.

"There are people suffering that could die because of lack of stem cells, it's easy to find out if you're a match and it's possible that you could save someone's life."

The group hope to help unlock matches for stem cell donors, plus give advice and support to families with children who have been diagnosed with leukaemia.

Unlock a Life for LocKEY is organising an event on Saturday, March 1, in Burnham where people can submit swab tests and donate during a day of live entertainment with a number of celebrities in attendance.

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B.C.-based genome research published this week is expected to help doctors target treatment of lymphoma tumours.

We found novel mutations in a gene that have not been described before in any cancer, said Dr. Christian Steidl, a scientist at the BC Cancer Agency and a professor in the University of British Columbias Department of Pathology who led the study team. Its a first description with a state-of-the-art technology.

Published in the scientific journal Nature Genetics Sunday, the work is part of a worldwide effort to identify gene mutations in all kinds of cancer tumours so treatment can be tailored to an individuals specific illness.

Thats what we mean by personalized medicine, that we dont just use a drug off the shelf and hope it works. Thats what we currently do. We use a drug combination that is very unspecific. It works in a proportion of patients, but we dont really know why.

Projecting five to 10 years in the future, this type of research will be the foundation of the shift that will happen in personalized medicine, said Steidl.

The study took samples from healthy cells and cancer tumours in about 100 patients, which were then analyzed using advanced gene sequencing techniques that have become available in only the last few years. Lead researcher Jay Gunawardana, a PhD student in pathology at UBC, found about 20 per cent of patients with Hodgkins lymphoma and a subtype of non-Hodgkin lymphoma (primary mediastinal B cell lymphoma) carry the same genetic mutation. While there is currently no therapy that can fix the damage caused by this mutation in the gene called PTPN1, experts say it opens the door for other scientists to find a treatment now that the target is known.

The term lymphoma covers about 50 different types of cancer that affect the glands of the lymphatic system that control the bodys immune response. It is divided into two groups, Hodgkin and non-Hodgkin lymphoma, and is the fifth most common cancer type in Canada. Its cause is unknown and it is rising among young adults, according to Lymphoma Canada. Each year, about 8,800 Canadians are diagnosed with lymphoma and more than 3,000 die from the disease.

Dr. Andrew Zelenetz, a lymphoma specialist at Memorial Sloan Kettering Cancer Center in New York who has no connection to the study, said in a telephone interview the discovery is incremental in adding one more piece to the advancement of cancer treatments. But it is a significant contribution to the understanding of lymphoma as diverse rather than a single ailment.

We often mistakenly think of cancer as one thing, that there will be a single magical cure, he said. What genomics has taught us is that we can walk up to three people with the same lymphoma, but if we look inside we see its three different diseases that should be treated in different ways. Today we dont have all the treatment tools that we need, but we would like to get away from having to use poisons as chemotherapy. Wed like to get away from drugs that work non-specifically.

The scale of interest in this area of research can be seen in the International Cancer Genome Consortium which aims to create a catalogue of gene abnormalities found in tumours from 50 different types of cancer. In the U.S., the Cancer Genome Atlas project is focused on specific cancers of the brain, lung and ovary. So far, the missteps in gene coding that cause tumour growth are known in only a tiny fraction of the myriad types of cancer

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Scientists at The Wistar Institute have developed a mathematical method for classifying forms of glioblastoma, an aggressive and deadly type of brain cancer, through variations in the way these tumor cells "read" genes. Their system was capable of predicting the subclasses of glioblastoma tumors with 92 percent accuracy. With further testing, this system could enable physicians to accurately predict which forms of therapy would benefit their patients the most.

Their research was performed in collaboration with Donald M. O'Rourke, M.D., a neurosurgeon at the University of Pennsylvania Brain Tumor Center, who provided the glioblastoma samples necessary to validate the Wistar computer model. Their findings were published online in the journal Nucleic Acids Research.

"It has become increasingly obvious that understanding the molecular makeup of each patient tumor is the key to personalizing cancer treatments for individual patients," said Ramana Davuluri, Ph.D., Wistar's Tobin Kestenbaum Family Professor and associate director of Wistar's Center for Systems and Computational Biology. "We have developed a computational model that will allow us to predict a patient's exact variety of glioblastoma based on the transcript variants a given tumor produces."

"A gene can produce multiple variants, in the form of transcript variants and protein-isoforms. We found that when you use the gene expression information at variant/isoform-level, the statistical analyses recaptured the four known molecular subgroups but with a significant survival difference among the refined subgroups." said Davuluri. "Using patient data, we found that certain subgroups when combined with patient age, for example, could predict better outcomes using a given course of therapy."

"As more targeted therapies come into use, this is exactly the sort of information clinicians will need to provide the best hope of survival for their patients," Davuluri said. "In time, we think this could form the basis of a clinical test that will help oncologists decide a patient's course of treatment."

Glioblastomamultiforme is the most lethal of the malignant adult brain tumors, and accounts for over 50 percent of all cases of brain cancer. Even with aggressive combination therapies, the prognosis remains bleak, with median patient survival of 15 months after diagnosis. The disease is also molecularly heterogeneous, that is, composed of subtypes that are not genetically alike or produce the same array of proteins. Genetic data from the Cancer Genome Atlas (TCGA) consortium has led to the identification of four subtypes of glioblastoma, but Davuluri and his researchers sought to find a way to quickly identify which patient was which subtype.

In previous studies, Davuluri and his Wistar colleagues have established how changes in the way a cell reads its own DNA can create multiple variations of a single protein. These variant proteins are called isoforms, and they are produced as cells alter how they transcribe a given gene into RNA. Slight changes in how the cellular machine reads a gene can result in protein isoforms with subtle differences in enzymatic activity or longevity.

For example, their earlier research determined how human brains produce different isoforms of specific proteins throughout their lives. Developing fetal brains produce different isoforms of certain genes than adult brains. They also found that changes that trigger the production of the wrong isoform at the wrong time could lead to cancer.

In the Nucleic Acids Research study, the researchers combined assays of these protein isoforms with a computer model they call PIGExClass, or the Platform-independent Isoform-level Gene-EXpression based Classification-system. To categorize glioblastomas with PIGExClass, Davuluri and his colleagues first began with Cancer Genome Atlas data to develop a set of 121 isoform variants whose combination of differences could denote a specific subtype of the brain cancer. PIGExClass is, essentially, a software that ranks gene isoform data into sets based on a set of pre-determined values. The researchers found that, by using this classification system, they could predict the subtype of glioblastoma in the database with 92 percent accuracy.

"When we knew what combination of isoforms could create a specific signature for each type of glioblastoma, we could then create a simple laboratory assay that would look for these differences in patient samples," Davuluri said. "In this case the test would measure variations in the RNA abundance associated with these 121 isoforms that make up the signature."

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19-Feb-2014

Contact: John Paul Gutierrez jpgutierrez@icahdq.org International Communication Association

Washington, DC (February 19 2014) The lifelong debate of nature versus nurture continuesthis time in what your children watch. A recent paper published in the Journal of Communication found that a specific variation of the serotonin-transporter gene was linked to children who engaged in increased viewing of violent TV and playing of violent video games.

Sanne Nikkelen, Helen Vossen, and Patti Valkenburg of the University of Amsterdam's School of Communication Research, in collaboration with researchers at the Erasmus University Medical Centre in Rotterdam, analyzed survey data of 1,612 parents of Dutch children ages 5-9. The parents noted how much violent TV programming their children viewed, as well as how often they played violent video games. DNA samples collected at the children's birth were then analyzed to determine a certain gene variant. The researchers found that children that had the specific variant of the serotonin-transporter gene on average consumed more violent media and displayed more ADHD-related behaviors. However, these links are subtle and more factors can influence these behaviors in children.

Earlier studies have shown that overall amount of media use is partly heritable. These studies, however, did not examine the use of specific media content and did not examine specific gene variants, but only looked at heritability. This study is the first to specifically examine violent media content and to examine a specific gene variant. There have been earlier studies looking at whether violent media use is related to ADHD-related behaviors, but these have found mixed results.

"Our results indicate that children's violent media use is partly influenced by genetic factors. This could mean that children with this gene variant are more likely to seek out stimulating activities, such as violent television viewing and video game playing," said Nikkelen. "It is important to study the relationship between media use and ADHD-related behaviors because children who show increased ADHD-related behaviors often face peer and academic difficulties and are at increased risk for substance abuse. Examining factors that may contribute to the development of these behaviors is essential."

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"Media Violence and Children's ADHD-Related Behaviors: A Genetic Susceptibility Perspective'" by Sanne Nikkelen, Helen Vossen, Patti Valkenburg, Fleur Velders, Dafna Windhorst, Vincent Jaddoe, Albert Hofman, Frank Verhulst, & Henning Tiemeier, Journal of Communication, Volume 64 No. 1, pgs. 42-60, 2014 doi:10.1111/jcom.12073

Contact: To schedule an interview with the author or a copy of the research, please contact John Paul Gutierrez, jpgutierrez@icahdq.org.

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Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, February 19, 2014Joseph C. Glorioso, III, PhD (University of Pittsburgh School of Medicine, PA) devoted much of his research career to developing herpes viruses as efficient vectors for delivering therapeutic genes into cells. In recognition of his leadership and accomplishments, he has received a Pioneer Award from Human Gene Therapy, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. Human Gene Therapy is commemorating its 25th anniversary by bestowing this honor on the leading 12 Pioneers in the field of cell and gene therapy selected by a blue ribbon panel* and publishing a Pioneer Perspective by each of the award recipients. The Perspective by Dr. Glorioso is available on the Human Gene Therapy website.

As he recounts in his essay "Herpes Simplex Viral Vectors: Late Bloomers with Big Potential," it took 30 years to create broadly applicable HSV vector designs and a useful gene delivery platform. Since herpes simplex virus has a natural affinity for the nervous system, Dr. Glorioso believes that "gene delivery to the brain represents the most important frontier for HSV-mediated gene therapy and provides a unique opportunity to study complex processes such as learning and memory and to treat complex genetic and acquired diseases, including brain degeneration, epilepsy, and cancer."

In addition, says Dr. Glorioso, some herpes viral delivery systems are proving useful for gene transfer in the emerging field of cellular reprogramming to produce stem cells for tissue regeneration.

"Joe began his work in gene therapy early in the development of the field focusing on the very challenging objective of targeting the central nervous system. His work with HSV vectors represents an incredibly elegant blending of basic virology and translational science," says James M. Wilson, MD, PhD, Editor-in-Chief of Human Gene Therapy, and Director of the Gene Therapy Program, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia.

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*The blue ribbon panel of leaders in cell and gene therapy, led by Chair Mary Collins, PhD, MRC Centre for Medical Molecular Virology, University College London selected the Pioneer Award recipients. The Award Selection Committee selected scientists that had devoted much of their careers to cell and gene therapy research and had made a seminal contribution to the field--defined as a basic science or clinical advance that greatly influenced progress in translational research.

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February 19, 2014

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Brett Smith for redOrbit.com Your Universe Online

Long-prized for their thick fur, the cuddly Eurasian beaver has been hunted by humans for thousands of years and a new genetic study from a large group of international researchers has found that predation by humans has significantly cut down the genetic diversity of these animals.

While beaver populations have been growing rapidly since the late 19th century when conservation efforts began, genetic diversity within modern beaver populations remains considerably reduced to what was present prior to the period of human hunting and habitat reduction, said study author Michi Hofreiter, a biology professor from the University of York in the United Kingdom.

In the study, which was published in the journal Molecular Ecology, the research team found that the Eurasian beaver can be divided into three different groups. The two predominant ones are in western and Eastern Europe and a now extinct, and previously unknown, third group inhabiting the Danube river basin. This population was around at least 6,000 years ago but vanished during the transition to modern society.

The rapid loss of diversity prior to conservation efforts appears to have established a very strong pattern for the geographic distribution of genetic diversity among present-day beaver populations, Hofreiter said.

After centuries of being hunted by humans, the Eurasian beaver had faded from the majority of its original range at the end of the 1800s, with approximately 1,200 beavers remaining. The researchers said they wanted to see if the lack of genetic diversity and strong distribution of genetic diversity seen today are caused by hunting or had already existed before the beavers range was diminished.

To reach their conclusion, the team analyzed DNA from 48 ancient beaver samples, ranging in age from a few hundred to about 11,000 years old, and over 150 modern beavers. The analytical work was performed at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany.

We found that overall there was more genetic diversity in the past, said study author Susanne Horn, from the institute. Apparently, already in ancient times an ancient contact zone existed between the eastern and western populations of beavers in the Oder River area. This is close to a present-day contact zone in Germany and Poland.

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Mendelian Genetics Law of Segregation tutorial
Genetics with Professor Matthew Schmidt and Dimitra Hasiotis For more information and to view the full video go to streamingtutors.com.

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KNIGHTSBRIDGE OG - Lady Sativa Genetics - Amsterdam Weed Review 2014
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Biology #flipclass Mendelian Genetics #bioHWHL
Our #flipclass introduction to Mendelian Genetics. Link for worksheet: https://www.dropbox.com/s/1jwvw1zafkd9o6f/01%20Autosomal%20Practice.pdf.

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Duke researchers use gene therapy to direct stem cells into becoming new cartilage on a synthetic scaffold even after implantation into a living body

By Ken Kingery

By combining a synthetic scaffolding material with gene delivery techniques, researchers at Duke University are getting closer to being able to generate replacement cartilage where it's needed in the body.

Performing tissue repair with stem cells typically requires applying copious amounts of growth factor proteinsa task that is very expensive and becomes challenging once the developing material is implanted within a body. In a new study, however, Duke researchers found a way around this limitation by genetically altering the stem cells to make the necessary growth factors all on their own.

They incorporated viruses used to deliver gene therapy to the stem cells into a synthetic material that serves as a template for tissue growth. The resulting material is like a computer; the scaffold provides the hardware and the virus provides the software that programs the stem cells to produce the desired tissue.

The study appears online the week of Feb. 17 in the Proceedings of the National Academy of Sciences.

An artistic rendering of human stem cells on the polymer scaffolds. Photo courtesy of Charles Gersbach and Farshid Guilak, Duke University

The traditional approach has been to introduce growth factor proteins, which signal the stem cells to differentiate into cartilage. Once the process is under way, the growing cartilage can be implanted where needed.

But a major limitation in engineering tissue replacements has been the difficulty in delivering growth factors to the stem cells once they are implanted in the body, said Guilak, who is also a professor in Dukes Department of Biomedical Engineering. Theres a limited amount of growth factor that you can put into the scaffolding, and once its released, its all gone. We need a method for long-term delivery of growth factors, and thats where the gene therapy comes in.

A microscopic view using electron microscopy of human stem cells and viral gene carriers adhering to the fibers of a polymer scaffold. Photo courtesy of Charles Gersbach and Farshid Guilak, Duke University

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Gene Therapy Might Grow Replacement Tissue Inside the Body

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