Archive for the ‘Gene Therapy Research’ Category

Most popular Genetic Medicine Austin TX
Hiring authorities actually mean alot as a result of that, we ensure our Genetic Medicine solutions are completed with professionals and specialist strategies. http://www.localpros.us/austin-tx/gen...

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London, UK (PRWEB) December 20, 2013

Nowadays, molecular diagnostics in generic testing introduces advanced analytical techniques to the treatment and diagnosis of various generic disorders. The burgeoning growth in the market is propelled by considerable breakthroughs in proteomics and genomics, as well as by the ongoing development of microarray devices to measure different analytes within body tissues and blood. The range of the major recent developments includes but is not limited to the introduction and rapid uptake of cell-free fetal DNA prenatal testing, advancements in the development of personalised medicine, the integration of gene expression profiling and specialty labs into clinical practice, expansion of the installed base of automated instruments used for molecular testing and also the considerable progress of companion diagnostics for drug development.

At present, generic testing forms one of the most profitable segments of the overall molecular diagnostics space. The generic testing area has a huge growth potential, which is poised to be the major area of interest in the upcoming years.

Discounted research report Molecular Diagnostics in Genetic Testing drawn up by TriMark Publications (TriMark) has been recently published by Market Publishers Ltd.

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Title: Molecular Diagnostics in Genetic Testing Published: November, 2013 Pages: 185 Price:US$ 3,060.00 http://marketpublishers.com/report/in_vitro_diagnostics/molecular_diagnostics/molecular-diagnostics-in-genetic-testing.html

The in-demand report presents a comprehensive guide to the emerging market for molecular diagnostics in generic testing globally and in the USA. It provides an in-depth assessment of this emerging field, offers a detailed analysis of its performance, estimates the size and growth potential of the molecular diagnostics in the genetic testing area. The research study contains a detailed examination of the major factors influencing the development of different market sectors, delves into the competitive environment and uncovers vital information on the performance of the leading companies engaged in the industry. The report characterises the regulative framework, describes the current market landscape and then thoroughly discusses the future growth prospects of molecular diagnostics in the generic testing universe.

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More insightful research reports by the publisher can be found at TriMark page.

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Molecular Diagnostics Prospects in Genetic Testing Area Discussed in Discounted Report by TriMark Published at ...

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20-Dec-2013

Contact: Jessica Studeny jessica.studeny@case.edu 216-368-4692 Case Western Reserve University

Many rare disorders are caused by gene mutation, like sickle cell anemia. Yet until now the underlying genetic cause of more common conditions for example, rheumatoid arthritis has evaded scientists for years.

New research from Case Western Reserve University School of Medicine to appear in the journal Genome Research finds that six common diseases arise from DNA changes located outside genes. The study from the laboratory of Peter Scacheri, PhD, shows that multiple DNA changes, or variants, work in concert to affect genes, leading to autoimmune diseases including rheumatoid arthritis, Crohn's disease, celiac disease, multiple sclerosis, lupus and colitis. Further, for each disease, multiple different genes are manipulated by several small differences in DNA.

"We've known that rare diseases are due to one change within one gene with major effects. The key take away is that common diseases are due to many changes with small effects on a handful of genes," said Scacheri, associate professor of genetics and genome sciences.

The research is in advanced online publication and can be found at http://tinyurl.com/okml3ag.

The human genome includes 3 billion letters of DNA. Only 1 to 2 percent of the letters are used as the blueprint for proteins, the body's building blocks. Scacheri's team is part of group of scientists investigating where and why DNA goes awry in the remaining 98 percent the regions between genes. These regions contain thousands of genetic switches that control the levels of genes. This new finding shows that in common diseases, the fine-tuning of those switches is not quite right, leading to incorrect expression of some key genes previously unidentified.

"This is a paradigm shift for the field with respect to pinpointing the genetic causes of common disease susceptibility," Scacheri said.

"The Scacheri lab's study provides a new model for understanding how genetic variants explain variation in common, complex diseases such as rheumatoid arthritis and colitis. That is, the effect of an individual variant may be very small, but when coupled with other nearby variants, the manifestations are much greater, said Anthony Wynshaw-Boris, MD, PhD, chair of the Department of Genetics and Genome Sciences at Case Western Reserve University School of Medicine and University Hospitals Case Medical Center and the James H. Jewell MD '34 Professor of Genetics at the School of Medicine. "This model may also help to explain why genetic studies of these and other common diseases have so far fallen short of providing a satisfactory explanation of the genetic pathways important for the development of these disorders."

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Common disorders: It's not the genes themselves, but how they are controlled

Minecraft FTB "Horizon" LP-EP08 "Advanced genetics"
Episode number 8 we hop into the technics of DNA and genetics!

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Bicuspid aortic valve: Prevalence, genetics and natural history.

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Bicuspid aortic valve: Prevalence, genetics and natural history. - Video

Genetics - Trinity Open Day 2013
A talk from Genetics at the Undergraduate Open Day, December 2013, Trinity College Dublin. http://www.tcd.ie/courses.

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Advances in Cattle Genetics
Knowing the genetics of your cattle is getting easier. Livestock genetics consultant Sean McGrath explains how experts can tell you the genetic traits of you...

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Scott Bill O #39;Malley Show: Genetics ReUpload Finalized
Cast: Dusan, Chris, Jesus, Nathan Sorry the audio is a bit soft at the end... Please raise volume at 5:56.

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Scott Bill O'Malley Show: Genetics ReUpload Finalized - Video

This article is about chimerism in animals. For chimerism in plants, see Chimera (plant).

Most organisms produced by sexual reproduction have at most two parents, one providing an egg and one providing sperm. However, sometimes fertilized eggs merge to form organisms with two sets of parents, giving them tissues that are a mixture of different genetic inheritance. This can result in male and female organs, two different blood types, or subtle variations in form. [1] Normally, chimerism is not visible on casual inspection; however, it has been detected in the course of proving parentage.

Another way that chimerism can occur is by organ transplantation, giving one individual tissues that developed from two different genomes. For example, a bone marrow transplant can change someone's blood type.

A chimera or chimaera is a single organism (usually an animal) that is composed of two or more different populations of genetically distinct cells that originated from different zygotes involved in sexual reproduction. If the different cells have emerged from the same zygote, the organism is called a mosaic. Chimeras are formed from at least four parent cells (two fertilized eggs or early embryos fused together). Each population of cells keeps its own character and the resulting organism is a mixture of tissues. Chimeras are typically seen in animals; there are some reports of human chimerism.[1]

This condition is either inherited or it is acquired through the infusion of allogeneic hematopoietic cells during transplantation or transfusion. In nonidentical twins, chimerism occurs by means of blood-vessel anastomoses. The likelihood of offspring being a chimera is increased if it is created via in vitro fertilization[citation needed]. Chimeras can often breed, but the fertility and type of offspring depends on which cell line gave rise to the ovaries or testes; varying degrees of intersexuality may result if one set of cells is genetically female and another genetically male.

Tetragametic chimerism is a form of congenital chimerism. This condition occurs through the fertilization of two separate ova by two sperm, followed by the fusion of the two at the blastocyst or zygote stages. This results in the development of an organism with intermingled cell lines. Put another way, the chimera is formed from the merging of two nonidentical twins (although a similar merging presumably occurs with identical twins, but as their DNA is almost identical, the presence would not be immediately detectable in a very early (zygote or blastocyst) phase). As such, they can be male, female, or hermaphroditic.

As the organism develops, it can come to possess organs that have different sets of chromosomes. For example, the chimera may have a liver composed of cells with one set of chromosomes and have a kidney composed of cells with a second set of chromosomes. This has occurred in humans, and at one time was thought to be extremely rare, though more recent evidence suggests that it is not as rare as previously believed.[1][2]

This is particularly true for the marmoset. Recent research shows most marmosets are chimeras, sharing DNA with their fraternal twins.[3] 95% of Marmoset fraternal twins trade blood through chorionic fusions, making them hematopoietic chimeras. [4][5]

Most chimeras will go through life without realizing they are chimeras. The difference in phenotypes may be subtle (e.g., having a hitchhiker's thumb and a straight thumb, eyes of slightly different colors, differential hair growth on opposite sides of the body, etc.) or completely undetectable. Chimeras may also show, under a certain spectrum of UV light, distinctive marks on the back resembling that of arrow points pointing downwards from the shoulders down to the lower back; this is one expression of pigment unevenness called Blaschko's lines.[6]

Affected persons may be identified by the finding of two populations of red cells or, if the zygotes are of opposite sex, ambiguous genitalia and hermaphroditism alone or in combination; such persons sometimes also have patchy skin, hair, or eye pigmentation (heterochromia). If the blastocysts are of opposite sex, genitals of both sexes may be formed, either ovary and testis, or combined ovotestes, in one rare form of intersexuality, a condition previously known as true hermaphroditism.

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GENE THERAPY PROF WAGIH P5

By: Asmaa Alhazmi

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Understanding Advances in Gene Therapy
Could a blood cancer patient #39;s own immune cells soon be used to fight their cancer? In chimeric antigen receptor (CAR) gene therapy, T-cells are taken from a...

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Understanding Advances in Gene Therapy - Video

GENE THERAPY PROF WAGIH P1

By: Asmaa Alhazmi

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GENE THERAPY PROF WAGIH P1 - Video

Stem Cell Therapy - Facet Syndrome Patients Relieve Back and Neck Pain Dr Robert Wagner - NSPC
How to know if the cause of your back or neck pain is Facet Syndrome. Discover how biologic regenerative treatments are able to pick up where traditional tre...

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Stem Cell Therapy - Facet Syndrome Patients Relieve Back and Neck Pain Dr Robert Wagner - NSPC - Video

Poway, CA (PRWEB) December 19, 2013

Amazing Grace Hamiltons banked stem cells from Vet-Stem, Inc. have recently helped her avoid hip surgery for the second time. Gracie is now nearly 12 years old and her owners noticed her activities had dramatically slowed in the last year. They turned to banked stem cells that Gracie had stored with Vet-Stem, Inc. in Poway, California to help with the discomfort and pain of arthritis that was slowing her down.

When Gracies owners brought her to Garden State Veterinary Specialists in Tinton Falls, New Jersey in October of this year the x-rays showed a severely deteriorated right hip. Dr. Thomas Scavelli and Dr. Michael Hoelzler were very concerned and recommended hip replacement. Gracies owners wanted to try stem cell therapy first, since it had given them such positive results five years before.

We needed to give the stem cells a try before going to the more invasive surgical approach, Mrs. Hamilton said. At the time of the procedure Dr. Hoelzler told me that Gracies hips were the worst he had seen, but in just a couple of days after the stem cell therapy we began to see a difference. Just shy of two weeks after the procedure I took her back to Dr. Hoelzler and he was very impressed. She was walking comfortably.

At three years Gracie had been diagnosed with hip dysplasia. By six years of age she had slowed to the point of great concern as her owners described it. The pain caused by arthritis from the hip dysplasia was beginning to interfere with her life.

Gracie was no longer running and jumping, and certain activities had become difficult (like climbing onto my husbands sailboat). She also had a noticeable limp, Mrs. Hamilton remembered the signs of pain and discomfort that prompted Gracies first stem cell therapy five years before.

Gracie was brought to Dr. Scavelli in 2008 with painful symptoms, and stem cell therapy for pets was the latest, cutting edge treatment. Gracies owners understood that without stem cell therapy Gracie would have faced hip surgery at the time.

We are grateful for stem cell therapy which has restored Gracies ability to enjoy her morning walks again, Mrs. Hamilton shared, She enjoys wrestling with us and playing with her toys. She looks forward to visiting her friends, and prances around like a puppy. Gracie is a happy dog and we are happy owners because she does not appear to be in pain anymore!

About Vet-Stem, Inc.

Vet-Stem, Inc. was formed in 2002 to bring regenerative medicine to the veterinary profession. The privately held company is working to develop therapies in veterinary medicine that apply regenerative technologies while utilizing the natural healing properties inherent in all animals. As the first company in the United States to provide an adipose-derived stem cell service to veterinarians for their patients, Vet-Stem, Inc. pioneered the use of regenerative stem cells in veterinary medicine. The company holds exclusive licenses to over 50 patents including world-wide veterinary rights for use of adipose derived stem cells. In the last decade over 10,000 animals have been treated using Vet-Stem, Inc.s services, and Vet-Stem is actively investigating stem cell therapy for immune-mediated and inflammatory disease, as well as organ disease and failure. For more on Vet-Stem, Inc. and Veterinary Regenerative Medicine visit http://www.vet-stem.com or call 858-748-2004.

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Stem Cell Therapy by Vet-Stem, a Surprising Alternative to Hip Surgery for a New Jersey Chocolate Labrador Retriever

Abba Zubair, medical and scientific director of the Cell Therapy Laboratory at the Mayo Clinic in Jacksonville, wants to test the feasibility of growing stem cells in outer space, cells that could be used to generate new tissue and even new organs in human beings.

There are reasons to believe that stem cells, which are hard to grow in the great quantity they are needed on Earth, will grow much more rapidly in the microgravity environment in space, Zubair thinks. Now the Center for the Advancement in Science in Space has given Zubair a $300,000 grant to test that by placing stem cells in a specialized cell bioreactor in the International Space Station.

It now takes a month to generate enough cells for a few patients, Zubair said. A clinical laboratory in space could provide the answer we all have been seeking for regenerative medicine. ... If you have a ready supply of these cells, you can treat almost any condition and can theoretically regenerate entire organs using a scaffold. Additionally, they dont need to come from individual patients. Anyone can use them without rejection.

The stem cells he plans to grow in space will be stem cells that can induce regeneration of neurons and blood vessels in patients who have suffered hemorrhagic strokes caused by blood clots.

I have a special personal interest in stroke, Zubair said. Thats what killed my mom years ago. I really would like to conquer and treat stroke.

The first step in growing stem cells in space is happening at the University of Colorado where engineers are building the cell bioreactor Zubair will use on the space station. Within a year, Zubair hopes to transport the bioreactor and stem cells to the space station, perhaps aboard a flight by SpaceX, a company expected to begin commercial flights to the space station soon.

Once the bioreactor and stem cells are aboard the space station, it will take about a month to grow them, Zubair said. The results will then be analyzed by the astronauts on the space station and by researches back in Zubairs Jacksonville laboratories.

We will be trying to determine if our notion that stem cells grow faster in microgravity is true, Zubair said. We also want to know how feasible it is to produce clinical grade cells in space that can be used in humans.

Hes optimistic his study will show that growing stem cells in space is a viable way to create stem cells in quantity.

Were quite excited, he said. I really think the future is full of promise. We just have to take the opportunity to make that a reality.

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Mayo cell therapy researcher plans to grow stem cells in space, where he thinks they will grow faster than on Earth

Dec 18, 2013 5:00pm

By Steven C. Moyo, M.D.

A gene mutation can increase your risk of heart attack and death as much as smoking does, new research suggests.

Duke University researchers reported today finding a link between a gene mutation known to increase the bodys response to stress and heart health. They found in a study of more than 6,000 patients with heart disease, carriers of this genetic mutation had a 38 percent increased risk of heart attack or death.

Genetic mutations are not just the stuff of movies and comic books. They are changes in our DNA code that affect the color of our eyes, our risks for cancer and, as this study shows, even our response to stress.

When we are stressed, it sets off a chain reaction of chemical signals in our bodies. The first of these is the release of a chemical called serotonin in the brain something that happens as soon as we get yelled at by our boss, for example, or get cut off in traffic. This release of serotonin lights the fuse for the explosive cascade of chemicals that follows, eventually leading to increased levels of cortisol in our system.

What this gene mutation does is produce a slightly different serotonin receptor in the brain one that causes an even greater than normal release of cortisol in response to stress.

This is bad news for our hearts. Specifically, increased cortisol has been shown to be associated with higher levels of calcium deposits in the hearts blood vessels, and blockage of these vessels is linked to increased risk of heart attack and death.

Men with this gene mutation have been shown to have a two- to three-times larger cortisol response to stress, said study investigator, Dr. Redford Williams, professor of medicine at Duke University. This higher-than-normal cortisol response from this gene, he said, boosts the risk of heart attack or death. Williams added that more than one in eight men and up to 2 percent of women in the general population are thought to carry this gene mutation, and that the increased risk associated with this gene is comparable to the increased risk associated with a smoking habit.

Williams said he hopes the findings will shed further light on the role of genes in stress-related heart ills a hope shared by heart disease experts not involved with the study.

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'Stress Gene' Ups Heart Attack, Death Risk

A gene linked to high stress levels has now been discovered to also increase a persons risk of having a heart attack, Medical News Today reported.

In a study published in PLoS ONE, researchers focused on the gene 5HTR2C, in order to examine how it affected cardiovascular health. Based on previous research, the study authors knew that a variation in the DNA of this gene was linked with extreme reactions to stress. In fact, men who carry this genetic variant have twice as much of the stress hormone cortisol in their blood, compared to men without the variant.

Knowing that high levels of cortisol were linked to an increased risk for heart attacks, the researchers decided to examine the effects of this genetic variant more closely.

For their study, researchers from the Duke University Medical Center in Durham, N.C., followed 6,100 white male and female heart patients for six years. Of the patients studied, 13 percent carried the genetic variation for extreme stress response.

Overall, researchers found that carriers of this gene variant had a 38 percent higher risk for heart attack or death. The researchers suspect this may be because of a blood compound called MMP9, which is known to increase as cortisol levels in the body rise. According to Medical News Today, MMP9 may soften plaque in the arteries, making them more likely to burst or clot leading to heart attacks or death.

Experts hope these findings might someday make it easier to prevent heart attack deaths.

"This research may one day help to identify patients who should be candidates for more intensive disease prevention and treatment strategies, said Dr. Peter Kaufmann, a deputy branch chief of the Clinical Applications and Prevention Branch at the National Heart, Lung, and Blood Institute.

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Stress gene linked to higher risk for heart attack

How To Be A Superhuman
Science stands at the brink of unlocking our primal instincts. Advancements in genetic engineering may soon free humans from the limitations that have linked...

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PUBLIC RELEASE DATE:

19-Dec-2013

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

New Rochelle, NY, December 19, 2013The natural ability of certain fungi to break down complex substances makes them very valuable microorganisms to use as cell factories in industrial processes. Advances in metabolic engineering and systems biology are helping to customize and optimize these fungi to produce specific bioproducts, as described in a Review article in Industrial Biotechnology, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Industrial Biotechnology website.

In the Review "Integrated Approaches for Assessment of Cellular Performance in Industrially Relevant Filamentous Fungi," Mhairi Workman, Mikael Anderson, and Jette Thykaer, Technical University of Denmark, Lyngby, focus on how to apply state-of-the-art analytical tools and technologies to characterize industrially relevant fungi, improve fungal cell factories, and "utilize fungal bioproduct diversity to its full potential."

The Review is part of an IB IN DEPTH special section on Fungal Biology led by Guest Editors Scott Baker, PhD, Pacific Northwest National Laboratory (PNNL), Richland, WA, and Adrian Tsang, PhD, Concordia University, Montreal, Canada. Additional Original Research articles include "Kinetic Modeling of -Glucosidases and Cellobiohydrolases Involved in Enzymatic Hydrolysis of Cellulose," by Marie Chauve, PhD, et al. from IFP Energies nouvelles (Solaize and Rueil-Malmaison, France), European Synchrotron Radiation Facility and Centre de Recherches sur les Macromolecules Vegetales (Grenoble, France); and "Comparative Genomics Analysis of Trichoderma reesei Strains," by Hideaki Koike, PhD, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan, and colleagues from the US Department of Energy (DOE) Joint Genome Institute (Walnut Creek, CA), and PNNL.

Also included in the Fungal Biology special section are two IB Interviews: with Randy Berka of Novozymes (Davis, CA); and Igor Grigoriev, PhD, US DOE Joint Genome Institute.

"Once again, one of IB's Editorial Board members has stepped forward to tell a compelling story of industrial biotechnology development," says Co-Editor-in-Chief Larry Walker, PhD, Professor, Biological & Environmental Engineering, Cornell University, Ithaca, NY. "The opportunities to exploit fungal biotechnology for industrial chemicals and energy are unlimited."

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Integrated approaches to customize fungal cell factories

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19-Dec-2013

Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego

Researchers at the University of California, San Diego School of Medicine, with colleagues in The Netherlands and United Kingdom, have produced the first map detailing the network of genetic interactions underlying the cellular response to ultraviolet (UV) radiation.

The researchers say their study establishes a new method and resource for exploring in greater detail how cells are damaged by UV radiation and how they repair themselves. UV damage is one route to malignancy, especially in skin cancer, and understanding the underlying repair pathways will better help scientists to understand what goes wrong in such cancers.

The findings will be published in the December 26, 2013 issue of Cell Reports.

Principal investigator Trey Ideker, PhD, division chief of genetics in the UC San Diego School of Medicine and a professor in the UC San Diego Departments of Medicine and Bioengineering, and colleagues mapped 89 UV-induced functional interactions among 62 protein complexes. The interactions were culled from a larger measurement of more than 45,000 double mutants, the deletion of two separate genes, before and after different doses of UV radiation.

Specifically, they identified interactive links to the cell's chromatin structure remodeling (RSC) complex, a grouping of protein subunits that remodel chromatin the combination of DNA and proteins that make up a cell's nucleus during cell mitosis or division. "We show that RSC is recruited to places on genes or DNA sequences where UV damage has occurred and that it helps facilitate efficient repair by promoting nucleosome remodeling," said Ideker.

The process of repairing DNA damage caused by UV radiation and other sources, such as chemicals and other mutagens, is both simple and complicated. DNA-distorting lesions are detected by a cellular mechanism called the nucleotide excision repair (NER) pathway. The lesion is excised; the gap filled with new genetic material copied from an intact DNA strand by special enzymes; and the remaining nick sealed by another specialized enzyme.

However, NER does not work in isolation; rather it coordinates with other biological mechanisms, including RSC.

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How cells remodel after UV radiation

A stress gene has been linked to having a higher risk of dying from a heart attack or heart disease.

Heart patients with the genetic change had a 38 per cent increased risk of heart attack or death, say US researchers.

Personalised medicine may lead to better targeting of psychological or drug treatment to those most at risk, they report in PLOS ONE.

The study adds to evidence stress may directly increase heart disease risk, says the British Heart Foundation.

A team at Duke University School of Medicine studied a single DNA letter change in the human genome, which has been linked to being more vulnerable to the effects of stress.

They found heart patients with the genetic change had a 38 per cent increased risk of heart attack or death from heart disease after seven years of follow up compared with those without, even after taking into account factors like age, obesity and smoking.

This suggests that stress management techniques and drug therapies could reduce deaths and disability from heart attacks, they say.

director of the Behavioural Medicine Research Center at Duke University School of Medicine, Dr Redford Williams, said the work is the first step towards finding genetic variants that identify people at higher risk of cardiovascular disease.

This is one step towards the day when we will be able to identify people on the basis of this genotype who are at higher risk of developing heart disease in the first place, he told BBC News.

Thats a step in the direction of personalised medicine for cardiovascular disease.

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Stress gene linked to heart attack – Study

Rebekah Eliason for redOrbit.com Your Universe Online

A new study from Duke reveals that the genetic trait responsible for predisposing some people to strong stress reactions may also cause the risk of heart attack or death to rise by 38 percent.

This discovery provides a new biological explanation for why some people are inclined towards cardiovascular disease. Since in these cases the disease is linked to stress, the findings suggest that behavior modification and drug therapies targeting stress reduction may lower heart attack related disability and deaths.

Redford B. Williams Jr., M.D., director of the Behavioral Medicine Research Center at Duke University School of Medicine and senior author of the paper, said, Weve heard a lot about personalized medicine in cancer, but in cardiovascular disease we are not nearly as far along in finding the genetic variants that identify people at higher risk. Here we have a paradigm for the move toward personalized medicine in cardiovascular disease.

Building on previous work at Duke and elsewhere, Williams and his colleagues were able to identify a variation in a DNA sequence known as single nucleotide polymorphism (SNP). In this sequence variation, one letter from the genetic code is swapped with another causing a change in the genes function. Specifically the team focused on the SNP occurring on the gene responsible for making a serotonin receptor that causes a hyperactive reaction to stress.

Last year, a study was published reporting that men with the genetic variation were found to contain twice as much cortisol in their blood after exposure to stress than men without the variant. Commonly known as the stress hormone, cortisol is designed to support the bodys biological response to stressful situations that cause negative emotions. This vital hormone is produced in the adrenal glands.

Beverly H. Brummett, PhD, associate professor of Psychiatry and Behavioral Sciences at Duke and lead author of the paper, said, It is known that cortisol has effects on the bodys metabolism, on inflammation and various other biological functions, that could play a role in increasing the risk of cardiovascular disease. It has been shown that high cortisol levels are predictive of increased heart disease risk. So we wanted to examine this more closely.

Several years of data from heart catheterization patients at Duke was formed into a large database used by researchers to run a genetic analysis of over 6,100 white participants. Of those studied, two-thirds were men and one-third was women. Approximately 13 percent of the group was found to possess the genetic variation for the overactive stress response.

Those found to carry the genetic variation corresponded with patients who had the highest rates of heart attacks and deaths when evaluating the median follow-up time of six years. Even when taking into account age, obesity, smoking history, other illnesses and the severity of their heartdisease, the studied genetic trait was found to be associated with a 38 percent increased risk of heart attack and death.

This finding requires independent replication and evaluation in a more diverse population, said Peter Kaufmann, Ph.D., deputy branch chief of the Clinical Applications and Prevention Branch at the NIHs National, Heart, Lung, and Blood Institute (NHLBI). This research may one day help to identify patients who should be candidates for more intensive disease prevention and treatment strategies.

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Stress Gene Linked To Higher Risk Of Heart Attack And Death

When Janet Rowley was accepted into the University of Chicago's medical school in 1944, the quota for women was already filled three in a class of 65.

So she had to wait a year.

Dr. Rowley made up for that early setback by becoming an internationally known scientist whose research in the 1970s redefined cancer as a genetic disease and led to a paradigm shift in how it is studied and treated.

An advisor to presidents and recipient of her nation's highest honors, Rowley achieved breakthroughs that prolonged the lives of countless cancer patients. She died Tuesday at age 88 at her home in the Chicago suburb of Hyde Park from complications of ovarian cancer.

"She was a pioneer in the field because, at that time, there was a big divide between what people thought caused cancer," said Dr. Funmi Olopade, director of the Center for Clinical Cancer Genetics at the University of Chicago. "She was able to show that genetic changes were defining specific types of cancers, and it was these genetic abnormalities that were really the trigger to explaining why cancer behaved the way it behaved."

Rowley graduated from medical school in 1948 at age 23. The next day she married fellow medical student Donald Rowley, who became a professor of pathology at the university. For many years while raising four sons, Rowley worked three days a week, including at a Chicago clinic for children with Down syndrome, a genetic disorder caused by an extra chromosome.

Her interest in chromosomes continued in the 1960s, when she traveled to Oxford University to learn new ways to analyze them.

Back home, a University of Chicago colleague gave Rowley some laboratory space, a microscope and a salary of $5,000 a year and encouraged her to study the chromosomes of leukemia patients.

Rowley's pivotal discovery came during one of her "off days" in 1972, while poring through images of chromosomes that she had spread out on the family dinner table.

At the time, scientists were befuddled by the relationship between genes and cancer, unsure why patients with a particular leukemia displayed one abnormally short chromosome a threadlike structure that carries genetic information.

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Janet Rowley dies at 88; scientist pinpointed genetic cause of leukemia

Researchers at the University of California, San Diego School of Medicine, with colleagues in The Netherlands and United Kingdom, have produced the first map detailing the network of genetic interactions underlying the cellular response to ultraviolet (UV) radiation.

The researchers say their study establishes a new method and resource for exploring in greater detail how cells are damaged by UV radiation and how they repair themselves. UV damage is one route to malignancy, especially in skin cancer, and understanding the underlying repair pathways will better help scientists to understand what goes wrong in such cancers.

The findings will be published in the December 26, 2013 issue of Cell Reports.

Principal investigator Trey Ideker, PhD, division chief of genetics in the UC San Diego School of Medicine and a professor in the UC San Diego Departments of Medicine and Bioengineering, and colleagues mapped 89 UV-induced functional interactions among 62 protein complexes. The interactions were culled from a larger measurement of more than 45,000 double mutants, the deletion of two separate genes, before and after different doses of UV radiation.

Specifically, they identified interactive links to the cell's chromatin structure remodeling (RSC) complex, a grouping of protein subunits that remodel chromatin the combination of DNA and proteins that make up a cell's nucleus during cell mitosis or division. "We show that RSC is recruited to places on genes or DNA sequences where UV damage has occurred and that it helps facilitate efficient repair by promoting nucleosome remodeling," said Ideker.

The process of repairing DNA damage caused by UV radiation and other sources, such as chemicals and other mutagens, is both simple and complicated. DNA-distorting lesions are detected by a cellular mechanism called the nucleotide excision repair (NER) pathway. The lesion is excised; the gap filled with new genetic material copied from an intact DNA strand by special enzymes; and the remaining nick sealed by another specialized enzyme.

However, NER does not work in isolation; rather it coordinates with other biological mechanisms, including RSC.

"DNA isn't free-floating in the cell, but is packaged into a tight structure called chromatin, which is DNA wound around proteins," said Rohith Srivas, PhD, a former research scientist in Ideker's lab and the study's first author. "In order for repair factors to fix DNA damage, they need access to naked DNA. This is where chromatin remodelers come in: In theory, they can be recruited to the DNA, open it up and allow repair factors to do their job."

Rohith said that other scientists have previously identified complexes that perform this role following UV damage. "Our results are novel because they show RSC is connected to both UV damage pathways: transcription coupled repair - which acts on parts of DNA being expressed - and global genome repair, which acts everywhere. All previous remodelers were linked only to global genome repair."

The scientists noted that the degree of genetic rewiring correlates with the dose of UV. Reparative interactions were observed at distinct low or high doses of UV, but not both. While genetic interactions at higher doses is not surprising, the authors said, the findings suggest low-dose UV radiation prompts specific interactions as well.

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How cells remodel after exposure to UV radiation

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