Archive for the ‘Gene Therapy Research’ Category

Genetics - The Musical Box (Parte 2) @ Teatro Coliseo, Bs As, 21/09/13.
Genetics, la banda tributo que mejor reproduce la música de Genesis en la era Gabriel, interpretando en vivo la majestuosa #39;Musical Box #39; en el teatro Coliseo...

By: Gino Zolezzi

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Genetics - The Musical Box (Parte 2) @ Teatro Coliseo, Bs As, 21/09/13. - Video

In a step that brings stem cells closer to the clinic, researchers in Japan have found that transplanting reprogrammed stem cells into the brains of primates elicits little rejection by their immune systems.

Induced pluripotent stem cells (iPSCs) are created when skin cells, for example, are genetically reprogrammed to an embryonic-like state. This kind of stem cells holds great potential for the treatment of disease, since the cells are genetically identical to the patient they are taken from.

However, studies in rodents have suggested that the immune system may still recognize cells derived from iPSCs as foreign, and mount an attack on them. This has cast doubt on the feasibility of similar cell therapy for humans.

To test this in an animal more closely related to humans, researchers studied macaques. Using cells taken from the monkeys mouths or from their bloodstream, the researchers created iPSCs which they then, in turn, transformed into neurons. These neurons were of a specific kind: dopamine-producing neurons, the type depleted by Parkinsons disease.

Each monkey got six injections of these neurons into its brainsome which had been made from their own cells and others which were from another individual and therefore mismatched. The team could then see what kind of immune response each type produced.

Over subsequent months of observation, the monkeys showed very little immune response to transplants of their own cells. Their immune response was much higher in response to cells from another monkey.

The team also tracked how well the neurons survived after transplantation. They found that even when there was an immune response from the primate, the dopamine-producing neurons survived. The study is published today in Stem Cell Reports.

Trials using iPSCs to treat people with Parkinsons disease could therefore be on the horizon. These findings give a rationale to start autologous transplantationat least of neural cellsin clinical situations, says senior author Jun Takahashi of Kyoto University.

Image by Oliver Sved / Shutterstock

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Stem Cell Therapy for Parkinson's Proves Safe in Primates

Paul Greenberg for Discovery News 2013-09-25 18:20:43 UTC

The war veteran who recoils at the sound of a car backfiring and the recovering drug addict who feels a sudden need for their drug of choice when visiting old haunts have one thing in common: Both are victims of their own memories. New research indicates those memories could actually be extinguished.

A new study from the Massachusetts Institute of Technology found a gene called Tet1 can facilitate the process of memory extinction. In the study, mice were put in a cage that delivered an electric shock. Once they learned to fear that cage, they were then put in the same cage but not shocked. Mice with the normal Tet1 levels no longer feared the cage once new memories were formed without the shock. Mice with the Tet1 gene eliminated continued to fear the cage even when there was no shock delivered.

We learned from this that the animals defective in the Tet1 gene are not capable of weakening the fear memory, Le-Huei Tsai, director of MIT's Picower Institute for Learning and Memory, told Discovery News. For more than a half century it has been documented that gene expression and protein synthesis are essential for learning and forming new memories. In this study we speculated that the Tet1 gene regulates chemical modifications to DNA.

SEE ALSO: Sleep Helps Reinforce Memory

The MIT researchers found that Tet1 changes levels of DNA methylation, the process of causing a chemical reaction. When methylation is prominent, the process of learning new memories is more efficient. When methylation is weaker, the opposite is true.

The results support the notion that once a fear memory is formed, to extinguish that memory a new memory has to form, Tsai said. The new memory competes with the old memory and eventually supersedes the old memory.

Experts in the study of memory and anxiety agree.

This is highly significant research in that it presents a completely new mechanism of memory regulation and behavior regulation, said Jelena Radulovic, a professor of bipolar disease at Northwestern University. The mechanism of manipulating DNA is likely to affect many other things. Now the question will be whether there will be patterns that emerge, whether there will be side effects on moods and emotions and other aspects. But the findings have real relevance.

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No More Bad Flashbacks: Scientists Find Gene That Erases Memories

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

Proterro, Inc., the only biofeedstock company that actually makes sucrose instead of extracting it from crops or deconstructing cellulosic materials, has named Timothy Cooper, Ph.D., vice president of engineering.

Dr. Cooper joins Proterros executive team with more than two decades of deep experience in bioprocessing. Prior to joining Proterro, he was responsible for Eastman Chemical Companys biotechnology effort, managing genetic engineering and fermentation development programs, and driving generation of intellectual property.

Before Eastman Chemical, Dr. Cooper was fermentation research leader at Dow AgroSciences LLC, where he was responsible for development and scale-up of new fermentation processes and managing the fermentation development efforts of three laboratories.

At Wyeth Pharmaceuticals, Inc., Dr. Cooper directed the companys fermentation and recovery development effort that solved key manufacturing obstacles of a complicated, multicomponent vaccine, successfully scaling the process to commercial volumes.

Dr. Coopers experience also includes:

A member of the American Chemical Society and the Society of Industrial Microbiology, Dr. Cooper earned a Bachelor of Science in chemical engineering from Tennessee Technological University and a Ph.D. in chemical engineering at the University of Wisconsin.

Other Proterro News

In a separate announcement today Proterro said it has reached new milestones in development. (See Proterro Meets Key Milestones)

About Proterro, Inc.

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Biofeedstock Company Proterro Names Bioprocessing Expert Engineering VP

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. 22 hours ago When rare "words" (codons) are present near the start of bacterial genes, working copies of the gene don't as readily into structures that block protein production. To find out the rare words themselves or lack of roadblocks increased protein production, Wyss Institute researchers synthesized 14,000 snippets of DNA with rare codons, roadblocks, both, or neither (individual pixels in this diagram), inserted them into genes, and measured how much protein they produced. Those with rare codons and roadblocks no longer made more protein (green pixels). That showed that rare codons work by removing roadblocks. Credit: Wyss Institute

Scientists routinely seek to reprogram bacteria to produce proteins for drugs, biofuels and more, but they have struggled to get those bugs to follow orders. But a hidden feature of the genetic code, it turns out, could get bugs with the program. The feature controls how much of the desired protein bacteria produce, a team from the Wyss Institute for Biologically Inspired Engineering at Harvard University reported in the September 26 online issue of Science.

The findings could be a boon for biotechnologists, and they could help synthetic biologists reprogram bacteria to make new drugs and biological devices.

By combining high-speed "next-generation" DNA sequencing and DNA synthesis technologies, Sri Kosuri, Ph.D., a Wyss Institute staff scientist, George Church, Ph.D., a core faculty member at the Wyss Institute and professor of genetics at Harvard Medical School, and Daniel Goodman, a Wyss Institute graduate research fellow, found that using more rare words, or codons, near the start of a gene removes roadblocks to protein production.

"Now that we understand how rare codons control gene expression, we can better predict how to synthesize genes that make enzymes, drugs, or whatever you want to make in a cell," Kosuri said.

To produce a protein, a cell must first make working copies of the gene encoding it. These copies, called messenger RNA (mRNA), consist of a specific string of words, or codons. Each codon represents one of the 20 different amino acids that cells use to assemble proteins. But since the cell uses 61 codons to represent 20 amino acids, many codons have synonyms that represent the same amino acid.

In bacteria, as in books, some words are used more often than others, and molecular biologists have noticed over the last few years that rare codons appear more frequently near the start of a gene. What's more, genes whose opening sequences have more rare codons produce more protein than genes whose opening sequences do not.

No one knew for sure why rare codons had these effects, but many biologists suspected that they function as a highway on-ramp for ribosomes, the molecular machines that build proteins. According to this idea, called the codon ramp hypothesis, ribosomes wait on the on-ramp, then accelerate slowly along the mRNA highway, allowing the cell to make proteins with all deliberate speed. But without the on-ramp, the ribosomes gun it down the mRNA highway, then collide like bumper cars, causing traffic accidents that slow protein production. Other biologists suspected rare codons acted via different mechanisms. These include mRNA folding, which could create roadblocks for ribosomes that block the highway and slow protein production.

To see which ideas were correct, the three researchers used a high-speed, multiplexed method that they'd reported in August in The Proceedings of the National Academy of Sciences.

First, they tested how well rare codons activated genes by mass-producing 14,000 snippets of DNA with either common or rare codons; splicing them near the start of a gene that makes cells glow green, and inserting each of those hybrid genes into different bacteria. Then they grew those bugs, sorted them into bins based on how intensely they glowed, and sequenced the snippets to look for rare codons.

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A hidden genetic code for better designer genes

Public release date: 26-Sep-2013 [ | E-mail | Share ]

Contact: Natasha Pinol npinol@aaas.org 202-326-6440 American Association for the Advancement of Science

Biology students at the University of Minnesota take a course in their very first semester in which they propose their own gene-based solution to a problem. Among the projects they have worked on was a camouflage military suit that could change color through the use of a gene that allows an octopus to camouflage itselfa technology that happened to be developed by the U.S. military a few years later.

"We've got these undergrads who propose amazingly practical, valuable, doable and sophisticated projects," Sue Wick, director of biology major undergraduate studies at the University of Minnesota and one of four professors there who developed the course.

Because of its effectiveness at teaching undergraduates how to think like professional biologists, the Genetic Engineering Proposal curriculum module has been chosen to receive the Science Prize for Inquiry-Based Instruction.

The Science Prize for Inquiry-Based Instruction (IBI) was developed to showcase outstanding materials, usable in a wide range of schools and settings, for teaching introductory science courses at the college level. The materials must be designed to encourage students' natural curiosity about how the world works, rather than to deliver facts and principles about what scientists have already discovered. Organized as one free-standing "module," the materials should offer real understanding of the nature of science, as well as provide an experience in generating and evaluating scientific evidence. Each month, Science publishes an essay by a recipient of the award, which explains the winning project. The essay about the Genetic Engineering Proposal, written by course co-creators Wick, Mark Decker, David Matthes and Robin Wright, will be published on September 27.

"We want to recognize innovators in science education, as well as the institutions that support them," says Bruce Alberts, editor-in-chief emeritus of Science. "At the same time, this competition will promote those inquiry-based laboratory modules with the most potential to benefit science students and teachers. The publication of an essay in Science on each winning module will encourage more college teachers to use these outstanding resources, thereby promoting science literacy."

From its inception, the Genetic Engineering Proposal course module has applied one main principle: that students should do biology, rather than just read about it. This idea was familiar to Wick, even when she was taking high school biology at her Milwaukee, Wisc., all-girls high school. Her teacher, a former medical technologist, made sure her students' science education was inquiry-based.

"There was inquiry, the idea of exploring, that we didn't know everything, that there were still so many things to discover, to explore and find out about," Wick says.

With her teacher's encouragement, Wick participated in a National Science Foundation summer high school program, took Advanced Placement biology, and ultimately went on to earn a PhD in the biological sciences.

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Genetic engineering course wins Science magazine prize

A type of DNA test the Apple CEO hoped might save his life is becoming widely available.

If you need proof of how information technology is influencing biotech, take a look at Foundation Medicine, the Boston-area diagnostics company that went public on Wednesday.

Its stock price quickly doubled after the IPO. And one reason is surely its links to stratospheric tech names from the West Coast. The company is backed by both Google and Bill Gates, and the core idea behind its technology was once tried out on Apple founder Steve Jobs.

Foundation sells a $5,800 test that looks in detail at the DNA of a person with cancer. The concept is that a comprehensive catalogue of genetic mutations in a persons tumor will show exactly whats driving the cancer and help doctors choose what drug will work best (see Foundation Medicine: Personalizing Cancer Drugs.)

It turns out that Jobs was one of the first peopleand certainly the best-knownto try this kind of all-in genetic strategy to beat cancer. As recounted in Walter Isaacsons biography of the Apple CEO, Jobs spent $100,000 to learn the DNA sequence of his genome and that of the tumors killing him. Jobs was jumping between treatments and hoped DNA would provide clues about where to turn next.

One of Jobss doctors I spoke to indicated that in the end DNA did not prove key to steering his treatment. But Jobs believed that medicine was taking strides. He famously said, Im either going to be one of the first to be able to outrun a cancer like this, or Im going to be one of the last to die from it.

According to Isaacson, some of the DNA analysis was done by the Broad Institute of MIT and Harvard, and his book tells how researchers travelled to California to brief Jobs five months before his death in 2011. While Broad wasnt able to confirm its role to me (events around Jobss illness are still closely guarded), by the time Jobs died four of the institute's top scientists were already deeply involved in setting up Foundation Medicine, which is based on their work studying cancer mutations.

The companys test, called FoundationOne, essentially offers the public the same type of DNA screening information that Jobs was among the first to get. Its a test that sequences 236 genes involved in cancer, detailing the dangerous mutations that are causing them to grow.

Google and Gates are two of the largest investors in Foundation Medicinethey own 9 percent and 4 percent of the company, respectively. One motive for their investment, I think, is that DNA is a profoundly digital molecule. And now that its become very cheap to decode, genetic data is piling up by the terabyte. Tech executives understand that and can see how to make a business out of it.

For a company like Foundation, which sprang out of genetics labs, having Google on board has been a big help. The search giant's venture arm, Google Ventures, which made the investment, has helped Foundation build software called the Interactive Cancer Explorer (see this promotional video) so doctors can access DNA reports on patients. Google also lends a hand recruiting technical personnel. And it sounds as if they may be helping Foundation launch a mobile app next year.

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From Steve Jobs to Google, tech leaders help drive personalized medicine

An upcoming film, The Perfect 46, is about a fictional genomics company with a not-so-fictional idea.

What if finding The One meant finding the person whose genome is most compatible with your own?

Thats the question raised by an upcoming movie called The Perfect 46. Writer/director Brett Ryan Bonowicz presented a near-final version of the film on Wednesday night at the Consumer Genetics Conference in Boston. Self-driving cars and disposable electronic package trackers set the film in an unspecified year in the future, but one that isnt so far away that you cant find a VCR or bulky television set.

The story centers around a genome-analysis company, The Perfect 46, that has developed an algorithm to determine the likelihood of prospective parents having a child with genetic disease. The promise is that future generations could be free of single-gene disorders like cystic fibrosis or even complex diseases like diabetes, if only everyone would work together to prevent these conditions in their children.

Sure, it sounds a bit like Gattaca, but unlike that 1997 film, The Perfect 46 does not feel like its happening in some distant era. In fact, I was struck by how unfuturistic it all seemed.

The real genetic analysis startup GenePeeks already says it can help sperm bank clients avoid donors whose genetic material may cause disease when combined with their own (see Genetic Screening Can Uncover Risky Matches at the Sperm Bank). And for couples planning to have a baby together, Counsyl and GoodStart Genetics can screen one or both partners to see whether they carry any DNA variants that could cause disease if combined with a similar genetic problem (see Better Screening for Deadly Genetic Diseases).

I met Bonowicz at the conference and he agreed that his science-fiction film is not that far outside the realm of possibility. Once I had the idea to write the film I realized I had to make it this year or not at all because a company is going to be doing this in four to five years, he says.

On a very small scale, genetic matchmaking is already happening, albeit not led by a company but by families affected by the disease and concerned medical groups. In the last few decades, the number of children born with Tay-Sachs diseasea neurodegenerative disorder that often takes a childs life by the age of fivehas been reduced by 90 percent in North American Ashkenazi Jews. Bulldozing that disease depended on gene-savvy matchmakers and in utero testing.

Another difference from Gattaca is the lack of a committed stance to whether genetic screening is a good or bad idea. The films protagonist heralds his matchmaking algorithm as a way to eliminate disease, but the film also touches on some of the fears surrounding genetic screening in reproductive medicine:What is a genetic defect and what is valuable human variation? Who decides what is healthy and what is not? When is it okay to intervene? And what if the screening doesnt go as planned? Bonowicz says he hopes that audiences will have conflicting opinions about the film. I wanted to start a conversation, he says. Thats the only way to push forward.

Bonowicz is looking to premiere a final version of the movie at a film festival next year.

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A Genetic Matchmaking Movie Isn't So Far-Fetched

A type of DNA test the Apple CEO hoped might save his life is becoming widely available.

Final slide: In 2011, Steve Jobs spent $100,000 to discover the genetic basis of the cancer that killed him.

If you need proof of how information technology is influencing biotech, take a look at Foundation Medicine, the Boston-area diagnostics company that went public on Wednesday.

Its stock price quickly doubled after the IPO. And one reason is surely its links to stratospheric tech names from the West Coast. The company is backed by both Google and Bill Gates, and the core idea behind its technology was once tried out on Apple founder Steve Jobs.

Foundation sells a $5,800 test that looks in detail at the DNA of a person with cancer. The concept is that a comprehensive catalogue of genetic mutations in a persons tumor will show exactly whats driving the cancer and help doctors choose what drug will work best (see Foundation Medicine: Personalizing Cancer Drugs.)

It turns out that Jobs was one of the first peopleand certainly the best-knownto try this kind of all-in genetic strategy to beat cancer. As recounted in Walter Isaacsons biography of the Apple CEO, Jobs spent $100,000 to learn the DNA sequence of his genome and that of the tumors killing him. Jobs was jumping between treatments and hoped DNA would provide clues about where to turn next.

One of Jobss doctors I spoke to indicated that in the end DNA did not prove key to steering his treatment. But Jobs believed that medicine was taking strides. He famously said, Im either going to be one of the first to be able to outrun a cancer like this, or Im going to be one of the last to die from it.

According to Isaacson, some of the DNA analysis was done by the Broad Institute of MIT and Harvard, and his book tells how researchers travelled to California to brief Jobs five months before his death in 2011. While Broad wasnt able to confirm its role to me (events around Jobss illness are still closely guarded), by the time Jobs died four of the institutes top scientists were already deeply involved in setting up Foundation Medicine, which is based on their work studying cancer mutations.

The companys test, called FoundationOne, essentially offers the public the same type of DNA screening information that Jobs was among the first to get. Its a test that sequences 236 genes involved in cancer, detailing the dangerous mutations that are causing them to grow.

Google and Gates are two of the largest investors in Foundation Medicinethey own 9 percent and 4 percent of the company, respectively. One motive for their investment, I think, is that DNA is a profoundly digital molecule. And now that its become very cheap to decode, genetic data is piling up by the terabyte. Tech executives understand that and can see how to make a business out of it.

View original post here:
Steve Jobs Left a Legacy on Personalized Medicine

Sep. 26, 2013 Although heavily studied, the specific genetic causes of "complex diseases," a category of disorders which includes autism, diabetes and heart disease, are largely unknown due to byzantine genetic and environmental interactions.

Now, scientists from the University of Chicago have created one of the most expansive analyses to date of the genetic factors at play in complex diseases -- by using diseases with known genetic causes to guide them. Analyzing more than 120 million patient records and identifying trends of co-occurrence among hundreds of diseases, they created a unique genetic map that has the potential to guide researchers and clinicians in diagnosing, identifying risk factors for and someday developing therapies against complex diseases. The work was published Sept. 26 in Cell.

"For the first time we've found that almost every complex disease has a unique set of associations with single-gene diseases. This essentially gives us 'barcodes' of specific gene loci, which we can use to help untangle the complex genetics of complex diseases," said Andrey Rzhetsky, PhD, professor of genetic medicine and human genetics at the University of Chicago, who led the study.

The majority of human diseases are complex and caused by a combination of genetic, environmental and lifestyle factors. On the other end of the spectrum are Mendelian diseases such as cystic fibrosis and sickle-cell anemia, which are caused by abnormalities to a single gene. Some Mendelian disorders are known to predispose patients to certain complex diseases, but these co-occurrences have thus far only been studied on a small-scale basis.

To expose any underlying shared genetic structures between these disease categories, Rzhetsky and his team developed computational algorithms to parse more than 120 million patient billing records from hospitals systems across the U.S. and from nearly the entire population of Demark. They looked for trends in comorbidity, or the occurrence of both complex and Mendelian disease in the same patient, that were higher than expected from random chance. They studied these correlations in 65 complex diseases affecting almost every system in the body, including arthritis, depression and lung cancer, and in 95 Mendelian disease groups (representing 213 disorders).

The team uncovered 2,909 statistically significant associations, as well as corresponding levels of relative risk between every disease pair. Some comorbidities were well known, such as the strong link between lipoprotein deficiencies and heart attack, but the vast majority were previously unknown. For example, Marfan syndrome, a connective tissue disorder, was found to have significant comorbidities with neuropsychiatric diseases such as autism, bipolar disorder and depression. Fragile X syndrome, an intellectual disability disorder, has significant associations with asthma, psoriasis and viral infection, highlighting a potential immune system dysfunction in these patients.

"Since the Mendelian diseases are associated with known genetic loci, we have essentially created a genetic map for complex disease using Mendelian disorders as markers," said David Blair, a graduate student at the University of Chicago and first author on the study. "These loci represent great candidates for uncovering subtle genetic variations, some which might not directly cause Mendelian disease but still impact the risk for developing complex diseases."

This genetic map is immediately useful for geneticists and clinicians as a gauge to the level of risk of developing complex disease among their patients with Mendelian diseases. But it also gives scientists a wealth of new data and a unique approach by which to better understand and develop therapeutics against complex diseases. The team also discovered that genetic insults underlying Mendelian diseases do not appear to independently contribute to complex diseases but likely interact in a combinatorial way to ultimately cause the disorders.

"Individuals with multiple Mendelian disease-causing genetic variants end up having a much higher risk for a complex disease than we would predict given that the variants act in isolation," Blair said.

The team hopes to expand their study to even more diseases and larger population data and to compare their predictions against the whole genome data of a broad population.

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Genetic map developed linking complex diseases

Eye genetics
Eye genetics.

By: Treyton Davis

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Eye genetics - Video

Genetics - Firth of Fifth [21.09.2013, Teatro Coliseo]
Genetics festejó los 40años de #39;Selling England by the Pound #39;, el disco más exitoso del Genesis de los 70s.

By: cdboxset

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Genetics - Firth of Fifth [21.09.2013, Teatro Coliseo] - Video

Paul on learning about his own DNA.
Paul, a genetics educator, shares why he decided to learn about his own DNA through the Personal Genome Project, and describes living with depression and how...

By: Personal Genetics Education Project - pgEd.org

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Paul on learning about his own DNA. - Video

Minecraft: Advanced Genetics mod - MORPH INTO MOBS AND USE THEIR ABILITIES!
Keep your eyes open for tomorrow #39;s video, it might just be one of the best vids I #39;ve made! Subscribe to my Gaming/Vlog channel [http://www.youtube.com/user/T...

By: TCTNGaming

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Minecraft: Advanced Genetics mod - MORPH INTO MOBS AND USE THEIR ABILITIES! - Video

Enrique on innovation and how genetics might change the world.
Enrique, a teacher in Boyle Heights and a champion of the i.am.angel foundation, shares his excitement about the potential of genetics to transform the world...

By: Personal Genetics Education Project - pgEd.org

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Enrique on innovation and how genetics might change the world. - Video

A revolutionary gene therapy developed in Colorado could relieve people's chronic pain, such as arthritis or fibromyalgia but first, it is being tested on pets with incredible results.

A Lafayette veterinarian is using cutting-edge research to heal dogs.

It may not look like it when 9-year-old Amos, a Labrador Retriever mix, is running happily after the ball, but he has arthritis, bad.

His owner, Vicki Riedel knew immediately.

"He is always by my side," said Riedel. "When I would go outside or downstairs,and he wouldn't come with me, I knew he was really hurting."

Their vet tried one medication after the next.

"And they all helped a little bit, but none of them really helped a lot, and he seemed to be getting worse and worse," said Riedel.

But a few weeks ago, Amos met pet pain specialist Dr. Rob Landry.

"Amos has a history of chronic pain in both his elbows," said Landry, a Lafayette veterinarian who has been testing a breakthrough gene therapy for chronic pain for the last two years.

"It's amazing," said Laundry with a smile.

The rest is here:
Gene therapy relieves pain in dogs

Jessica Soho Reports- STEM CELL therapy and LAMININE
visit http://www.mylifepharm.com/junvillomo.

By: Jun Villomo

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Jessica Soho Reports- STEM CELL therapy and LAMININE - Video

26.09.2013 - (idw) Universitt Konstanz

ERC Advanced Grant for the chemist Professor Dr. Andreas Marx from Konstanz for research on gene modification The chemist Professor Dr. Andreas Marx from Konstanz was awarded the renowned ERC Advanced Grant by the European Research Council (ERC) for developing new diagnostic procedures on the basis of DNA methylation. Similar to a diabetes quick test the new DNA methylation diagnostic is a universal and simplified procedure for an early diagnosis of diseases, among other things cancer. Moreover, the procedure provides the opportunity to tailor therapies more exactly to the patient and thus opens the door to personalised disease control, that is exactly matched to the organism of the patient and therefore shows fewer side effects. The five-year research project at the University of Konstanz is being supported by the European Research Council with approximately 2.5 million euros.

DNA methylation is considered as the most important epigenetic modification in human beings. The degree of methylation of cells is an important indicator of diseases and can be used for the early recognition of cancer, among other things. Present methods of testing methylation, however, have not only been work-intensive and time-consuming, but also bear a high risk of sample contamination. These test procedures have been too complex and too expensive for a broad medical application so far.

"Our approach of combining chemistry with biochemistry and biotechnology significantly simplifies these methods, thus enabling every diagnostic laboratory to run the test with established devices", comments Andreas Marx on the background of his research project EvoEPIGEN. "If we are successful, a test will no longer take some 16 hours, as is currently the case, but only two hours. This will safe nearly two days of work and the costs and risks will be substantially reduced: the test becomes suitable for large-scale use", Marx explains the importance of the simplified test procedure.

"The aim of our project is not only to promote biochemistry and its application in the medical field, but also to enhance the understanding of the effect of DNA methylation", explains Andreas Marx. The chemist and his research group intend to advance basic research in the field of epigenetics in order to tap new medical potential. "My thanks go to the European Research Council for the trust placed in me and in particular to all parties involved, as they played an important part in the preparatory work and made the project possible in the first place", Andreas Marx acknowledges.

Note to editors: You can download a photo of Prof. Dr. Andreas Marx here: http://www.pi.uni-konstanz.de/2013/marx.jpg

Contact: University of Konstanz Communications and Marketing Phone: 07531 / 88-3603 Email: kum@uni-konstanz.de

Prof. Dr. Andreas Marx University of Konstanz Department of Chemistry Organic chemistry / cellular chemistry Universittsstrae 10 78464 Konstanz Phone: 07531 / 88-5139 Email: Andreas.Marx@uni-konstanz.de

http://www.uni-konstanz.de

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Health & Medicine for Senior Citizens

Fat and Obesity Gene also Affects Hip Fracture: 82 Percent Risk Increase for Women

Women in study all over 60, bone health was followed between 1989 and 2007; during period, 102 had hip fractures

Sept. 25, 2013 - Australian researchers have demonstrated a strong association between the FTO (fat and obesity) gene and hip fracture in women. While the gene is already well known to affect diabetes and body fat, this is the first study to show that its high-risk variant can increase the risk of hip fracture by as much as 82%.

The study, undertaken by Dr Bich Tran and Professor Tuan Nguyen from Sydneys Garvan Institute of Medical Research, examined six gene variants (single nucleotide polymorphisms, or SNPs) of the FTO gene, taken from the DNA of 934 women in the Dubbo Osteoporosis Epidemiology Study (DOES). The women were all over 60, and their bone health was followed between 1989 and 2007. During that period, 102 women had hip fractures.

On average, the risk of fracture is about 11%. The study showed that if a woman has a low-risk genotype, or gene variant, the risk of fracture is 10%. If she has a high-risk genotype, it is 16%.

Now published online in Clinical Endocrinology, the authors believe that the findings have the potential to improve prediction of hip fracture. Known risk factors, also to be taken into account, include advancing age, falls, history of fracture, low bone mineral density, low body mass index (BMI) and genetic make-up.

We found that for a woman of the same age and same clinical risk factors, those with the high-risk genotype have an increased risk of fracture of 82% - a very high effect in genetic terms, said Professor Tuan Nguyen.

A genome-wide association study published in 2007 suggested that genetic variants in the FTO gene were associated with variation in BMI. This led us to hypothesise that they might also be associated with variation in hip fracture risk.

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Fat and Obesity Gene also Affects Hip Fracture: 82 Percent Risk Increase for Women

Public release date: 26-Sep-2013 [ | E-mail | Share ]

Contact: Graham Shaw graham.shaw@icr.ac.uk 44-020-715-35380 Institute of Cancer Research

Scientists have used a brand new technique for examining individual stem cells to uncover dramatic differences in the gene expression levels which genes are turned 'up' or 'down' between apparently identical 'sister' pairs.

The research, published today (Thursday) in Stem Cell Reports, was conducted and funded by The Institute of Cancer Research, London. It provides the latest evidence that despite having identical DNA, sister stem cells can display considerable differences in their molecular characteristics.

The study showed that DNA methylation, a process that controls which genes are expressed in cells, plays an important role in generating non-genetic (or 'epigenetic') differences between sister cells.

DNA methylation could therefore be one of the reasons for the major molecular variation between different cancer cells in the same tumour and drugs to reduce methylation might help control variation and make cancers easier to treat.

In the new research, scientists at The Institute of Cancer Research (ICR) developed a novel micro-dissection technique to separate pairs of sister embryonic stem cells for single cell RNA analysis [1].

Using their new high-tech method, researchers separated and isolated mouse stem cells from their sister pairs and measured the behaviour of key genes known to be expressed in those cells. By comparing which of these genes were up or down regulated, they determined the levels of similarity between sister cells at the molecular level for the first time.

They found that under normal conditions, pairs of sister stem cells displayed considerable differences to each other, showing nearly as much diversity as two cells from different sister pairs.

The researchers then looked at cells grown in the presence of a chemical cocktail called 2i, which reverts cells back to their most primitive stem cell state where they can make identical copies of themselves. They found that the cells had reduced levels of two enzymes critical for DNA methylation and they produced more similar sister cells.

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Study of 'sister' stem cells uncovers new cancer clue

Public release date: 26-Sep-2013 [ | E-mail | Share ]

Contact: Hannes Lohi hannes.lohi@helsinki.fi 358-919-25085 University of Helsinki

Professor Hannes Lohi's research group at the University of Helsinki and Folkhlsan Research Center has identified a mutation in ITGA10 gene, causing chondrodysplasia in two dog breeds, the Norwegian Elkhound and the Karelian Bear Dog. The research revealed a new chondrodysplasia gene in dogs, and a candidate gene for human chondrodysplasias. The finding has implications on bone biology as well as canine health. A genetic test can now be used to identify mutation carriers in the two affected dog breeds. The study was published on the scientific journal PLOS ONE on 25 September 2013.

The ITGA10 mutation causes autosomal recessive disproportionate short-stature dwarfism of varying severity. The appearance of affected dogs is characterized considerably shorter limbs than normal dogs, and other skeletal abnormalities may follow, including bowed forearms, abnormal digits, and malformed femoral heads.

The ITGA10 gene codes for an integrin subunit that assembles into a cartilage-specific collagen receptor, found in the growth plates of long bones. The receptor is important for the process of endochondral ossification, in which the cartilage cells first proliferate, and are then replaced by bone tissue. Accordingly, several abnormalities have been found in the growth plates of affected dogs both in radiographic and histological examinations.

Collagen-receptor mutation causes growth disturbances

The causative mutation was mapped to a specific region on canine chromosome 17 by comparing the genomes of affected and healthy dogs. Further analysis of this chromosomal region revealed a single nucleotide change in the ITGA10 gene, which disrupts the gene by introducing signal that prematurely ends the production of the encoded integrin subunit. "Because of the premature stop codon, the full length integrin subunit is never made, and consequently, there are no functional receptors in the affected dogs' growth plates. This causes the growth disturbances", explains Professor Lohi, and continues: "Several collagen mutations have been previously found in different growth disorders but this is only the second collagen receptor that has been linked to inherited chondrodysplasia. Our canine disease model offers new possibilities to study growth plate biology".

The results of the study may have implications to human medicine as well. "Humans also suffer from different types of inherited chondrodysplasia, and the ITGA10 gene could represent a good candidate gene for some of these disorders, which still have an unknown genetic cause", tells Kaisa Kystil, the first author of the paper. "We have already begun screening human patients for mutations in the gene", she adds.

A gene test recognizes mutation carrier dogs

The studied canine chondrodysplasia was initially described in Norwegian Elkhounds in the 1980's, and the current study identifies a corresponding problem in Karelian Bear Dogs. "Both breeds have now benefited from a genetic test that is available for dog owners", tells Professor Lohi. "The test is used to recognize mutation carriers, and the long-term aim is to eradicate the mutation and the disease from the dog breeds", he concludes.

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New dwarfism mutation identified in dogs

Public release date: 25-Sep-2013 [ | E-mail | Share ]

Contact: Connie Hughes connie.hughes@wolterskluwer.com 646-674-6348 Wolters Kluwer Health

Philadelphia, Pa. (September 25, 2013) - A specific gene variant is more frequent among elite athletes in power sports, reports a study in the October issue of The Journal of Strength and Conditioning Research, official research journal of the National Strength and Conditioning Association (NSCA). The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

A "functional polymorphism" of the angiotensiogen (AGT) gene is two to three times more common in elite power athletes, compared to nonathletes or even elite endurance athletes, according to the new research by Pawe Ciszczyk, PhD, of University of Szczecin, Poland, and colleagues. They write, "[T]he M23T variant in the AGT may be one of the genetic markers to investigate when an assessment of predisposition to power sports is made."

Gene Variant More Common in Elite Power Athletes

The researchers analyzed DNA samples from two groups of elite Polish athletes: 100 power-oriented athletes, from sports such as power-lifting, short-distance runners, and jumpers; and 123 endurance athletes, such as long-distance runners and swimmers and rowers. All athletes competed at the international leveleg, World and European Championships, World Cups, or Olympic Games. A group of 344 nonathletes were studied for comparison.

The analysis focused on the genotype of the M235T polymorphism of the gene AGT. "Polymorphisms" are genes that can appear in two different forms (alleles). A previous study found that the "C" allele of the AGT gene (as opposed to the "T" allele) was more frequent among elite athletes in power sports.

The genetic tests found that elite power athletes were more likely to have two copies of the C allelein other words, they inherited the C allele from both parents. This "CC" genotype was found 40 percent of the power athletes, compared to 13 percent of endurance athletes and 18 percent of nonathletes.

Power athletes were three times more likely to have the CC genotype compared to endurance athletes, and twice as likely compared to nonathletes. At least one copy of the C allele was present in 55.5 percent of power athletes, compared to about 40 percent of endurance athletes and nonathletes.

But Functional Significance Not Yet Clear

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Do elite 'power sport' athletes have a genetic advantage?

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Chapter 08 Microbial Genetics and Genetic Engineering - Cowan - Dr. Mark Jolley - Video

Public release date: 26-Sep-2013 [ | E-mail | Share ]

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

New Rochelle, NY, September 26, 2013Traumatic brain injury (TBI) during childhood can have long-term effects on cognitive and psychosocial functioning, including poor academic achievement. Pediatric TBI can cause significant deficits in working memory, as demonstrated in a study published in Journal of Neurotrauma, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Neurotrauma website at http://www.liebertpub.com/neu.

Working memory is the ability to collect, retain, and use information needed to perform tasks and respond to immediate demands. Amery Treble and coauthors from University of Houston, Texas and University of Texas Health Science Center at Houston used brain imaging studies to measure verbal and visuospatial working memory in a group of children who sustained TBI and a control group who did not. The comparison showed poorer visuospatial working memory in the pediatric TBI group, which was associated with disruptions in brain connectivity between neural networks that underlie working memory.

In the article "Working Memory and Corpus Callosum Microstructural Integrity after Pediatric Traumatic Brain Injury: A Diffusion Tensor Tractography Study," the authors propose that the identification of neuroanatomical biomarkers indicative of these changes in brain microstructure might allow for early identification of children at increased risk for impaired working memory and for earlier intervention.

"While confirming the longstanding belief that the corpus callosum is consistently involved with traumatic brain, this study's exquisite regionally specific analyses of callosal integrity, together with its evaluation of working memory in a pediatric brain-injured population, make this a particularly important contribution to the field of pediatric TBI," says John T. Povlishock, PhD, Editor-in-Chief of Journal of Neurotrauma and Professor, VCU Neuroscience Center, Medical College of Virginia, Richmond.

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About the Journal

Journal of Neurotrauma is an authoritative peer-reviewed journal published 24 times per year in print and online that focuses on the latest advances in the clinical and laboratory investigation of traumatic brain and spinal cord injury. Emphasis is on the basic pathobiology of injury to the nervous system, and the papers and reviews evaluate preclinical and clinical trials targeted at improving the early management and long-term care and recovery of patients with traumatic brain injury. Journal of Neurotrauma is the official journal of the National Neurotrauma Society and the International Neurotrauma Society. Complete tables of content and a sample issue may be viewed on the Journal of Neurotrauma website at http://www.liebertpub.com/neu.

About the Publisher

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Can traumatic brain injury impair a child's working memory?