(CBS News) A new study of patients with heart failure found a novel treatment approach might reverse the damage that has long been considered irreversible: Fixing their damaged hearts using stem cells derived by their own skin cells.

Stem cells heal heart attack scars, regrow healthy muscle Stem cells cure heart failure? What "breakthrough" study shows

In what scientists are calling a first, skin cells were taken from heart failure patients and transformed into stem cells, which were then turned into heart muscle cells capable of beating - albeit in a petri dish.

The treatment approach has scientists buzzing because it avoids the risk of possible immune system rejection from transplanting "foreign" stem cells, since the cells came from patients' own bodies.

"What is new and exciting about our research is that we have shown that it's possible to take skin cells from an elderly patient with advanced heart failure and end up with his own beating cells in a laboratory dish that are healthy and young - the equivalent to the stage of his heart cells when he was just born," the study's author Professor Lior Gepstein, professor of cardiology and physiology at the Technion-Israel Institute of Technology in Haifa, said in a news release.

Just how do skin cells become heart cells? Researchers took skin cells from two male patients with heart failure, a 51 and 61-year-old, and genetically reprogrammed them by injecting a cocktail of "transcription factors" and a virus into the nucleus of the skin cell, followed by removing the virus and transcription factors that have been linked to cancerous tumor growth. The goal was to reprogram the cells into human-induced pluripotent stem cells (hiPSCs) that could help repair hearts.

"One of the obstacles to using hiPSCs clinically in humans is the potential for the cells to develop out of control and become tumours," explained Prof Gepstein in using the technique.

Once in stem cell-form, the cells differentiated in a petri dish to become heart muscle cells called cardiomyocytes, which the researchers then combined with heart tissue and cultured them into healthy heart muscle tissue. Within 48 hours, the tissues were beating together.

"The tissue was behaving like a tiny microscopic cardiac tissue comprised of approximately 1000 cells in each beating area," Gepstein said in a statement.

The researchers then transplanted the new human tissue into rats, finding it grafted to the rat's host cardiac tissues. Their research is published in the May 22 issue of the European Heart Journal.

Follow this link:
Skin cells transformed into beating heart tissue, fueling heart failure treatment hopes

Recommendation and review posted by Bethany Smith

23-05-2012 09:53 Dr Ragai Mitry, Head of Liver processing at Kings College London, talks about implanting cells into a patient to replace failing liver function, at an event organised by TAPb Progress in Transplantation, Organ Donation and Research

Read the original post:
Ragai Mitry - Cell Therapy and Liver Disease - Video

Recommendation and review posted by Bethany Smith

05/24/2012 . (Classic Rock) Former Iron Maiden singer Paul Di'Anno wants his ex-bandmate Clive Burr to undergo stem cell therapy, despite the costs and risks associated with the procedure.

Burr, the drummer with Maiden from 1979 until 1982, has been in a wheelchair as a result of multiple sclerosis, which has been attacking his nervous system since before he was diagnosed in 2002.

MS reduces the ability of the brain and spinal cord to communicate with each other, resulting in a wide range of potentially severe symptoms. The cause is unknown and there is no cure; but in 2009 researchers made the first breakthrough in reversing symptoms through stem cell therapy.

Di'Anno tells Talking Metal Pirate Radio Burr's condition is "not very good at all." He had a lot to say, read it here.

Classic Rock Magazine is an official news provider for antiMusic.com. Copyright Classic Rock Magazine- Excerpted here with permission.

antiMUSIC News featured on RockNews.info and Yahoo News

...end

Read the rest here:
Di'Anno Wants Former Iron Maiden Bandmate To Undergo Stem Cell Therapy

Recommendation and review posted by Bethany Smith

TRADITION Three former Treasure Coast high school students have been awarded the first $3,000 internships at the Vaccine and Gene Therapy Institute's research laboratories in the Tradition Center for Innovation.

The Summer Undergraduate Research Foundation at VGTI, known as SURF-VGTI, pairs each student with a faculty mentor who will then work on research project for six weeks starting June 11. Their research findings will be presented in late July, according to the VGTI website.

Daniel Rosenberg and Lysa Vola, both graduates of Jensen Beach High School, and Robert Tack, a graduate of Port St. Lucie High School all now college students are this year's first interns, said John Schatzle, principle investigator and director of scientific affairs at VGTI.

For the past few years, Torrey Pines Institute for Molecular Studies, also located in Tradition, has been offering similar type summer internships to area college students and public school teachers.

VGTI concentrated on offering internships to students from the Treasure Coast and providing them real-world research experience, Schatzle said. "They will be working like any other researcher would be in the lab."

VGTI opened the doors of its new $47 million, 100,000-square-foot research facility in February to develop vaccines and immunotherapies for diseases such as AIDS, cancer, tuberculosis and diseases associated with emerging viral infections.

Rosenberg, 19, who now is a biomedical engineering student at the University of Miami, will be paired with a mentor who is studying HIV, Schatzle said.

"We've actually found one of its major hiding places in the body and trying to figure out how to purge it, and effectively have a cure for HIV," he said. "(Rosenberg's) lab is working on that project."

Rosenberg said he is excited to be working on such an important study.

"The last semester I took a physiology class and I learned a lot about AIDS and now I can apply that knowledge," Rosenberg said. "It astounds me that it impacts so many people every year and we have not found a solid cure for the disease."

The rest is here:
Tradition-based VGTI offers its first summer research internships

Recommendation and review posted by Bethany Smith

Featured Article Academic Journal Main Category: Fertility Also Included In: Genetics;Men's Health Article Date: 25 May 2012 - 2:00 PDT

Current ratings for: 'Sperm Gene Discovery May Lead To Non-Hormonal Male Contraceptive'

Currently, the only male contraceptives available rely on disrupting the production of hormones like testosterone, which can cause unpleasant side effects such as acne, irritability and mood swings.

First author Dr Lee Smith is Reader in Genetic Endocrinology at the University of Edinburgh's Centre for Reproductive Health. He told the media:

"If we can find a way to target this gene in the testes, we could potentially develop a non-hormonal contraceptive."

The gene, called Katnal1, is critical to enabling sperm to mature in the testes.

Finding a way to regulate the gene could potentially stop the sperm maturing and render them ineffective.

Not only could this form the basis of a new type of male contraceptive that does not involve disrupting hormone levels, it could also lead to new treatments for male infertility caused by a faulty Katnal1 gene.

"The important thing is that the effects of such a drug would be reversible because Katnal1 only affects sperm cells in the later stages of development, so it would not hinder the early stages of sperm production and the overall ability to produce sperm," explained Smith.

"Although other research is being carried out into non-hormonal male contraceptives, identification of a gene that controls sperm production in the way Katnal1 does is a unique and significant step forward in our understanding of testis biology," he added.

Link:
Sperm Gene Discovery May Lead To Non-Hormonal Male Contraceptive

Recommendation and review posted by Bethany Smith

ScienceDaily (May 24, 2012) Researchers at NYU School of Medicine have, for the first time, identified a single gene that simultaneously controls inflammation, accelerated aging and cancer.

"This was certainly an unexpected finding," said principal investigator Robert J. Schneider, PhD, the Albert Sabin Professor of Molecular Pathogenesis, associate director for translational research and co-director of the Breast Cancer Program at NYU Langone Medical Center. "It is rather uncommon for one gene to have two very different and very significant functions that tie together control of aging and inflammation. The two, if not regulated properly, can eventually lead to cancer development. It's an exciting scientific find."

The study, funded by the National Institutes of Health, appears online ahead of print May 24 in Molecular Cell and is scheduled for the July 13 print issue.

For decades, the scientific community has known that inflammation, accelerated aging and cancer are somehow intertwined, but the connection between them has remained largely a mystery, Dr. Schneider said. What was known, due in part to past studies by Schneider and his team, was that a gene called AUF1 controls inflammation by turning off the inflammatory response to stop the onset of septic shock. But this finding, while significant, did not explain a connection to accelerated aging and cancer.

When the researchers deleted the AUF1 gene, accelerated aging occurred, so they continued to focus their research efforts on the gene. Now, more than a decade in the making, the mystery surrounding the connection between inflammation, advanced aging and cancer is finally being unraveled.

The current study reveals that AUF1, a family of four related genes, not only controls the inflammatory response, but also maintains the integrity of chromosomes by activating the enzyme telomerase to repair the ends of chromosomes, thereby simultaneously reducing inflammation, preventing rapid aging and the development of cancer, Dr. Schneider explained.

"AUF1 is a medical and scientific trinity," Dr. Schneider said. "Nature has designed a way to simultaneously turn off harmful inflammation and repair our chromosomes, thereby suppressing aging at the cellular level and in the whole animal."

With this new information, Dr. Schneider and colleagues are examining human populations for specific types of genetic alterations in the AUF1 gene that are associated with the co-development of certain immune diseases, increased rates of aging and higher cancer incidence in individuals to determine exactly how the alterations manifest and present themselves clinically.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

More here:
Key gene found responsible for chronic inflammation, accelerated aging and cancer

Recommendation and review posted by Bethany Smith

Gene Findings in African-Americans May Pave Way Toward Better Quit-Smoking Treatments

By Denise Mann WebMD Health News

Reviewed by Laura J. Martin, MD

May 22, 2012 -- A "smoking gun" gene may play a role in how many cigarettes certain smokers puff each day.

Researchers from 50 medical institutions across the country analyzed genetic material of more than 32,000 African-American smokers and non-smokers to see if certain genes predicted when they began smoking, how many cigarettes they smoked, and how easily they were able to quit.

According to the new study, a variant in a nicotine receptor gene predicts about one extra cigarette smoked per day. This same general location has been implicated in smoking behavior among white Europeans. Among African-Americans, the new genetic marker appears on a different spot on the same gene.

The findings appear in the May 22 issue of Translational Psychiatry. They are part of the Study of Tobacco in Minority Populations (STOMP) Genetics Consortium.

"This region is really important for addiction biology, regardless of race or ethnicity," says researcher Helena Furberg, PhD, an assistant attending epidemiologist at Memorial Sloan-Kettering Cancer Center in New York City.

This is somewhat surprising, she says. "Smoking behaviors differ among ethnic groups." For example, African-Americans typically start smoking at later ages than their counterparts of European descent and smoke fewer cigarettes each day. But they have a higher risk for lung cancer and are less likely to quit smoking.

The findings hold potential for tailoring smoking cessation treatments down the road, Furberg says. "The next research step would be to see if currently available smoking cessation medications would work better or differently among people who carry these variants."

See the article here:
Smoking Gene May Reveal Why Some People Smoke More

Recommendation and review posted by Bethany Smith

OMAHA, Neb.--(BUSINESS WIRE)--

Transgenomic, Inc. (TBIO.OB) today announced it has entered into an agreement with Gene Logic, Inc., an Ocimum Biosolutions Company, to acquire its biorepository assets for $250,000 in cash. The biorepository contains thousands of human biological samples that can be used to validate diagnostic assays developed by Transgenomic. Transgenomic will use the samples to develop and validate its REVEAL family of proprietary ICE COLD-PCR-based oncology assays, as well as its WAVE MCE System and SURVEYOR Scan Mutation Detection Kits.

This transaction significantly strengthens Transgenomics position in translational medicine services, providing a deep source of clinical samples allowing us to validate new drug-associated genetic targets, said Craig Tuttle, Chief Executive Officer of Transgenomic. The biorepository provides not only strategic and operational benefits, but also long-term cost savings. Acquiring specimens on a case-by-case basis is expensive and time-consuming; such expenditure would quickly surpass the cost of acquiring this asset.

The Gene Logic biorepository consists of a high quality, diverse collection of human tissue samples and extracted DNA specimens with linked clinical information. The 60,000 samples and specimens cover multiple disease areas, including many thousands of cancer tissue specimens.

About Transgenomic

Transgenomic, Inc. (www.transgenomic.com) is a global biotechnology company advancing personalized medicine in cancer and inherited diseases through its proprietary molecular technologies and world-class clinical and research services. The Company has three complementary business divisions: Transgenomic Pharmacogenomic Services is a contract research laboratory that specializes in supporting all phases of pre-clinical and clinical trials for oncology drugs in development. Transgenomic Clinical Laboratories specializes in molecular diagnostics for cardiology, neurology, mitochondrial disorders, and oncology. Transgenomic Diagnostic Tools produces equipment, reagents, and other consumables that empower clinical and research applications in molecular testing and cytogenetics. Transgenomic believes there is significant opportunity for continued growth across all three businesses by leveraging their synergistic capabilities, technologies, and expertise. The Company actively develops and acquires new technology and other intellectual property that strengthen its leadership in personalized medicine.

Forward-Looking Statements

Certain statements in this press release constitute forward-looking statements of Transgenomic within the meaning of the Private Securities Litigation Reform Act of 1995, which involve known and unknown risks, uncertainties and other factors that may cause actual results to be materially different from any future results, performance or achievements expressed or implied by such statements. Forward-looking statements include, but are not limited to, those with respect to management's current views and estimates of future economic circumstances, industry conditions, company performance and financial results, including the ability of the Company to grow its involvement in the diagnostic products and services markets. The known risks, uncertainties and other factors affecting these forward-looking statements are described from time to time in Transgenomic's filings with the Securities and Exchange Commission. Any change in such factors, risks and uncertainties may cause the actual results, events and performance to differ materially from those referred to in such statements. Accordingly, the Company claims the protection of the safe harbor for forward-looking statements contained in the Private Securities Litigation Reform Act of 1995 with respect to all statements contained in this press release. All information in this press release is as of the date of the release and Transgenomic does not undertake any duty to update this information, including any forward-looking statements, unless required by law.

Originally posted here:
Transgenomic Acquires Clinical Sample Biorepository from Gene Logic

Recommendation and review posted by Bethany Smith

Public release date: 24-May-2012 [ | E-mail | Share ]

Contact: Tara Womersley tara.womersley@ed.ac.uk 44-131-650-9836 University of Edinburgh

A new type of male contraceptive could be created thanks to the discovery of a key gene essential for sperm development.

The finding could lead to alternatives to conventional male contraceptives that rely on disrupting the production of hormones, such as testosterone and can cause side-effects such as irritability, mood swings and acne.

Research, led by the University of Edinburgh, has shown how a gene Katnal1 is critical to enable sperm to mature in the testes.

If scientists can regulate the Katnal1 gene in the testes, they could prevent sperm from maturing completely, making them ineffective, without changing hormone levels.

The research, which is published in the journal PLoS Genetics, could also help in finding treatments for cases of male infertility, when malfunction of the Katnal1 gene hampers sperm development.

Dr Lee Smith, Reader in Genetic Endocrinology at the Medical Research Council Centre for Reproductive Health at the University of Edinburgh, said: "If we can find a way to target this gene in the testes, we could potentially develop a non-hormonal contraceptive.

"The important thing is that the effects of such a drug would be reversible because Katnal1 only affects sperm cells in the later stages of development, so it would not hinder the early stages of sperm production and the overall ability to produce sperm.

"Although other research is being carried out into non-hormonal male contraceptives, identification of a gene that controls sperm production in the way Katnal1 does is unique and a significant step forward in our understanding of testis biology."

Read the rest here:
Gene discovery points towards new type of male contraceptive

Recommendation and review posted by Bethany Smith

Public release date: 24-May-2012 [ | E-mail | Share ]

Contact: Tara Womersley Tara.Womersley@ed.ac.uk 44-131-650-9836 Public Library of Science

A new type of male contraceptive could be created thanks to the discovery of a key gene essential for sperm development.

The finding could lead to alternatives to the conventional male contraceptives that rely on disrupting the production of hormones, such as testosterone. These treatments can cause side-effects such as irritability, mood swings and acne.

Research, led by the University of Edinburgh, has shown how a gene Katnal1 is critical to enable sperm to mature in the testes.

If scientists can regulate the Katnal1 gene in the testes, they could prevent sperm from maturing completely, making them ineffective without changing hormone levels.

The research, which is published in the journal PLoS Genetics, could also help in finding treatments for cases of male infertility when malfunction of the Katnal1 gene hampers sperm development.

Dr Lee Smith, Reader in Genetic Endocrinology at the University of Edinburgh's Centre for Reproductive Health, said: "If we can find a way to target this gene in the testes, we could potentially develop a non-hormonal contraceptive.

"The important thing is that the effects of such a drug would be reversible because Katnal1 only affects sperm cells in the later stages of development, so it would not hinder the early stages of sperm production and the overall ability to produce sperm.

"Although other research is being carried out into non-hormonal male contraceptives, identification of a gene that controls sperm production in the way Katnal1 does is a unique and significant step forward in our understanding of testis biology."

Read more:
Gene study could pave way for non-hormonal male contraceptive

Recommendation and review posted by Bethany Smith

DARPA, the science arm of the US Department of Defense, is trying to find a way to create a streamlined manufacturing process for purpose-specific engineering of plants and animals, reports Popular Science's Rebecca Boyle. This program, called Living Foundries, "sets up an assembly line paradigm for life and its constituent parts," Boyle says. "Under this program, genetic engineering would no longer be limited to modification of existing organisms instead, scientists would be able to concoct anything they wanted from scratch, using a suite of ingredients and processes that could apply in any situation." And DARPA's first grants for the program have just been announced $15.5 million spread among six institutions and companies, including the J. Craig Venter Institute. This last pick is particularly appropriate, she says, given the group's work in synthetic biology.

The purpose of the grants is to build a basic library of modularized parts that can be used in assembling various organisms, Boyle says, like wires or circuits that can be used to build electronics. "The ultimate goal is a genetic starter set that could be snapped together like so many Legos, forming any system the military might require," she adds.

Our sister publication GenomeWeb Daily News has more on the project here.

Go here to read the rest:
DARPA's Synthetic Army

Recommendation and review posted by Bethany Smith

LOS ANGELES Understanding the genetic diversity within and between populations has important implications for studies of human disease and evolution. This includes identifying associations between genetic variants and disease, detecting genomic regions that have undergone positive selection and highlighting interesting aspects of human population history.

Now, a team of researchers from the UCLA Henry Samueli School of Engineering and Applied Science, UCLA's Department of Ecology and Evolutionary Biology and Israel's Tel Aviv University has developed an innovative approach to the study of genetic diversity called spatial ancestry analysis (SPA), which allows for the modeling of genetic variation in two- or three-dimensional space.

Their study is published online this week in the journal Nature Genetics.

With SPA, researchers can model the spatial distribution of each genetic variant by assigning a genetic variant's frequency as a continuous function in geographic space. By doing this, they show that the explicit modeling of the genetic variant frequency the proportion of individuals who carry a specific variant allows individuals to be localized on a world map on the basis of their genetic information alone.

"If we know from where each individual in our study originated, what we observe is that some variation is more common in one part of the world and less common in another part of the world," said Eleazar Eskin, an associate professor of computer science at UCLA Engineering. "How common these variants are in a specific location changes gradually as the location changes.

"In this study, we think of the frequency of variation as being defined by a specific location. This gives us a different way to think about populations, which are usually thought of as being discrete. Instead, we think about the variant frequencies changing in different locations. If you think about a person's ancestry, it is no longer about being from a specific population but instead, each person's ancestry is defined by the location they're from. Now ancestry is a continuum."

The team reports the development of a simple probabilistic model for the spatial structure of genetic variation, with which they model how the frequency of each genetic variant changes as a function of the location of the individual in geographic space (where the gene frequency is actually a function of the x and y coordinates of an individual on a map).

"If the location of an individual is unknown, our model can actually infer geographic origins for each individual using only their genetic data with surprising accuracy," said Wen-Yun Yang, a UCLA computer science graduate student.

"The model makes it possible to infer the geographic ancestry of an individual's parents, even if those parents differ in ancestry. Existing approaches falter when it comes to this task," said UCLA's John Novembre, an assistant professor in the department of ecology and evolution.

SPA is also able to model genetic variation on a globe.

Read more from the original source:
New genetic method pinpoints geographic origin

Recommendation and review posted by Bethany Smith

BOSTON The great promise of the Human Genome Project is that if we can crack the genetic code in each of our cells, we may be able to predict what diseases we might get and prevent them. But more than a decade into this project, no medical miracles have been produced. Now, a new study by the Harvard School of Public Health has more disappointing news. WBURs All Things Considered host Sacha Pfeiffer spoke with the studys senior author, Peter Kraft, an associate professor of epidemiology at Harvard.

Sacha Pfeiffer: Your study looked at one of the possible key reasons for why simply mapping the human genome as huge a scientific accomplishment as that is might not alone be enough to start curing or preventing diseases. What else have researchers thought might be necessary to do that?

Peter Kraft: Weve actually been fabulously successful, in the last five years especially, in finding genetic variants that are associated with disease risk. But when people looked and asked the question, Do these actually help us predict whos going to be at high risk? the answer was mostly no. And one of reasons that might have been is that people looked at these variants in isolation, one at a time. But if you considered how they work together, and how they work together with the environment, to influence cancer risk or disease risk generally, people thought that might help boost the predictive ability.

So in terms of how genes work with other genes, or how genes react if you smoke, or if youre overweight, or if youve taken hormones that kind of thing?

Right, exactly. So the models up till now have assumed that a gene is a gene and its effect is the same whether you smoke or not. But, of course, that may not be the case and in fact probably isnt the case.

And so in your study you took those factors into account environmental and lifestyle factors. What did you find?

We sort of played a thought experiment and said, What if we knew how actually these things worked together? And given that information we tried to predict who was at high risk and who was at low risk. And we found that even knowing that information, which were a long way from knowing and understanding but even if we knew it, the change in the risk estimates would not be all that great. Its giving us a 1 to 3 percent increase of our ability to detect people who are at high risk.

Is that not a very useful increase?

Well, it depends on the context, but not necessarily. It seems to be in the range where your decision as a patient and your clinicians recommendations wouldnt really change that much. So given what they knew before they drew your blood and looked at your genetics, their recommendation would probably be the same.

So your study tells us that if we get our genes mapped, we might learn a little bit more if were at risk of a disease, but not very much to help our doctors. So where does that leave us in terms of our hopes for the Humane Genome Project and this idea that we could create personalized medicine customized for every individual?

Follow this link:
Study: Knowing Genetic Makeup May Not Help Predict Disease Risk

Recommendation and review posted by Bethany Smith

May 23, 2012

Isabel Teotonio

In a landmark study examining the smoking behaviour of more than 32,300 African Americans, researchers have identified a genetic marker linked to how much a person smokes.

The findings of the study, which were published Tuesday in Translational Psychiatry, may prove useful in helping develop treatments to help smokers butt out.

This kind of research has been done in the past on white populations, but studying those who are non-European is important given their greater genetic diversity.

If we want to think about a future where we can use biological markers and psychosocial history to really tailor treatments, we need to understand the genetic architecture of smoking in multiple populations, said clinical associate professor of medicine at Stanford University Sean David, the studys lead author.

We havent found the cure to smoking with this study, said David, referring to the Study of Tobacco in Minority Populations Genetics Consortium, called STOMP. But we have found an informative genetic marker of smoking quantity that we think could inform future research to help move the field forward.

Researchers combined the findings of 13 previous studies, which provided a sample size of 32,389 men and women of African ancestry. This enabled them to better see links that may have been too subtle to spot in smaller studies. Genome-wide association studies are used to identify common genetic factors that influence health and disease.

The STOMP study, which included 78 researchers from 50 academic institutions across the United States, is the first meta-analysis of genome-wide association studies for smoking behaviours in African Americans. (Meta-analysis is a statistical technique for combining the results of independent studies.)

Investigators gathered a variety of data, including when people smoked their first cigarette, when they began smoking regularly and if they were heavy, or light, smokers.

Continue reading here:
Genetic marker predicts smoking behaviour in African Americans

Recommendation and review posted by Bethany Smith

(CNN) -

Getting personalized genetic tests that can pinpoint your risk of developing a number of diseases like cancer, diabetes, Alzheimer's or heart disease are not yet "ready for prime time" according to a new recommendation Tuesday from the American College of Obstetricians and Gynecologists. ACOG says while these tests could be important tools down the road, right now, they should only be used in a clinical trial setting, where experts can put the information into a proper context.

The College published their opinion "Personalized Genomic Testing for Disease Risk" in the June issue of Obstetrics & Gynecology. The advocacy group says the lack of rigorous scientific evidence that the tests are valuable and improve clinical care was the basis for the opinion.

Experts are concerned that a genetic test could tell a patient they have no markers for colon cancer, which could lead someone to get the false impression that they won't get the disease and possibly forego colon screening. On the flip side, genetic testing may reveal that a woman has a 1% risk of getting breast cancer, which could get her very freaked out about getting breast cancer, even though her risk may still be minimal compared to other women without the genetic marker.

"All results require careful interpretation since the result will be affected by other factors such as medical or family history. There is also the potential hazard of a misinterpreted or inaccurate test result, " says Dr. Nancy Rose, Chairman of ACOG's Committee on Genetics.

Dr. Melissa Fries, Director of Genetics and Fetal Medicine at MedStar Washington Hospital Center in Washington, DC supports the new directive. "Genetic testing in general has great power if done for specific indications. We do not know yet the value of tests that may measure minor increases or decrease in the development of disease."

Since the human genome was mapped in 2001 the promise of personalized medicine and genetic testing has been one of medicine's holy grails. Hundreds of genetic variations have been linked to diseases like cancer, but few have been the focus of research that has translated into treatments for patients. As for when these kinds of test will be "ready for prime time?" Rose says the timeframe is currently unknown.

In 2008, ACOG announced their position discouraging people from getting the DNA tested by using home genetic tests you can buy on the internet because they were concerned about " the potential harm of misinterpreted or inaccurate results."

However ACOG does support patients get genetic testing for certain diseases like the BRCA 1 & 2 mutation that increases the risk of breast cancer, Cystic Fibrosis, Fragile X syndrome, the most common form of learning disability and cognitive impairment (occurring predominately in boys), and Tay-Sachs disease, a fatal genetic disorder.

Read more from the original source:
Personalized genetic testing not ready

Recommendation and review posted by Bethany Smith

Public release date: 23-May-2012 [ | E-mail | Share ]

Contact: Wileen Wong Kromhout wwkromhout@support.ucla.edu 310-206-0540 University of California - Los Angeles

Understanding the genetic diversity within and between populations has important implications for studies of human disease and evolution. This includes identifying associations between genetic variants and disease, detecting genomic regions that have undergone positive selection and highlighting interesting aspects of human population history.

Now, a team of researchers from the UCLA Henry Samueli School of Engineering and Applied Science, UCLA's Department of Ecology and Evolutionary Biology and Israel's Tel Aviv University has developed an innovative approach to the study of genetic diversity called spatial ancestry analysis (SPA), which allows for the modeling of genetic variation in two- or three-dimensional space.

Their study is published online this week in the journal Nature Genetics.

With SPA, researchers can model the spatial distribution of each genetic variant by assigning a genetic variant's frequency as a continuous function in geographic space. By doing this, they show that the explicit modeling of the genetic variant frequency the proportion of individuals who carry a specific variant allows individuals to be localized on a world map on the basis of their genetic information alone.

"If we know from where each individual in our study originated, what we observe is that some variation is more common in one part of the world and less common in another part of the world," said Eleazar Eskin, an associate professor of computer science at UCLA Engineering. "How common these variants are in a specific location changes gradually as the location changes.

"In this study, we think of the frequency of variation as being defined by a specific location. This gives us a different way to think about populations, which are usually thought of as being discrete. Instead, we think about the variant frequencies changing in different locations. If you think about a person's ancestry, it is no longer about being from a specific population but instead, each person's ancestry is defined by the location they're from. Now ancestry is a continuum."

The team reports the development of a simple probabilistic model for the spatial structure of genetic variation, with which they model how the frequency of each genetic variant changes as a function of the location of the individual in geographic space (where the gene frequency is actually a function of the x and y coordinates of an individual on a map).

"If the location of an individual is unknown, our model can actually infer geographic origins for each individual using only their genetic data with surprising accuracy," said Wen-Yun Yang, a UCLA computer science graduate student.

See original here:
Researchers develop new genetic method to pinpoint individuals' geographic origin

Recommendation and review posted by Bethany Smith

CAMBRIDGE, Mass.--(BUSINESSWIRE)--

- Global studies showed significant and sustained improvements in lung function and other measures of disease among people with a specific genetic mutation -

Vertex Pharmaceuticals Incorporated (Nasdaq: VRTX) announced today that the European Committee for Medicinal Products for Human Use (CHMP) has issued a positive opinion by consensus recommending the approval of KALYDECO (ivacaftor) for people with cystic fibrosis (CF) ages 6 and older who have at least one copy of the G551D mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. KALYDECO is the first medicine to treat the underlying cause of CF, a rare, genetic disease caused by defective or missing CFTR proteins resulting from mutations in the CFTR gene. In people with the G551D mutation, KALYDECO helps the defective CFTR protein function more normally. An estimated 1,100 people in Europe have this mutation.

The CHMP opinion was based on positive findings from two global Phase 3 studies in which KALYDECO demonstrated unprecedented improvements in breathing and other measures of disease for people ages 6 and older with this specific genetic mutation. People treated with KALYDECO experienced significant and sustained improvements in lung function, weight gain and certain quality of life measurements compared to those on placebo. In addition, people who took KALYDECO were 55 percent less likely to have pulmonary exacerbations, or periods of worsening in the signs and symptoms of the disease that often require treatment with antibiotics and hospital visits, than those who received placebo. Fewer people in the KALYDECO treatment groups discontinued treatment due to adverse events than in the placebo groups. The majority of adverse events associated with KALYDECO were mild to moderate. Adverse events most commonly observed in those taking KALYDECO included headache, upper respiratory tract infection (common cold), stomach pain and diarrhea.

While there has been great progress in cystic fibrosis treatment during the last few decades, we are still only treating the symptoms and complications of the disease, said Stuart Elborn, M.D., KALYDECO investigator and President of the European Cystic Fibrosis Society. KALYDECO is a fundamentally different approach to the way we treat cystic fibrosis because it targets the underlying cause of the disease. In clinical trials, KALYDECO helped people with a specific genetic mutation breathe more easily, gain weight and generally feel better.

The CHMPs positive opinion will now be reviewed by the European Commission, which has the authority to approve medicines for the European Union. The European Commission generally follows the recommendation of the CHMP and typically issues marketing approval within three to four months.

Since 1998, Vertex has been committed to developing new medicines to treat the underlying cause of cystic fibrosis, said Peter Mueller, Ph.D., Chief Scientific Officer and Executive Vice President of Global Research and Development at Vertex. KALYDECO represents an important achievement in this ongoing effort. We look forward to working with the European Medicines Agency to bring KALYDECO, our first new medicine in Europe, to people with CF as quickly as possible.

KALYDECO was discovered as part of a collaboration with Cystic Fibrosis Foundation Therapeutics, Inc., the nonprofit drug discovery and development affiliate of the Cystic Fibrosis Foundation.

About Cystic Fibrosis

Cystic fibrosis is a rare, life-threatening genetic disease affecting approximately 35,000 people in Europe and 70,000 people worldwide. Today, the median predicted age of survival for a person with CF is approximately 38 years but the median age of death remains in the mid-20s. There are more than 1,800 known mutations in the CFTR gene. Some of these mutations, which can be determined by a genetic, or genotyping test, lead to CF by creating non-working or too few CFTR proteins at the cell surface. The absence of working CFTR proteins results in poor flow of salt and water into and out of the cell in a number of organs, including the lungs. This leads to the buildup of abnormally thick, sticky mucus that can cause chronic lung infections and progressive lung damage.

Read the original here:
Vertex Receives European CHMP Positive Opinion for KALYDECO™ (ivacaftor), the First Medicine to Treat the Underlying ...

Recommendation and review posted by Bethany Smith

ASTANA, Kazakhstan, May 24, 2012 /PRNewswire/ --Sir Richard Roberts, the eminent British biologist and Nobel Prize laureate, said today European opposition to genetically modified organisms is political rather than scientific in nature.

He also said "personal medicine" based on human genome research holds large-scale promise to improve the health of the world's people on an individualized basis.

Roberts, who won the Nobel in 1993 for his shared discovery of split genes, made his remarks at the Astana Economic Forum, a global conference of scientists, academics, multinational executives and government leaders.

"On a political level, governments must embrace genetically modified organisms (GMOs) and not give way to European prophets of doom, who oppose the use of GMOs for purely political reasons," said Roberts. "It is important to note there is a complete absence of evidence that GMOs can cause any harm. Indeed to any well-informed scientist, traditionally bred plants seem much more likely to be harmful than GMOs."

Roberts predicted growing knowledge of the human genome will yield better medical treatments and diagnostics. "It is just as important that we learn more about the bacteria that colonize our bodies since they are an essential part of what it means to be human," he said.

He also predicated synthetic biology will enable scientists to build novel microorganisms from "scratch."

"Most exciting is the promise of stem cells where the challenge is to understand how they drive their differentiation into all of the other cell types in our bodies," Roberts said. "While I do not advocate prolonging life indefinitely, I am very much in favor of ensuring that as we age, the quality of our life does not diminish."

The annual Astana Economic Forum this year has drawn thousands of participants from more than 80 nations to this rapidly growing Central Asian nation. There has been much focus at the current sessions on the Greek financial crisis and turbulence in the Euro currency, in addition to the broader economic, scientific and international trade issues that are a traditional mainstay at Astana.

Deal making is a big part of both the official and the unofficial agenda at Astana. Multinationals represented include Chevron, Toyota, Nestle, Microsoft, BASF, Total, General Electric.

Go here to see the original:
Nobelist Speaks Out on Genetic Modification, Synthetic Biology, Stem Cell Research

Recommendation and review posted by Bethany Smith

Public release date: 24-May-2012 [ | E-mail | Share ]

Contact: Marge Dwyer mhdwyer@hsph.harvard.edu 617-432-8416 Harvard School of Public Health

Boston, MA Harvard School of Public Health (HSPH) researchers have found that detailed knowledge about your genetic makeupthe interplay between genetic variants and other genetic variants, or between genetic variants and environmental risk factorsmay only change your estimated disease prediction risk for three common diseases by a few percentage points, which is typically not enough to make a difference in prevention or treatment plans. It is the first study to revisit claims in previous research that including such information in risk models would eventually help doctors either prevent or treat diseases.

"While identifying a synergistic effect between even a single genetic variant and another risk factor is known to be extremely challenging and requires studies with a very large number of individuals, the benefit of such discovery for risk prediction purpose might be very limited," said lead author Hugues Aschard, research fellow in the Department of Epidemiology.

The study appears online May 24, 2012 and will appear in the June 8, 2012 print issue of The American Journal of Human Genetics.

Scientists have long hoped that using genetic information gleaned from the Human Genome Project and other genetic research could improve disease risk prediction enough to help aid in prevention and treatment. Others have been skeptical that such "personalized medicine" will be of clinical benefit. Still others have argued that there will be benefits in the future, but that current risk prediction algorithms underperform because they don't allow for potential synergistic effectsthe interplay of multiple genetic risk markers and environmental factorsinstead focusing only on individual genetic markers.

Aschard and his co-authors, including senior author Peter Kraft, HSPH associate professor of epidemiology, examined whether disease risk prediction would improve for breast cancer, type 2 diabetes, and rheumatoid arthritis if they included the effect of synergy in their statistical models. But they found no significant effect by doing so. "Statistical models of synergy among genetic markers are not 'game changers' in terms of risk prediction in the general population," said Aschard.

The researchers conducted a simulation study by generating a broad range of possible statistical interactions among common environmental exposures and common genetic risk markers related to each of the three diseases. Then they estimated whether such interactions would significantly boost disease prediction risk when compared with models that didn't include these interactions since, to date, using individual genetic markers in such predictions has provided only modest improvements.

For breast cancer, the researchers considered 15 common genetic variations associated with disease risk and environmental factors such as age of first menstruation, age at first birth, and number of close relatives who developed breast cancer. For type 2 diabetes, they looked at 31 genetic variations along with factors such as obesity, smoking status, physical activity, and family history of the disease. For rheumatoid arthritis, they also included 31 genetic variations, as well as two environmental factors: smoking and breastfeeding.

But, for each of these disease models, researchers calculated that the increase in risk prediction sensitivitywhen considering the potential interplay between various genetic and environmental factorswould only be between 1% and 3% at best.

Continue reading here:
Knowing genetic makeup may not significantly improve disease risk prediction

Recommendation and review posted by Bethany Smith

ANN ARBOR, Mich.--(BUSINESS WIRE)--

RetroSense Therapeutics, a gene therapy company dedicated to vision restoration, announced completion of a pre-IND meeting with the Center for Biological Evaluation and Research (CBER) division of the FDA that took place on May 22nd 2012 regarding RetroSenses lead biologic, RST-001 for vision restoration in retinal degenerative conditions.

The purpose of the meeting was to obtain CBERs guidance for the clinical path to a Biologics License Application (BLA) for RST-001 in the US, and clarity on the steps required for Investigational New Drug (IND) submission. The discussions included manufacturing criteria, the scope and design of the preclinical studies, and the scope and design of Phase I and IIa clinical trials.

Sean Ainsworth, CEO, noted,"We were quite encouraged by the FDA's feedback and comments and identified nothing that will hinder our path to the clinic. RetroSense remains on schedule to bring RST-001 to the clinic safely and expeditiously.

Peter Francis, MD, PhD, Clinical Director, led the meeting. Dr. Francis stated, It was a successful, productive interaction with the FDA. We were thankful to have representation by Foundation Fighting Blindness, who have been supportive of our novel approach to vision restoration.

We are very excited about the potential for this innovative treatment to restore vision in people who are blind from retinal degenerations, says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. It is an elegant and powerful approach to overcoming devastating eye diseases.

About RetroSense Therapeutics

RetroSense Therapeutics is a biotechnology company developing a game-changing gene therapy to restore vision in patients suffering from blindness due to retinitis pigmentosa (RP) and advanced dry age-related macular degeneration (advanced dry-AMD). There are currently no FDA approved therapies to improve or restore vision in patients with these retinal degenerative conditions. RetroSense is led by a team of seasoned veterans with deep experience in taking products from the discovery stage through to the clinic. For more information about RetroSense, visit http://www.retro-sense.com/.

About Foundation Fighting Blindness

The Foundation Fighting Blindness is a national non-profit organization driving research that will lead to preventions, treatments and cures for retinitis pigmentosa, macular degeneration, Usher syndrome and the entire spectrum of retinal degenerative diseases that affect more than 10 million Americans. Since 1971, the Foundation has raised over $450 million as the leading non-governmental funder of retinal research. Breakthrough Foundation-funded studies using gene therapy have restored significant vision in children and young adults who were previously blind, paving the way for using this method to treat a variety of retinal degenerative diseases, and proving a cure is in sight. With a network of 50 chapters, the Foundation also provides support, education and resources to affected individuals and their families in communities across the country.

Go here to read the rest:
RetroSense Therapeutics Completes pre-IND Meeting for RST-001

Recommendation and review posted by Bethany Smith

Public release date: 24-May-2012 [ | E-mail | Share ]

Contact: Sarah Jackson press_releases@the-jci.org Journal of Clinical Investigation

Severe combined immunodeficiency is defect in the immune system that results in a loss of the adaptive immune cells known as B cells and T cells. Mutations in several different genes can lead to the development of severe combined immunodeficiency, including mutation of the adenosine deaminase (ADA) gene. Traditional treatment options, such as enzyme replacement therapy, are of limited efficacy, but bone marrow transplant from a compatible donor leads to a better response. A recent clinical trial indicated that gene therapy to insert the correct ADA gene in the patient's own bone marrow cells can also lead to a good response.

However, patients were noted to have defects in B cell tolerance, meaning that some B cells that react to antigens from the body fail to be eliminated, leading to an autoimmune response. Dr. Eric Meffre and colleages at Yale University in New Haven, Connecticut and Alessandro Aiuti in Milan, Italy joined together to better understand why patients developed B cell tolerance problems. They found that loss of the ADA gene directly contributes to B cell tolerance problems and that these defects are mostly corrected after gene therapy. Their results point to a previously unknown role for ADA in B cell response and support the use of gene therapy as an effective treatment option for ADA-deficient severe combined immunodeficiency patients.

###

TITLE:

Defective B cell tolerance in adenosine deaminase deficiency is corrected by gene therapy

AUTHOR CONTACT:

Eric Meffre Yale University School of Medicine, New Haven, CT, USA Phone: 1-203-737-4535; Fax: 1-203-785-7903; E-mail: eric.meffre@yale.edu

ACCOMPANYING COMMENTARY

Link:
Gene therapy can correct forms of severe combined immunodeficiency

Recommendation and review posted by Bethany Smith

Scientists on Wednesday reported that they have for the first time taken skin cells from heart attacks patients and turned them into healthy heart tissue that could hopefully be used to one day repair damaged heart muscle.

The healthy, beating heart tissue was grown successfully in the lab from human-induced pluripotent stem cells (hiPSCs), and while scientists said they were not safe enough to put back into human patients, they appeared to work well with other cells when implanted into rats. HiPSCs are a recently discovered source far less controversial than use of embryonic stem cells. And, because the transplanted hiPSCs come from the individual, it could resolve the problems seen with tissue and organ rejection.

While the technique has shown promise in rats, the scientists say there are numerous obstacles to overcome and it could take up to ten years or longer before clinical trials could be available for humans. Even so, it is a significant advance in the quest for replacement cell therapy for heart failure patients.

More people are surviving following a heart attack than ever before and therefore the number of people living with a damaged heart and heart failure is increasing, Nicholas Mills, a consultant cardiologist at Edinburgh University, told The Guardian. Unfortunately, the body has only very limited capacity to repair the heart following a heart attack. There is therefore an urgent need to develop effective and safe treatments to regenerate the heart.

Recent research has shown that hiPSCs could be derived from young and healthy people and are capable of transforming into heart cells. However, researchers have not been able to obtain those cells from elderly and diseased patients. And until now, researchers have not been able to show that heart cells created from hiPSCs could integrate with existing heart tissue.

What is new and exciting about our research is that we have shown that its possible to take skin cells from an elderly patient with advanced heart failure and end up with his own beating cells in a laboratory dish that are healthy and young the equivalent to the stage of his heart cells when he was just born, said lead researcher Professor Lior Gepstein, of Sohnis Research Laboratory for Cardiac Electrophysiology and Regenerative Medicine, Technion-Israel Institute of Technology and Rambam Medical Center in Haifa, Israel.

For their study, published in the European Heart Journal, Limor Zwi-Dantsis, a PhD student in the Sohnis Research Laboratory, Gepstein and colleagues took skin cells from two male heart failure patients (ages 51 and 61) and reprogrammed them with three genes (Sox2, Klf4 and Oct4), followed by a small molecule (valproic acid) to the cell nucleus.

The team also used an alternative strategy that involved a virus that delivered reprogramming information to the cell nucleus but which was capable of being removed afterward to avoid insertional oncogenesis.

Using these methods, the hiPSCs were able to differentiate to become cardiomyocytes (heart muscle cells) just as effectively as hiPSCs that had been developed from healthy, young volunteers. The researchers were then able to make cardiomyocytes develop into heart muscle tissue, which they cultured together with pre-existing cardiac tissue. The tissues were beating together within 48 hours, said the researchers.

The researchers transplanted the new tissue into the hearts of healthy rats and found that the grafted tissue started to establish connections with the cells in the host tissue.

View original post here:
Human Skin Cells Turned Into Healthy Heart Muscle

Recommendation and review posted by sam

On a special surface that could help advance stem cell therapies, UM researchers have turned human skin cells into adult-derived stem cells, coaxed them into bone cells and then transplanted them into holes in the skulls of mice. The cells produced four times as much new bone growth as in the mice without the extra bone cells. In this pink-stained image, the black outline partially encloses the new bone growth in the skull. Image credit: Villa-Diaz, L.G., Brown, S.E., Liu, Y. Ross, A.M., Lahann, J.M., Krebsbach, P.H., University of Michigan

ANN ARBOR University of Michigan researchers have proven that a special surface, free of biological contaminants, allows adult-derived stem cells to thrive and transform into multiple cell types. Their success brings stem cell therapies another step closer.

To prove the cells regenerative powers, bone cells grown on this surface were then transplanted into holes in the skulls of mice, producing four times as much new bone growth as in the mice without the extra bone cells.

An embryos cells really can be anything they want to be when they grow up: organs, nerves, skin, bone, any type of human cell. Adult-derived induced stem cells can do this and better. Because the source cells can come from the patient, they are perfectly compatible for medical treatments.

In order to make them, Paul Krebsbach, professor of biological and materials sciences at the UM School of Dentistry, said, We turn back the clock, in a way. Were taking a specialized adult cell and genetically reprogramming it, so it behaves like a more primitive cell.

Specifically, they turn human skin cells into stem cells. Less than five years after the discovery of this method, researchers still dont know precisely how it works, but the process involves adding proteins that can turn genes on and off to the adult cells.

Before stem cells can be used to make repairs in the body, they must be grown and directed into becoming the desired cell type. Researchers typically use surfaces of animal cells and proteins for stem cell habitats, but these gels are expensive to make, and batches vary depending on the individual animal.

You dont really know whats in there, said Joerg Lahann associate professor of chemical engineering and biomedical engineering.

For example, he said that human cells are often grown over mouse cells, but they can go a little native, beginning to produce some mouse proteins that may invite an attack by a patients immune system.

The polymer gel created by Lahann and his colleagues in 2010 avoids these problems because researchers are able to control all of the gels ingredients and how they combine.

Excerpt from:
UM: Stem-Cell-Growing Surface Enables Bone Repair

Recommendation and review posted by sam

A growth factor isolated from human stem cells shows promising results in a mouse model of multiple sclerosis.

Human mesenchymal stem cells (hMSCs) have become a popular potential therapy for numerous autoimmune and neurological disorders. But while these bone marrow-derived stem cells have been studied in great detail in the dish, scientists know little about how they modulate the immune system and promote tissue repair in living organisms.

Now, one research team has uncovered a molecular mechanism by which hMSCs promote recovery in a mouse model of multiple sclerosis (MS).

According to research, published online Sunday (May 20) in Nature Neuroscience, a growth factor produced by hMSCs fights MS in two ways: blocking a destructive autoimmune response and repairing neuronal damage. The finding could help advance ongoing clinical trials testing hMSCs as a therapy for MS.

The researchers have identified a unique factor that has surprisingly potent activity mediating neuron repair, said Jacques Galipeau, a cell therapy researcher at Emory University in Atlanta, Georgia, who was not involved in the research. The magnitude of the effect on a mouse model of MS is a big deal.

MS is an autoimmune disease in which the immune system attacks myelin sheaths that surround and protect nerve cells. The attack leaves nerves exposed and unable to send signals to the brain and back, resulting in the loss of motor skills, coordination, vision, and cognitive abilities. There is no cure for MS, and most current therapies work to simply suppress the immune system, preventing further neuronal damage. None have demonstrated an ability to also repair damaged myelin and promote recovery.

In 2009, Robert Miller and colleagues at Case Western Reserve University in Cleveland, Ohio, demonstrated that hMSCs dramatically reversed the symptoms of multiple sclerosis in a mouse model of the disorder. The animals got better, recalled Miller. The team hypothesized that the stem cells suppress the immune response and promote remyelination.

But Miller wanted to know exactly what the cells were doing. To find out, his team isolated the medium on which the hMSCs were grown to determine if the cells or something they secreted was responsible for the observed recovery. The medium alone was enough to induce recovery in mice, pointing to the latter.

To find out exactly which molecule or molecules in the medium were responsible, the researchers separated the proteins in the fluid based on the molecular weight and injected each isolate into mice exhibiting symptoms of MS. The mid-weight solution, of proteins with masses between 50 and 100 kilodaltons (kDa), caused recovery. That eliminated a huge number of potential candidates, said Miller.

The researchers then narrowed the field again with a literature search for a molecule that fit their criteria: secreted by hMSCs, 50-100 kDa in size, and involved in tissue repair. They identified hepatocyte growth factor (HGF), a cytokine made by mesenchymal cells that has been shown to promote tissue regeneration and cell survival in numerous experiments. Sure enough, HGF alone was enough to promote recovery in the MS mouse models, and blocking the receptor for HGF in those mice blocked recovery. The team also demonstrated that HGF suppresses immune responses in vivo and accelerates remyelination of neurons in vitro. Finally, they saw that HGF causes remyelination in rats with a lesion on their spinal cord.

Go here to read the rest:
Could Stem Cells Cure MS?

Recommendation and review posted by sam

Editor's Choice Main Category: Multiple Sclerosis Article Date: 24 May 2012 - 14:00 PDT

Current ratings for: 'Recovery From Multiple Sclerosis By Growth Factor In Stem Cells'

5 (2 votes)

4.5 (2 votes)

Animals that were injected with hepatocyte growth factor were noted to have grown new neural cells and lower levels of inflammation. Most significantly, the researchers noted that the protective envelope of myelin, the myelin sheath, which surrounds the core of a nerve fiber and facilitates the transmission of nerve impulses, re-grew and covered lesions that were caused by MS.

Robert H. Miller, professor of neurosciences at the School of Medicine and vice president for research at Case Western Reserve University declared: "The importance of this work is we think we've identified the driver of the recovery."

MS is caused by damage to the myelin sheath, the protective covering that surrounds nerve cells. The nerve damage is caused by inflammation, which occurs when the body's own immune cells attacks the nervous systems located in areas of the brain, the optic nerve, and spinal cord. This damage can cause an interruption of the nerve signals, which results in loss of balance and coordination, cognitive ability, as well as in other functions and in time, these intermittent losses may become permanent. In 2009, Caplan and Miller discovered that mice with MS injected with human mesenchymal stem cells recovered from the type of damage that was brought on by MS. A clinical trial is currently underway based on their research, whereby patients with MS are injected with their own stems cells.

During this trial, the team decided to first establish whether the presence of stem cells or other cells induce recovery. They injected a total of 11 animals with MS with the medium, in which mesenchymal stem cells that were taken from bone marrow grew, discovering that all animals displayed a rapid reduction in functional deficits. An analysis demonstrated that unless the injected molecules had a certain size or weight, i.e. between 50 and 100 kiloDaltons, the course of the disease remained unchanged.

Other research, as well as the team's own studies, suggested that this was likely to be instigated by the hepatocyte growth factor, which is secreted by mesenchymal stem cells.

The team then injected the animals with either 50 or 100 nanograms of the growth factor on alternate days for a 5-day period and observed a decrease in the level of signaling molecules that promote inflammation, whilst the level of signaling molecules that oppose inflammation increased. The researchers noted a growth of neural cells, whilst nerves that were exposed because of MS were rewrapped with myelin. Recovery was marginally better in those mice that received the 100-nanogram injections compared with those receiving the 50-nanogram injections.

See more here:
Recovery From Multiple Sclerosis By Growth Factor In Stem Cells

Recommendation and review posted by sam