ABC Dr Julia Ellyard said the research will allow scientists to individually tailor treatment.

Scientists from the Australian National University (ANU) have been able to identify the genetic cause of lupus in a specific individual for the first time.

Lead researcher from the ANU, Dr Julia Ellyard, said scientists have used personalised medicine to identify the cause of the autoimmune disease in a 10-year-old girl.

Lupus causes various tissues in the body to become inflamed, swollen and painful.

The disease can affect the skin and joints of a patient, but can also target major organs.

While it has been previously known that there are genetic causes for the disease, it is not known what triggers lupus.

It might be triggered by injury, illness or a period of stress.

"Using DNA sequencing, the approach we've taken, we've been able to identify the specific cause of this child's disease," Dr Ellyard said.

"(It is an) increased amount of a particular molecule, called interferon-alpha, being produced."

Dr Ellyard said while any treatment would target the girl's specific condition, it could lead to new ways of treating other people with lupus.

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Lupus: Australian scientists identify genetic cause of disease in 10yo girl

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Hyderabad, Aug 18:

Cancer Genetics Inc. (Nasdaq; CGIX), a DNA-based cancer diagnostics company, today closed the acquisition of BioServe Biotechnologies (India) Pvt Ltd, a genomics services provider serving research and clinical markets in India.

BioServe India, which operates out of a 14,000 sq. ft. genomics facility in Hyderabad, has serviced over 200 clients with genomics services, sequencing, genotyping and DNA synthesis.

According to a statement, CGI will benefit from immediate revenue through BioServe Indias long-term contracts with academic and research institutions and its capabilities in genetic research, test development and genomic analysis.

BioServe Indias clients include some of the leaders in the Indian life sciences industry, including Dr. Reddys Laboratories, Natco Pharmaceuticals, Piramal Life Sciences, the Indian Institute of Science Education and Research and the Centre for Cellular and Molecular Biology.

We are excited to be joining Cancer Genetics, said Venkatadri Bobba, general partner of Ventureast, and a board member at BioServe India.

Cancer diagnostics

Cancer Genetics CEO, Panna Sharma, said the acquisition places the company in a unique position to meet the growing need for genomic-based cancer diagnostics in this market.

He anticipates wide adoption of CGIs proprietary tests for non-Hodgkins lymphomas and leukemia, kidney cancer and cervical cancer.

The expansion into India will also allow Cancer Genetics to leverage its resources and scale its operations, while strengthening its capabilities in molecular testing, DNA synthesis, biomarker analysis and generation sequencing, Sharma said.

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Cancer Genetics completes acquisition of BioServe India

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(Rick Egan | The Salt Lake Tribune) Donald A. McClain, endocrinologist and a professor of internal medicine, Josef Prchal, a professor of internal medicine at the U. School of Medicine, and Tsewang Tashi, a Tibetan who is a hematologist and researcher at the Huntsman Cancer Institute, in Prchal's lab at the University of Utah Medical Center, Friday, August 15, 2014. University of Utah scientists are the lead researchers on a study publishing Sunday in the journal Nature Genetics. The study concludes that Tibetans who thrive in the thin air of the Tibetan Plateau (average elevation 14,800) do so because of a genetic mutation 8,000 years ago.

Genetics A mutation 8,000 years ago made them fit for high areas.

Thriving at high altitude, where most mortals suffer from oxygen deprivation? Theres a gene for that.

A study led by University of Utah researchers has identified for the first time the genetic reason Tibetans can live without medical complications on the Tibetan Plateau, which has an average elevation of 14,800 feet.

The results of the study, led by senior author Josef Prchal, an internist and hematologist at the U., were published online Sunday in the journal Nature Genetics.

By taking blood samples from 26 Tibetans living in Utah and Virginia as well as dozens more from Tibetans and other Asians living in China and India they found the gene EGLN1 changed by a single DNA base pair.

Lowlanders who lack the genetic mutation suffer in thin air because their blood becomes thick with oxygen-carrying red blood cells in an attempt to feed oxygen-starved tissues. That can lead to long-term complications such as acute mountain sickness or heart failure, Prchal said.

But Tibetans bodies do not react to high altitude by producing extra red blood vessels.

The mutation apparently began 8,000 years ago and "spread like fire" through the population, he said. Those who had it thrived and, by natural selection, their offspring did, too.

Today, 88 percent of Tibetans have the genetic variation, but it is virtually absent in closely related lowland Asians, the study found.

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Salk Institute for Biological Studies

Salk researchers discover a master gene responsible for sleep and wake cycles, offering hope for a drug that could help reset sleep

Scientists at the Salk Institute for Biological Studies have identified a gene that regulates sleep and wake rhythms.

The discovery of the role of this gene, called Lhx1, provides scientists with a potential therapeutic target to help night-shift workers or jet lagged travelers adjust to time differences more quickly. The results, published in eLife, can point to treatment strategies for sleep problems caused by a variety of disorders.

Its possible that the severity of many dementias comes from sleep disturbances, says Satchidananda Panda, a Salk associate professor who led the research team. If we can restore normal sleep, we can address half of the problem.

Every cell in the body has a clock an abundance of proteins that dip or rise rhythmically over approximately 24 hours. The master clock responsible for establishing these cyclic circadian rhythms and keeping all the bodys cells in sync is the suprachiasmatic nucleus (SCN), a small, densely packed region of about 20,000 neurons housed in the brains hypothalamus.

More so than in other areas of the brain, the SCNs neurons are in close and constant communication with one another. This close interaction, combined with exposure to light and darkness through vision circuits, keeps this master clock in sync and allows people to stay on essentially the same schedule every day. The tight coupling of these cells also helps make them collectively resistant to change. Exposure to light resets less than half of the SCN cells, resulting in long periods of jet lag.

In the new study, researchers disrupted the light-dark cycles in mice and compared changes in the expression of thousands of genes in the SCN with other mouse tissues. They identified 213 gene expression changes that were unique to the SCN and narrowed in on 13 of these that coded for molecules that turn on and off other genes. Of those, only one was suppressed in response to light: Lhx1.

No one had ever imagined that Lhx1 might be so intricately involved in SCN function, says Shubhroz Gill, a postdoctoral researcher and co-first author of the paper. Lhx1 is known for its role in neural development: its so important, that mice without the gene do not survive. But this is the first time it has been identified as a master regulator of light-dark cycle genes.

By recording electrical activity in the SCN of animals with reduced amounts of the Lhx1 protein, the researchers saw that the SCN neurons werent in sync with one another, despite appearing rhythmic individually.

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Single Gene Provides A Potential Therapeutic Target To Help Night-Shift Workers Or Jet Lagged Travelers

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August 17, 2014

Herb Booth, University of Texas, Arlington

A computer science and engineering associate professor and her doctoral student graduate are using a genetic computer network inference model that eventually could predict whether a person will suffer from bipolar disorder, schizophrenia or another mental illness.

The findings are detailed in the paper Inference of SNP-Gene Regulatory Networks by Integrating Gene Expressions and Genetic Perturbations, which was published in the June edition of Biomed Research International. The principal investigators were Jean Gao, an associate professor of computer science and engineering, and Dong-Chul Kim, who recently earned his doctorate in computer science and engineering from UT Arlington.

We looked for the differences between our genetic computer network and the brain patterns of 130 patients from the University of Illinois, Gao said. This work could lead to earlier diagnosis in the future and treatment for those patients suffering from bipolar disorder or schizophrenia. Early diagnosis allows doctors to provide timely treatments that may speed up aid to help affected patients.

The UT Arlington researchers teamed with Jiao Wang of the Beijing Genomics Institute at Wuhan, China; and Chunyu Liu, visiting associate professor at the University of Illinois Department of Psychiatry, on the project.

Gao said the findings also could lead to more individualized drug therapies for those patients in the early stages of mental illnesses.

Our work will allow doctors to analyze a patients genetic pattern and apply the appropriate levels of personalized therapy based on patient-specific data, Gao said.

One key to the research is designing single nucleotide polymorphism or SNP networks, researchers said.

SNPs are regulators of genes, said Kim, who joins the University of Texas-Pan American this fall as an assistant professor. Those SNPs visualize how individual genes will act. It gives us more of a complete picture.

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Understanding the genetic coding also opens up the possibility of developing ways of turning microbial genes on or off to generate production of a specific antibiotic.

Pampering leafcutter ants with fragrant rose petals and fresh oranges may seem an unlikely way to rescue modern medicine, but scientists at a lab in eastern England think its well worth trying.

As the world cries out for new antibiotics, researchers at the John Innes Centre (JIC) in Norwich are also taking a bet on bacteria extracted from the stomachs of giant stick insects and cinnabar caterpillars with a taste for highly toxic plants.

Their work is part of a new way of thinking in the search for superbug-killing drugs turning back to nature in the hope that places as extreme as insects insides, the depths of the oceans, or the driest of deserts may throw up chemical novelties and lead to new drugs.

Natural products fell out of favor in the pharmaceutical sphere, but now is the time to look again, says Mervyn Bibb, a professor of molecular microbiology at JIC who collaborates with many other geneticists and chemists. We need to think ecologically, which traditionally people havent been doing.

The quest is urgent. Africa provides a glimpse of what the world looks like when the drugs we rely on to fight disease and prevent infections after operations stop working.

In South Africa, patients with tuberculosis that has developed resistance to all known antibiotics are already simply sent home to die, while West Africas Ebola outbreak shows what can happen when there are no medicines to fight a deadly infection in this case due to a virus rather than bacteria.

Scant financial rewards and lack of progress with conventional drug discovery have prompted many Big Pharma companies to abandon the search for new bacteria-fighting medicines. Yet for academic microbiologists these are exciting times in antibiotic research thanks to a push into extreme environments and advances in genomics.

Its a good time to be researching antibiotics because there are a lot of new avenues to explore, said Christophe Corre, a Royal Society research fellow in the department of chemistry at the University of Warwick.

Extreme locations, smart techniques

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Extreme medicine: The search for new antibiotics

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Newswise (SALT LAKE CITY) In an environment where others struggle to survive, Tibetans thrive in the thin air of the Tibetan Plateau, with an average elevation of 14,800 feet. A study led by University of Utah scientists is the first to find a genetic cause for the adaptation a single DNA base pair change that dates back 8,000 years and demonstrate how it contributes to the Tibetans ability to live in low oxygen conditions. The work appears online in the journal Nature Genetics on Aug. 17, 2014.

These findings help us understand the unique aspects of Tibetan adaptation to high altitudes, and to better understand human evolution, said Josef Prchal, M.D., senior author and University of Utah professor of internal medicine.

The story behind the discovery is equally about cultural diplomacy as it is scientific advancement. Prchal traveled several times to Asia to meet with Chinese officials, and representatives of exiled Tibetans in India, to obtain permissions to recruit subjects for the study. But he quickly learned that without the trust of Tibetans, his efforts were futile. Wary of foreigners, they refused to donate blood for his research.

After returning to the U.S., Prchal couldnt believe his luck upon discovering that a native Tibetan, Tsewang Tashi, M.D., had just joined the Huntsman Cancer Institute at the University of Utah as a clinical fellow. When Prchal asked for his help, Tashi quickly agreed. I realized the implications of his work not only for science as a whole but also for understanding what it means to be Tibetan, said Tashi. In another stroke of luck, Prchal received a long-awaited letter of support from the Dalai Lama. The two factors were instrumental in engaging the Tibetans trust: more than 90, both from the U.S. and abroad, volunteered for the study.

Their hard work was worth it, for the Tibetans DNA had a fascinating tale to tell. About 8,000 years ago, the gene EGLN1 changed by a single DNA base pair. Today, a relatively short time later on the scale of human history, 88% of Tibetans have the genetic variation, and it is virtually absent from closely related lowland Asians. The findings indicate the genetic variation endows its carriers with an advantage.

Prchal, collaborated with experts throughout the world, to determine what that advantage is. In those without the adaptation, low oxygen causes their blood to become thick with oxygen-carrying red blood cells - an attempt to feed starved tissues - which can cause long-term complications such as heart failure. The researchers found that the newly identified genetic variation protects Tibetans by decreasing the over-response to low oxygen.

These discoveries are but one chapter in a much larger story. The genetic adaptation likely causes other changes to the body that have yet to be understood. Plus, it is one of many as of yet unidentified genetic changes that collectively support life at high altitudes.

Prchal says the implications of the research extend beyond human evolution. Because oxygen plays a central role in human physiology and disease, a deep understanding of how high altitude adaptations work may lead to novel treatments for various diseases, including cancer. There is much more that needs to be done, and this is just the beginning, he said.

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Data, data everywhere and now as ever researchers need the best tools to make the data useful. In medicine, searching through genomic data can take some time. A startup called One Codex hopes to make difference with their genetic search platform that can process data sets quickly. A report on their work on Friday in TechCrunch noted the advantage of One Codex speed. "Currently," wrote Julian Chokkattu, "the most commonly used tool for genome searching is by using an algorithm called BLAST, Basic Local Alignment Search Tool, which compares primary biological sequence information." For Nick Greenfield, cofounder of One Codex, uploading a file to BLAST took two minutes and 30 seconds to process, compared with the One Codex system where the number was less than 1/20th of a second. The company defines One Codex as a search engine for genomic data. The TechCrunch piece describes what they offer as a service platform for genomics. Apart from using search technology," said Chokkattu, the platform also acts as an indexed, curated reference.

The company said that it can search the world's largest index of bacterial, viral, and fungal genomes. A key advantage is speed. The product can, said the company, "process next-generation datasets in minutes, not days (millions of DNA base pairs per second)."

The two founders are Nick Greenfield, former data scientist, and Nik Krumm, who has a PhD in genome sciences from the University of Washington.

Sample applications would be in clinical diagnostics, food safety and biosecurity. Right now, said TechCrunch, the company is focusing on testing their platform with hospitals and agencies. One Codex is in open beta.

Scientific interest in being able to search genomic data faster has been in evidence for some years. In 2012, MIT's news office reported on a study in Nature Biotechnology, where MIT and Harvard researchers described an algorithm "that drastically reduces the time it takes to find a particular gene sequence in a database of genomes. Moreover, the more genomes it's searching, the greater the speedup it affords, so its advantages will only compound as more data is generated."

The authors of that paper, titled "Compressive genomics," said, "In the past two decades, genomic sequencing capabilities have increased exponentially, outstripping advances in computing power. Extracting new insights from the data sets currently being generated will require not only faster computers, but also smarter algorithms." They stated that although compression schemes for BLAST and BLAT that they presented yield an increase in computational speed and in scaling, "they are only a first step."

Explore further: Team develops tool to better visualize, analyze human genomic data

More information: One Codex: onecodex.com/

2014 Phys.org

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Six years ago, a 250-year ban on importing cow genetics on to the island of Jersey came to an end. Aly Balsom speaks to two producers with varying views on introducing international genetics to the island breed

Choosing from many cow families across the world is something most breeders take for granted, yet until 2008, dairy producers on the island of Jersey were limited to using bulls produced on the island, which measures nine by five miles.

Ironically for the island that gave birth to the Jersey breed, a ban on imported genetics put in place in 1763 to protect trading, led to many farmers fearing for the future viability of the islands Jersey cow population.

The ban had originally remained in place as farmers found their isolation created a unique selling point that was beneficial for export. However, the development of bull proving schemes around the world meant the Jersey island cow was quickly getting left behind, explains David Hambrook of Jersey Island Genetics.

It was a numbers game. There just wasnt the opportunity for large scale proving schemes on the island, he says.

The island did introduce a bull proving scheme, but it flat-lined in terms of genetic gain after 15 years. Around 2008, there was a group of farmers looking to invest in the next generation and they didnt think there was a viable future without looking at global genetics.

Yield in particular was a significant driver. In 2008, on average, the island Jersey breed was lagging behind the UK Jersey breed by 22% in terms of milk production. Many producers felt the island cow had hit a genetic glass ceiling and was unable to convert feed any more efficiently. Such a trait is particularly important on the island, considering feed has to be imported across The Channel, making feed costs for Jersey farmers one of the highest in the world.

Following several failed attempts over the decades to get the policy overturned, in 2008 the ban on genetic imports came to an end. Most dairy herds immediately took advantage of the new world of genetics available to them. However, two of the islands 24 herds have chosen to continue just using island genetics.

Tom Perchard believes imported genetics have helped secure a future for the family business at La Ferme, St Martin, by driving yield increases and efficiencies.

Having been one of the first farms on the island to import genetics in 2008, the Perchard family has since witnessed a 650 litre a cow a year increase from similar feed inputs.

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Jersey dairy cow six years after genetics ban

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Melbourne researchers have revealed the critical importance of highly specialized immune cells, called natural killer cells, in killing melanoma cells that have spread to the lungs.

These natural killer cells could be harnessed to hunt down and kill cancers that have spread in the body.

The team, from the Walter and Eliza Hall Institute, also found natural killer cells were critical to the body's rejection of donor bone marrow transplants and in the runaway immune response during toxic shock syndrome.

The discoveries came after the team showed that a protein called MCL-1 was crucial for survival of natural killer cells, in research published today in the journal Nature Communications. The discovery will help to determine how natural killer cells can be manipulated to fight cancers and other disorders.

Dr Nick Huntington, Dr Priyanka Sathe and Ms Rebecca Delconte from the Walter and Eliza Hall Institute said MCL-1 could be a target for boosting or depleting natural killer cell populations to treat disease. Natural killer cells are immune predators, scouring the body in search of foreign invaders such as viruses, and sensing changes in our own cells that are associated with cancer.

Dr Huntington said the team showed natural killer cells were needed to fight off invading tumor cells that had spread past the original cancer site.

"We discovered MCL-1 is absolutely essential for keeping natural killer cells alive," Dr Huntington said. "Without natural killer cells, the body was unable to destroy melanoma metastases that had spread throughout the body, and the cancers overwhelmed the lungs."

"Knowing how important natural killer cells are for detecting and destroying cancer cells as they spread suggests they would be a good target for boosting immune defenses to treat cancer."

Natural killer cells are present in high frequency in our blood and patrol the body's 'frontlines' -- the lungs, intestines, mucous membranes and skin -- to detect and destroy diseased cells. However these predatory natural killer cells are a double-edged sword.

Dr Huntington said the team showed natural killer cells also played a role in death from toxic shock (sepsis), and in rejecting bone marrow transplants.

Link:
Immune cell discovery could help to halt cancer spread

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ALAMEDA, Calif.--(BUSINESS WIRE)--BioTime, Inc. (NYSE MKT: BTX) today reported financial results for the first quarter ended June 30, 2014 and highlighted recent corporate accomplishments.

We are pleased with our success to date in building toward our goal of developing both near-term commercial applications of our technologies and maintaining our focus on the power of pluripotent stem cells to create innovative human therapeutics, said Dr. Michael D. West, BioTimes Chief Executive Officer. Near-term product development underway includes our subsidiary OncoCyte Corporations three cancer diagnostic products undergoing clinical studies, mobile health product development in our subsidiary LifeMap Solutions, Inc., our Renevia pivotal clinical trial in Europe, steps to prepare for the marketing of our recently FDA-cleared wound healing product Premvia, and growing research product sales by our ESI BIO division.

BioTimes longer-term major therapeutic product opportunities are based on the broad range of cell-based regenerative therapies planned for development from its pluripotent stem cell technology platform. This platform is protected by over 600 patents and patent applications worldwide within the BioTime family of companies. Our subsidiary Asterias Biotherapeutics, Inc. has submitted an amended IND to the FDA for a Phase 1/2a clinical trial of AST-OPC1 for the treatment of cervical spinal cord injury and is currently awaiting clearance from the FDA for that trial. Asterias is also currently undertaking process development of AST-VAC2, a cancer immunotherapy targeting the important antigen called telomerase, for a potential clinical trial in lung cancer. This progress, along with the appointment of Pedro Lichtinger as Asterias CEO and the award of a $14 million grant from the California Institute for Regenerative Medicine, should fuel the development of these first-in-class therapeutic products. Recently, Asterias shares began to trade publicly under the symbol ASTYV, the first of our subsidiaries to have its shares trade publicly. Lastly, we expect that BioTimes subsidiary Cell Cure Neurosciences Ltd. will soon file its IND to begin a clinical trial of OpRegen for the treatment of age-related macular degeneration. Additional important cell-based product development is underway in our disease-focused subsidiaries OrthoCyte Corporation and ReCyte Therapeutics.

As we saw in the first quarter of this year, our expenses have risen compared to recent quarters, but our progress during the second quarter in streamlining our workforce through shared core resources among our subsidiaries should reduce our cash burn rate in the third quarter. We would like to thank those who share our goal of better health in the coming era of regenerative medicine. Their continued support and the diligent efforts of our collaborators at leading academic medical institutions is critical in advancing our products from the lab bench to the clinic, where they are desperately needed.

Second Quarter and Recent Highlighted Corporate Accomplishments

Financial Results

Revenue

For the six months ended June 30, 2014, on a consolidated basis, total revenue was $2.2 million, up $0.3 million or 19% from $1.8 million for the same period one year ago. The increase in revenue is primarily attributable to a $0.4 million increase in grant income primarily from a grant awarded to BioTimes subsidiary Cell Cure Neurosciences Ltd. (Cell Cure Neurosciences) from Israels Office of the Chief Scientist, offset in part by the decline in license fees of $0.1M primarily due to full recognition of the unamortized balance of the Summit license fees received in advance during the fourth quarter of 2013 as a result of the termination of our license agreements with Summit in 2013.

Expenses

Operating expenses for the six months ended June 30, 2014 were $26.0 million, compared to expenses of $18.0 million for the same period of 2013. The increase in operating expenses is primarily attributable to an increase in staffing, and the expansion of research and development efforts, including additional expenses in the Renevia clinical safety trial program, the development of OpRegen by BioTimes subsidiary Cell Cure Neurosciences for the treatment of dry age related macular degeneration, and the increased staffing and operations of Asterias in connection with the Geron stem cell asset acquisition and by LifeMap Solutions. In addition, during the first six months in 2014, operating expenses included $1.5 million of amortization expense of intangible assets recorded in connection with the Geron stem cell asset acquisition in October 2013.

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Newswise A genetic variation linked to schizophrenia, bipolar disorder and severe depression wreaks havoc on connections among neurons in the developing brain, a team of researchers reports. The study, led by Guo-li Ming, M.D., Ph.D., and Hongjun Song, Ph.D., of the Johns Hopkins University School of Medicine and described online Aug. 17 in the journal Nature, used stem cells generated from people with and without mental illness to observe the effects of a rare and pernicious genetic variation on young brain cells. The results add to evidence that several major mental illnesses have common roots in faulty wiring during early brain development.

This was the next best thing to going back in time to see what happened while a person was in the womb to later cause mental illness, says Ming. We found the most convincing evidence yet that the answer lies in the synapses that connect brain cells to one another.

Previous evidence for the relationship came from autopsies and from studies suggesting that some genetic variants that affect synapses also increase the chance of mental illness. But those studies could not show a direct cause-and-effect relationship, Ming says.

One difficulty in studying the genetics of common mental illnesses is that they are generally caused by environmental factors in combination with multiple gene variants, any one of which usually could not by itself cause disease. A rare exception is the gene known as disrupted in schizophrenia 1 (DISC1), in which some mutations have a strong effect. Two families have been found in which many members with the DISC1 mutations have mental illness.

To find out how a DISC1 variation with a few deleted DNA letters affects the developing brain, the research team collected skin cells from a mother and daughter in one of these families who have neither the variation nor mental illness, as well as the father, who has the variation and severe depression, and another daughter, who carries the variation and has schizophrenia. For comparison, they also collected samples from an unrelated healthy person. Postdoctoral fellow Zhexing Wen, Ph.D., coaxed the skin cells to form five lines of stem cells and to mature into very pure populations of synapse-forming neurons.

After growing the neurons in a dish for six weeks, collaborators at Pennsylvania State University measured their electrical activity and found that neurons with the DISC1 variation had about half the number of synapses as those without the variation. To make sure that the differences were really due to the DISC1 variation and not to other genetic differences, graduate student Ha Nam Nguyen spent two years making targeted genetic changes to three of the stem cell lines.

In one of the cell lines with the variation, he swapped out the DISC1 gene for a healthy version. He also inserted the disease-causing variation into one healthy cell line from a family member, as well as the cell line from the unrelated control. Sure enough, the researchers report, the cells without the variation now grew the normal amount of synapses, while those with the inserted mutation had half as many.

We had our definitive answer to whether this DISC1 variation is responsible for the reduced synapse growth, Ming says.

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Stem Cells Reveal How Illness-Linked Genetic Variation Affects Neurons

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Gene therapy can offer an effective treatment for drug-resistant radio-insensitive cancer. However, progress has been hampered by the difficulties in developing an appropriate delivery mechanism. Now researchers have demonstrated for the first time that magnetic nanoparticles provide safe, effective and targeted "suicide-gene" delivery to cells of a particularly prevalent and highly resilient type of liver cancer. Because the nanoparticles are magnetic they can also be used for hyperthermia treatments, where magnetic energy is converted into heat to elevate the temperature of the surrounding cancerous tissue, increasing the overall therapeutic effect of the gene therapy.

"Our in vivo and in vitro experiments showed that the gene therapy combined with the heating treatment was very effective," explains Chenyan Yuan, a researcher from Southeast University in China. "In mice, we saw that the tumour growth rate, volume and mass were significantly less in the combined treatment group compared to gene therapy and hyperthermia therapy alone."

Yuan and colleagues from the Affiliated Zhong Da Hospital of Southeast University and Jiangsu Key Laboratory for Biomaterials and Devices in China equipped the magnetic nanoparticles with a tumour-specific promoter gene to specifically tackle hepatocellular carcinoma, which is the most common form of liver cancer and causes more than 600,000 deaths worldwide each year. The promoter gene could be easily replaced to track down and treat other cancers in the body.

For several years, gene therapy has been acknowledged as a promising candidate to treat a wide range of diseases and genetic disorders. The concept of gene therapy is fairly straightforward, tackling disease at the DNA level by replacing defective, disease-causing genes with healthy genes, but it has proved to be very difficult in practice, with one of the main issues being the choice of a suitable vehicle, or vector, to transport and introduce healthy genes into cells.

Scientists have traditionally used genetically engineered viruses as a vector because they are naturally programmed to insert their DNA into a foreign cell. However, the viruses have been known to randomly integrate themselves onto chromosomes and also provoke an immune response in the host, causing major complications. As a result, scientists have proposed using functional nanoparticles as a vector to avoid these issues and enhance the therapeutic effect of the delivered genes.

As Yuan points out, "magnetic nanoparticles have proven to be an extremely effective alternative to traditionally used vectors. They are very efficient when it comes to delivering DNA into a cell and do not provoke an immune response in the host. They are also safe, simple to use and easy to produce on a large scale."

In their study, the researchers fabricated iron-oxide magnetic nanoparticles, which were around 2030nm wide and coated them with a positive charge so that the negatively charged DNA molecules could bind strongly to them.

The DNA that they attached to the magnetic nanoparticles included the "suicide gene", which stops the cells in the tissue proliferating and promotes cell death, as well as a tumour-specific "promoter" gene that acts as the driver of the vehicle, directing the magnetic nanoparticle to the specific tissue.

The magnetic nanoparticles were assessed to see how well the different genes combined, and then tested in vitro on human liver cancer cells and in vivo on healthy female mice. During the tests, the magnetic nanoparticles were exposed to magnetic energy through an alternating magnetic field, which they were able to convert into heat, raising the temperature of the surrounding cancerous tissue to 4244C.

"Our results showed that the magnetic nanoparticles could elevate the temperature of the selected tissue into an effective therapeutic range, and avoid unwanted cell death and heating to normal tissues," says Yuan.

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Nanoparticles tackle cancer with heat and 'suicide genes'

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When Isaac Patterson awoke one Saturday morning last month to find his father resting on the couch, the 7-year-old was curious.

The previous day, his father had undergone surgery to donate bone marrow, and Isaac had questions.

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Race gathers money, recruits for bone-marrow donations

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In a boon to stem cell research and regenerative medicine, scientists at Boston Children's Hospital, the Wyss Institute for Biologically Inspired Engineering at Harvard University and Boston University have created a computer algorithm called CellNet as a "roadmap" for cell and tissue engineering, to ensure that cells engineered in the lab have the same favorable properties as cells in our own bodies. CellNet and its application to stem cell engineering are described in two back-to-back papers in the August 14 issue of the journal Cell.

Scientists around the world are engaged in culturing pluripotent stem cells (capable of forming all the body's tissues) and transforming them into specialized cell types for use in research and regenerative medicine. Available as an Internet resource for any scientist to use, CellNet provides a much needed "quality assurance" measure for this work.

The two papers also clarify uncertainty around which methods are best for stem cell engineering, and should advance the use of cells derived from patient tissues to model disease, test potential drugs and use as treatments. For example, using CellNet, one of the studies unexpectedly found that skin cells can be converted into intestinal cells that were able to reverse colitis in a mouse model.

"To date, there has been no systematic means of assessing the fidelity of cellular engineering -- to determine how closely cells made in a petri dish approximate natural tissues in the body," says George Q. Daley, MD, PhD, Director of the Stem Cell Transplantation Program at Boston Children's and senior investigator on both studies. "CellNet was developed to assess the quality of engineered cells and to identify ways to improve their performance."

Gene Signatures

CellNet applies network biology to discover the complex network of genes that are turned on or off in an engineered cell, known as the cell's Gene Regulatory Network or GRN. It then compares that network to the cell's real-life counterpart in the body, as determined from public genome databases. Through this comparison, researchers can rigorously and reliably assess:

"CellNet will also be a powerful tool to advance synthetic biology -- to engineer cells for specific medical applications," says James Collins, PhD, Core Faculty member at the Wyss Institute and the William F. Warren Distinguished Professor at Boston University, co-senior investigator on one of the studies.

Putting CellNet to the Test

The researchers -- including co-first authors Patrick Cahan, PhD and Samantha Morris, PhD, of Boston Children's, and Hu Li, PhD, of the Mayo Clinic, first used CellNet to assess the quality of eight kinds of cells created in 56 published studies.

In a second study, they applied CellNet's teachings to a recurring question in stem cell biology: Is it feasible to directly convert one specialized cell type to another, bypassing the laborious process of first creating an iPS cell? This study looked at two kinds of directly converted cells: liver cells made from skin cells, and macrophages made from B cells.

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Tissue development 'roadmap' created to guide stem cell medicine

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TO SOME people, the term stem cell may seem kind of taboo. I personally would not want something from animals injected into my system. But Im okay with non-invasive treatments, so I was interested to try out a plant-based stem cell facial.

After cleansing and toning, cotton pads moistened with a clear solution were laid on my eyelids to protect them from a three-minute steaming session. This was followed by a special tool called a scrubber that kind of looks like a computer mouse, but helps to remove dead skin cells and unblock pores without using the rather painful pricking tool.

Next, a rejuvenating gel was applied, followed by the plant-derived stem cell formula. A unique cooling machine was used to massage it into the skin for 10 minutes. Using this machine for cold electrophoresis helps the skin absorb serums and vitamins, without having to use injections. This was great for someone like me, who is wary of invasive treatments. The cooling machine feels like having an ice-cold metal ball massaged on the face; very invigorating, indeed.

Just when I thought my skin already got a lot of pampering, the stem cell was followed by a face mask full of natural vitamins. While it penetrated into my skin, I was given an arm and foot massage, which was nice for further relaxation.

With my combination skin, I looked pretty greasy right afterwards. When I woke up the next day, I didnt see a visible difference in my skin, but it was very smooth and supple to the touch. You may not see instant results with a treatment like this, but its a good treatment to maintain radiance, softness and hydration from beneath the surface of the skin.

This type of facial is not recommended for those with oily or acne-prone skin because the added oiliness may exacerbate problems, but it is ideal for those with dry or mature skin, as it is deeply nourishing and moisturizing. After the first treatment or over time, depending on the condition of your skin, stem cell diminishes fine lines, prevents wrinkles, and promotes cell renewal (a process that slows with age) to give that glowing look that signifies healthy, youthful skin.

I tried out the stem cell facial at Lohas skin and slimming center on Paseo Saturnino, Banilad. Its a more upscale experience here with your own room, as opposed to being in one large room with dividers, in case privacy is an issue for you. All of their machines and products are brought in from Korea and their staff, like my therapist Jennylyn, are highly knowledgeable and know just how much pressure to apply during the treatment. The service, facilities and products used add up to a luxurious treatment session that makes one feel very pampered.

Published in the Sun.Star Cebu newspaper on August 15, 2014.

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Trying out a stem cell facial

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Dartmouth cancer researchers at Norris Cotton Cancer Center found a means of causing the elimination of a protein that maintains cancer cell viability; the results of the study appear in the August 8 issue of The Journal of Biological Chemistry.

"These findings may lead to a new target for chemoresistant cancer cells," said Ruth W. Craig, PhD, professor of Pharmacology & Toxicology, Geisel School of Medicine at Dartmouth, Hanover, NH, who is primary author of the peer reviewed article. "These cells are resistant to multiple types of standard chemotherapeutic agents because of over-expression of Myeloid Cell Leukemia-1 (Mcl-1), however, Mcl-1 expression plummets when we inhibit one particular enzyme and then cancer cells subsequently die."

The Mcl-1 protein is frequently over-expressed in cancer; it is present not only in leukemia and lymphoma but also in a host of solid tumors. While Mcl-1 is expressed in a highly-controlled fashion in normal cells, its over-expression and lack of destruction maintains the viability of cancer cells and renders them resistant to chemotherapy. When high levels of this protein are maintained, the patient's cancer cells survive multiple types of drug treatment.

The research found that an enzyme that removes phosphate groups from Mcl-1 is critical in terms of maintaining its expression in cancer. This enzyme, known as protein phosphatase 2A (PP2A), can be inhibited to stop the removal of phosphate groups from a regulatory motif in Mcl-1 referred to as the PEST region (enriched with amino acids Proline, glutamic acid, Serine, and Threonine). Inhibition of the removal of phosphate groups, such as at Threonine-163 and Serine-159, targets the Mcl-1 protein for rapid destruction and, shortly thereafter, the cancer cells die.

"PP2A is a complex multi-subunit enzyme and we hope to identify more specifically which form of PP2A is involved in dephosphorylating Mcl-1," said Craig. "This could give a more specific way of causing Mcl-1 destruction."

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The above story is based on materials provided by Norris Cotton Cancer CenterDartmouth-Hitchcock Medical Center. Note: Materials may be edited for content and length.

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Researchers target rapid destruction of protein responsible for cancer cell resistance to therapy

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PUBLIC RELEASE DATE:

13-Aug-2014

Contact: Lester Kok lesterkok@ntu.edu.sg 65-679-06804 Nanyang Technological University

A research team led by Nanyang Technological University (NTU) scientists have made a key finding which is expected to open up improved treatment possibilities for children suffering from leukaemia.

They found that two in three cases of acute lymphoblastic leukaemia, a type of cancer of the white blood cells, may be caused by mutations in one of the two key genes found in children. These genes are however more prevalent in those with Down syndrome.

This means that scientists can design better tailored treatment protocols, depending on which mutating gene is carried by the patient. Such treatments may include lower doses of anti-cancer drugs thus leading to fewer side effects.

Acute lymphoblastic leukaemia is the most common cancer in children, with 50 to 100 children diagnosed each year in Singapore. This gene discovery is good news for those with Down syndrome and the 20 per cent of children who do not respond well to standard therapy.

Children with Down syndrome have a 20 to 50 fold greater risk of developing this blood cancer. They are also prone to suffer a relapse and have a higher risk of dying from the side effects of therapy.

The discovery, made by an international team led by Professor Dean Nizetic from NTU's Lee Kong Chian School of Medicine, was published in the prestigious academic journal Nature Communications last week.

Prof Nizetic's team of experts in ageing and Down syndrome collaborated with researchers from the Queen Mary University in London and the universities of Geneva and Padua on this study.

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NTU gene research promises better treatment procedures for children with leukemia

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A new research has developed a fresh computational method to study the function of disease-causing genes with a new discovery of a gene associated with malaria.

Dr. Olivier Lichtarge, professor of molecular and human genetics and director of the Computational and Integrative Biomedical Research Center at Baylor said that today, rapidly falling costs meant that high throughput sequencing projects were revealing the entire gene sequences of ever more species, but the biological functions of most of these genes remain unknown.

The researchers came up with a computational method that allowed biological information to flow from gene to gene across a massive network across many genomes, known as the "supergenomic" network.

Dr. Andreas Martin Lisewski, an instructor in Lichtarge's lab at Baylor, asserted that the network connected millions of genes from hundreds of species based on their interactions within the organism or based on their ancestral relations between different species and normally computing the flow of functional information would be costly and slow, but they developed a compression method that reduced this gigantic network into one that was much smaller and now computationally tractable.

The study is published in the journal Cell.

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New malaria research studies function of disease-causing gene

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Newswise DALLAS August 14, 2014 UTSouthwestern Medical Center researchers successfully used a new gene editing method to correct a mutation that leads to Duchenne muscular dystrophy (DMD) in a mouse model of the condition.

Researchers used a technique called CRISPR/Cas9-mediated genome editing, which can precisely remove a mutation in DNA, allowing the bodys DNA repair mechanisms to replace it with a normal copy of the gene. The benefit of this approach over other gene therapy techniques is that the new method can permanently correct the defect in a gene rather than just transiently adding a functional one, said Dr. Eric Olson, Director of the Hamon Center for Regenerative Science and Medicine at UTSouthwestern and Chairman of Molecular Biology.

Using CRISPR/Cas9, the Hamon Center team was able to correct the genetic defect in a mouse model of DMD and thus prevent the development of features of the disease, which in boys causes progressive muscle weakness and degeneration, often along with breathing and heart complications.

Our findings show that CRISPR/Cas9 can correct a genetic mutation that leads to DMD, at least in mice, said Dr. Olson, holder of the Pogue Distinguished Chair in Research on Cardiac Birth Defects, the Robert A. Welch Distinguished Chair in Science, and the Annie and Willie Nelson Professorship in Stem Cell Research. Even in mice with only a small percentage of corrected cells, we saw widespread and progressive improvement of the condition over time, likely reflecting a survival advantage of the corrected cells and their contribution to regenerating muscle. He also pointed out this research sets the stage for possible clinical application of the approach in the future. Skeletal muscle is one of the largest tissues in the human body and current gene therapy methods are only able to affect a portion of the muscle. If the corrected tissue can replace the diseased muscle, then patients may get greater clinical benefit.

Although the genetic cause of DMD has been known for nearly 30 years, there are no treatments that can cure the condition. Duchenne muscular dystrophy breaks down muscle fibers and replaces them with fibrous and/or fatty tissue causing the muscle to gradually weaken.

DMD affects an estimated 1 in 3,6006,000 male births in the United States, according to the Centers for Disease Control (CDC). Left untreated, those with DMD eventually require use of a wheelchair between age 8 and 11, and have a life expectancy of 25 years. Initial symptoms include difficulty running and jumping, and delays in speech development. DMD can be detected through high levels of a protein called creatine kinase in the blood stream, and is confirmed by genetic testing.

Genome editing through the CRISPR/Cas9 system is not currently feasible in humans. However, it may be possible, through advances in the technology, to develop therapies for DMD in the future, Dr. Olson said.

At the moment, we still need to overcome technical challenges, in particular to find better ways to deliver CRISPR/Cas9 to the target tissue and to scale up, Dr. Olson said. But in the future we might be able to use this technique therapeutically, for example to directly target and correct a mutation in muscle stem cells and muscle fibers. We are working on a more clinically feasible method to correct mutations in adult tissues, and have made some progress added Chengzu Long, a graduate student in the Olson lab.

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New Gene Editing Method Shows Promising Results for Correcting Muscular Dystrophy

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A computer science and engineering associate professor and her doctoral student graduate are using a genetic computer network inference model that eventually could predict whether a person will suffer from bipolar disorder, schizophrenia or another mental illness.

The findings are detailed in the paper "Inference of SNP-Gene Regulatory Networks by Integrating Gene Expressions and Genetic Perturbations," which was published in the June edition of Biomed Research International. The principal investigators were Jean Gao, an associate professor of computer science and engineering, and Dong-Chul Kim, who recently earned his doctorate in computer science and engineering from UT Arlington.

"We looked for the differences between our genetic computer network and the brain patterns of 130 patients from the University of Illinois," Gao said. "This work could lead to earlier diagnosis in the future and treatment for those patients suffering from bipolar disorder or schizophrenia. Early diagnosis allows doctors to provide timely treatments that may speed up aid to help affected patients."

The UT Arlington researchers teamed with Jiao Wang of the Beijing Genomics Institute at Wuhan, China; and Chunyu Liu, visiting associate professor at the University of Illinois Department of Psychiatry, on the project.

Gao said the findings also could lead to more individualized drug therapies for those patients in the early stages of mental illnesses.

"Our work will allow doctors to analyze a patient's genetic pattern and apply the appropriate levels of personalized therapy based on patient-specific data," Gao said.

One key to the research is designing single nucleotide polymorphism or SNP networks, researchers said.

"SNPs are regulators of genes," said Kim, who joins the University of Texas-Pan American this fall as an assistant professor. "Those SNPs visualize how individual genes will act. It gives us more of a complete picture."

The paper is a culmination of four years of work.

Khosrow Behbehani, dean of the College of Engineering, said the research merges the power of computer science and engineering, psychology and genetics.

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Earlier diagnosis, treatment of mental illness? Genetic computer network inference model

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By Shane Huntington

Neuropsychiatrist Prof Chris Pantelis and neural engineering researcher Prof Stan Skafidas discuss the potential for the use of genetics to improve the diagnosis of autism.

SHANE HUNTINGTON I'm Dr Shane Huntington. Thanks for joining us. Human beings are social animals. We rely on language and the subtle social cues that accompany our words to communicate with each other. But for people with Autism Spectrum Disorder, or ASD for short, the simple acts of communicating and interacting with others in a social setting can be baffling or even terrifying. Currently ASD diagnosis is complex. Psychological assessments and interviews are combined with behavioural observations by parents and teachers and a multitude of other mental disorders need to be carefully ruled out. But we know from twin studies that there's a genetic component to ASD, so why don't we have a genetic test for this condition? Are behavioural observations really the best we can do for desperate parents seeking answers for the challenging behaviour in their children? Surely our extraordinary advances in genetics hint at effective DNA based tests. Today on Up Close we speak to a neuropsychiatrist and an electrical engineer about how we might one day test for ASD based on our genetics. Chris Pantelis is Professor of Neuropsychiatry and Scientific Director of the Melbourne Neuropsychiatry Centre at the University of Melbourne and Melbourne Health. Stan Skafidas is Professor of Neural Engineering at the Department of Electrical and Electronic Engineering; leads the Melbourne School of Engineering's research in nanoelectronics and is the Director of the Centre for Neural Engineering. Welcome to Up Close Stan and Chris.

STAN SKAFIDAS Thank you.

CHRIS PANTELIS Thank you.

SHANE HUNTINGTON Chris, I might start with you. What sorts of tests are currently available to diagnose someone with Autism Spectrum Disorder?

CHRISTOS PANTELIS So the diagnosis of Autism Spectrum Disorder relies very much on clinical observation. It requires careful considered observation of behaviour, social interaction and particularly looking at language and communication; also observations related to stereotype, the repetitive behaviours that many of these children manifest. The disorder is diagnosed early. The onset is before the age of three and it's the observation that children are not engaging, not socialising appropriately, that they're delayed in their language and that they may have stereotyped or repetitive behaviours. So very much the diagnosis is based on clinical observation at this point in time. Now as you rightly point out it is clear that there is a genetic component to this disorder. It runs in families. Those twins that are monozygotic have a high concordance, which means that if one twin has the disorder there's a high likelihood that the co-twin is also affected. This means that we should be able to examine the genetics of this disorder and see if we can come up with a test if you like that might help us in our clinical diagnosis.

SHANE HUNTINGTON You mentioned we can look at children as young as three. It would seem difficult that you'd be able to extract the sort of behavioural anomalies that you're talking about at that age, given the wide variety of developmental speeds that we find out kids growing up with. Now some kids learn language very quick, others don't. How successful is it in terms of determining if a child is positive at age three?

CHRISTOS PANTELIS Again a very good and I think the important thing here is that one needs to take account of the trajectory of development of any individual child. And often clinicians looking at these children will assess them over a lengthy period of time. The diagnosis might be suspected but may not be confirmed for a considerable period of time, perhaps a number of years. It depends on the severity of the presentation, the range of symptoms and how they're developing.

SHANE HUNTINGTON You mentioned the possibility of genetic testing. It would seem that we have a genetic test for every second illness at the moment. There are a lot of new ones around, the most commonly known ones such as those for breast cancer and so forth. There is definitely a genetic component to this as you say from twin studies. Why is it that we don't have a genetics test at this point for autism?

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Screening along the spectrum: The search for a genetic test for autism

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William Smith's disease has grim milestones.

At 2, the Gambrills triplet known as Mick couldn't walk or talk as well as his siblings. In kindergarten, he started losing language and motor skills. At 12, he needed a wheelchair and a feeding tube.

Doctors at Johns Hopkins Hospital dedicated to treating his symptoms said he had an undiagnosed progressive neuromuscular disease.

But a new test may provide something the family has long sought: a name.

"The idea that there is something out there that can tell you [what's wrong] is huge," said Cathy Smith, Mick's mother. "There is a lot of pain that comes from not knowing what is wrong with your kid."

The test, called whole exome sequencing, stems from the decades-long push to map all the genes in the human body and translate that knowledge into diagnostic tools and therapies.

The test has been commercially available for less than three years ,and doctors say it still doesn't offer definitive information for most patients with genetic disorders. The largest published study, by scientists at Baylor College of Medicine in Houston, found diagnoses a quarter of the time, though the success rate appears to be rising.

Data analysis takes three to four months, and the test is so new there is no insurance billing code and often no coverage for the average $7,000 cost even though insurers may pay more for a series of smaller genetic tests and potentially ineffective therapies.

Unlike tests that look for one or a small number of genetic mutations, such as the BRCA test for breast cancer, exome sequencing allows analysis of thousands of genes at once.

The exome is composed of about 22,000 genes, about 1 percent of the human genome. But it is believed to be where functionally important DNA is housed, and where 85 percent of harmful mutations are found.

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New genetic test helps identify some mystery illnesses

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An Iowa drug developer is preparing to test a possible Ebola vaccine in humans, as scientists race to develop ways to prevent or fight a virus that has killed more than 1,000 people in a West African outbreak.

NewLink Genetics is planning an initial phase of testing involving up to 100 healthy volunteers and is talking with regulators about the study, said Brian Wiley, the company's vice president for business development. He declined to say whether the drug developer has submitted an application for the research to the Food and Drug Administration.

Chief Financial Officer Gordon Link said Thursday the timing of the testing, which would involve up to 100 healthy volunteers, is uncertain.

"We're getting a lot of assistance from a number of sources to accelerate this, so exactly how long it's going to take is a little uncertain because people are greasing the paths as much as they can," he said.

There is no proven treatment or vaccine for Ebola, and the current outbreak, which also has sickened nearly 2,000 people, is the largest in history. The outbreak was first detected in March in Guinea and spread to Liberia, Sierra Leone and Nigeria.

Other possible Ebola vaccines under development include one developed at the National Institutes of Health that is set to begin early-stage testing in humans this fall.

On Wednesday, Canadian drugmaker Tekmira Pharmaceuticals Corp. said it wasn't ready to make its experimental Ebola drug available in Africa.

NewLink Genetics Corp. is planning to test a vaccine that was discovered by scientists working for the Canadian government. The U.S. drugmaker has an exclusive license to take it through clinical trials and then sell it if regulators grant approval.

NewLink said the vaccine has been 100 percent effective in preventing deadly Ebola infections in non-human primates, and it acts quickly enough to show effectiveness in animals that received a typically lethal dose of the virus.

The vaccine contains an antigen from the Ebola virus, and it essentially teaches a person's immune system how to fight the virus.

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NewLink Genetics: Ready to Test Ebola Vaccine

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Australian scientists studying zebrafish have stumbled upon what they say is one of the most significant discoveries in stem cell research.

In research published on Thursday in the journal Nature, the Monash University scientists revealed that they uncovered how one of the most important stem cells in blood and bone marrow, the haematopoietic stem cell (HSC), is formed.

Professor Peter Currie, from Monash University's Australian Regenerative Medicine Institute, said the discovery brought researchers closer to growing HSCs in a lab.

"HSCs are the basis of bone marrow transplantations as a therapy, so when a leukaemia patient receives bone marrow, it's really these HSCs that do the heavy lifting," Professor Currie said.

"So when clinicians do bone marrow transplants, they need to find a matching donor recipients and we know that's a hit-or-miss procedure.

"So for many years people have been trying to make HSCs in the dish, and they've had very little success in doing this."

Professor Currie, who led the study, said the discovery brought scientists much closer to achieving that aim.

"It's the discovery of a completely new cell type that basically is required to give instructions to the HSC to make it become what it needs to become," he said.

"It means we now understand how HSC form in the body better, we can use that information to try to grow these cells in the dish and we hope that will lead to better treatment for people with leukaemia and blood disorders."

Professor Currie said he specialises in muscle stem cell biology and accidentally came across the discovery while studying muscle stem cells in zebrafish.

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Stem cell discovery: Australian scientists make significant find while studying zebrafish

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