PUBLIC RELEASE DATE:

17-Aug-2014

Contact: Henry Stanley henry@bg-rf.org.uk 44-208-133-5518 Biogerontology Research Foundation

Scientists from the Biogerontology Research Foundation (BGRF), a UK-based charity founded to support ageing research and address the challenges of a rapidly ageing population, propose a new concept for signalome-wide analysis of changes in intracellular pathways, called OncoFinder, which allows for accurate and robust cross-platform analysis of gene expression data. This new technique will allow scientists to derive useful information from and compare the hundreds of thousands of data sets obtained using legacy equipment as well as data sets obtained from biological samples preserved in paraffin blocks and partially-degraded samples.

The original research, published in the journal Frontiers in Molecular Biosciences, shows that the OncoFinder method significantly reduces errors introduced by transcriptome-wide experimental techniques. Scientists compared gene expression data for the same biological samples obtained by both next generation sequencing (NGS) and microarray methods, finding that these different techniques have almost no correlation between the gene expression values for all datasets analysed. In contrast, when the OncoFinder algorithm is applied to the data, a clear correlation between next generation sequencing and microarray gene expression datasets was seen.

"For several years the potential for the use of gene expression data in research and clinical applications has been underappreciated due to the inconsistency of the data coming from the various types of equipment. There is just too much variation and complexity when comparing the massive number of individual genes. But when this complexity is reduced and the gene expression is mapped onto signalling pathways, we can evaluate the pathway activation drift and analyse the changes and transitions much more effectively. The OncoFinder algorithm enables scientists to characterise the functional states of transcriptomes more accurately than before and we hope that this will become a method of choice in genetics, physiology, biomedicine and molecular diagnostics," said Alex Zhavoronkov, PhD, director of the BGRF and co-author of the study.

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The original research paper is available to view and download at http://journal.frontiersin.org/Journal/10.3389/fmolb.2014.00008/abstract.

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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BGRF announces OncoFinder algorithm for reducing errors in transcriptome analysis

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PUBLIC RELEASE DATE:

18-Aug-2014

Contact: Nicole Baritot press@aats.org 978-299-4520 American Association for Thoracic Surgery

Beverly, MA, August 18, 2014 Investigators from the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) have successfully transplanted hearts from genetically engineered piglets into baboons' abdomens and had the hearts survive for more than one year, twice as long as previously reported. This was achieved by using genetically engineered porcine donors and a more focused immunosuppression regimen in the baboon recipients, according to a study published in The Journal of Thoracic and Cardiovascular Surgery, an official publication of the American Association for Thoracic Surgery.

Cardiac transplantation is the treatment of choice for end stage heart failure. According to the NHLBI, approximately 3,000 people in the US are on the waiting list for a heart transplant, while only 2,000 donor hearts become available each year. For cardiac patients currently waiting for organs, mechanical assist devices are the only options available. These devices, however, are imperfect and experience issues with power supplies, infection, and problems with blood clots and bleeding.

Transplantation using an animal organ, or xenotransplantation, has been proposed as a valid option to save human lives. "Until we learn to grow organs via tissue engineering, which is unlikely in the near future, xenotransplantation seems to be a valid approach to supplement human organ availability. Despite many setbacks over the years, recent genetic and immunologic advancements have helped revitalized progress in the xenotransplantation field," comments lead investigator Muhammad M. Mohiuddin, MD, of the Cardiothoracic Surgery Research Program at the NHLBI.

Dr. Mohiuddin's group and other investigators have developed techniques on two fronts to overcome some of the roadblocks that previously hindered successful xenotransplantation. The first advance was the ability to produce genetically engineered pigs as a source of donor organs by NHLBI's collaborator, Revivicor, Inc. The pigs had the genes that cause adverse immunologic reactions in humans "knocked out" and human genes that make the organ more compatible with human physiology were inserted. The second advance was the use of target-specific immunosuppression, which limits rejection of the transplanted organ rather than the usual generalized immunosuppression, which is more toxic.

Pigs were chosen because their anatomy is compatible with that of humans and they have a rapid breeding cycle, among other reasons. They are also widely available as a source of organs.

In this study, researchers compared the survival of hearts from genetically engineered piglets that were organized into different experimental groups based on the genetic modifications introduced. The gene that synthesizes the enzyme alpha 1-3 galactosidase transferase was "knocked out" in all piglets, thus eliminating one immunologic rejection target. The pig hearts also expressed one or two human transgenes to prevent blood from clotting. The transplanted hearts were attached to the circulatory systems of the host baboons, but placed in the baboons' abdomens. The baboons' own hearts, which were left in place, maintained circulatory function, and allowed the baboons to live despite the risk of organ rejection.

The researchers found that in one group (with a human gene), the average transplant survival was more than 200 days, dramatically surpassing the survival times of the other three groups (average survival 70 days, 21 days, and 80 days, respectively). Two of the five grafts in the long-surviving group stopped contracting on postoperative days 146 and 150, but the other three grafts were still contracting at more than 200 to 500 days at the time of the study's submission for publication.

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7 hours ago A Batwa young man in Bwindi Impenetrable Forest National Park, Uganda. Credit: George Perry, Penn State

The small body size associated with the pygmy phenotype is probably a selective adaptation for rainforest hunter-gatherers, according to an international team of researchers, but all African pygmy phenotypes do not have the same genetic underpinning, suggesting a more recent adaptation than previously thought.

"I'm interested in how rainforest hunter-gatherers have adapted to their very challenging environments," said George H. Perry, assistant professor of anthropology and biology, Penn State. "Tropical rainforests are difficult for humans to live in. It is extremely hot and humid with limited food, especially when fruit is not in season."

A phenotype is the outward expression of genetic makeup and while two individuals with the same phenotype may look alike, their genes may differ substantially. The pygmy phenotype exists in many parts of Africa, Southeast Asia, the Philippines and potentially in South America. The phenotype is usually associated with rainforest hunter-gathers, groups of people who do not farm, but obtain resources by hunting large and small animals and gathering fruit, nuts, insects and other available resources.

Perry and colleagues looked at the genetics of the Batwa rainforest hunter-gatherers of Uganda and compared them to their farming neighbors, the Bakiga, with whom they traditionally traded forest products for grain, and sometimes intermarry. The researchers also looked at the Baka rainforest hunter-gatherers and their farming neighbors the Nzebi/Nzime in central Africa. They report their results online today (Aug. 18) in the Proceedings of the National Academies of Science.

The average height for Batwa men is five foot and for women it is four foot eight inches. Their short stature is not caused by a single genetic mutation as occurs in many forms of dwarfism, but is the result of a variety of genetic changes throughout the genome that influence height.

The researchers investigated 16 different genetic locations that were associated with short stature when they looked at individuals who were an admixture of Batwa and Bakiga. Several of these regions contained genes known to be involved with growth in humans. They then studied these regions to look for indications that the changes were ones that persisted because they were adaptive.

Genetic mutations occur in populations all the time. If they have a negative impact on the individual, they tend to disappear from the population quickly. If they have no noticeable impact for the good or bad, they might disappear as well, although more slowly. Mutations which have positive influence on individuals, making them more fit for their environment, tend to spread through the population.

Short stature may be adaptive for rainforest individuals for a variety of reasons, according to Perry. Small bodies require less food, which is adaptive for a food-limited location like the rainforest. Small bodies also generate less heat, which, in the heat and humidity of the rainforest, is adaptive. It is also easier for small, agile individuals to move through dense undergrowth and to climb trees.

The results of the genetic comparison indicated that there was a statistical difference between the two groups indicative of multi gene adaptation.

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Pygmy phenotype developed many times, adaptive to rainforest

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PUBLIC RELEASE DATE:

18-Aug-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, August 18, 2014While much attention has focused on the link between violent video game playing and aggression among youths, a new study finds significantly increased signs of depression among preteens with high daily exposure to violent video games. The details and implications of this important new study are described in Cyberpsychology, Behavior, and Social Networking, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Cyberpsychology, Behavior, and Social Networking website.

Susan R. Tortolero, PhD and coauthors from The University of Texas Health Science Center at Houston School of Public Health, RAND Corporation (Santa Monica, CA), The University of Alabama at Birmingham, Centers for Disease Control and Prevention (Atlanta, GA), and Boston Children's Hospital and Harvard Medical School (Boston, MA) recorded significantly more depressive symptoms over the course of a year among fifth-graders from three U.S. cities who reported playing high-violence video games for 2 or more hours a day, compared to those who reported playing low-violence video games for less than 2 hours a day. This association was consistent across all racial/ethnic subgroups and among boys, according to the study results presented in the article "Daily Violent Video Game Playing and Depression in Preadolescent Youth."

"One of the strengths of this study is its large and ethnically diverse sample," says Editor-in-Chief Brenda K. Wiederhold, PhD, MBA, BCB, BCN, Interactive Media Institute, San Diego, California and Virtual Reality Medical Institute, Brussels, Belgium.

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About the Journal

Cyberpsychology, Behavior, and Social Networking is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that explores the psychological and social issues surrounding the Internet and interactive technologies plus cybertherapy and rehabilitation, plus cybertherapy and rehabilitation. Complete tables of contents and a sample issue may be viewed on the Cyberpsychology, Behavior, and Social Networking website.

About the Publisher

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Are children who play violent video games at greater risk for depression?

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8 hours ago Cold Spring Harbor Laboratory researchers have found that miRNAs, short RNA molecules, are responsible for sexual differences in fruit flies. Shown here are testes from a male fruit fly where a hormone that controls a key miRNA has been inactivated. The abnormal testes fail to make sperm. They now produce sex determinants (shown in red) that are found in the ovaries of female flies. Credit: D. Fagegaltier/ Cold Spring Harbor Laboratory

Men and women differ in plenty of obvious ways, and scientists have long known that genetic differences buried deep within our DNA underlie these distinctions. In the past, most research has focused on understanding how the genes that encode proteins act as sex determinants. But Cold Spring Harbor Laboratory (CSHL) scientists have found that a subset of very small genes encoding short RNA molecules, called microRNAs (miRNAs), also play a key role in differentiating male and female tissues in the fruit fly.

A miRNA is a short segment of RNA that fine-tunes the activation of one or several protein-coding genes. miRNAs are able to silence the genes they target and, in doing so, orchestrate complex genetic programs that are the basis of development.

In work published in Genetics, a team of CSHL researchers and colleagues describe how miRNAs contribute to sexual differences in fruit flies. You've probably never noticed, but male and female flies differ visibly, just like other animals. For example, females are 25% larger than males with lighter pigmentation and more abdominal segments.

The team of researchers, including Delphine Fagegaltier, PhD, lead author on the study, and CSHL Professor and Howard Hughes Medical Institute Investigator Greg Hannon, identified distinct miRNA populations in male and female flies. "We found that the differences in miRNAs are important in shaping the structures that distinguish the two sexes," says Fagegaltier. "In fact, miRNAs regulate the very proteins that act as sex determinants during development."

The team found that miRNAs are essential for sex determination even after an animal has grown to adulthood. "They send signals that allow germ cells, i.e., eggs and sperm, to develop, ensuring fertility," Fagegaltier explains. "Removing one miRNA from mature, adult flies causes infertility." More than that, these flies begin to produce both male and female sex-determinants. "In a sense, once they have lost this miRNA, the flies become male and female at the same time," according to Fagegaltier. "It is amazing that the very smallest genes can have such a big effect on sexual identity."

Some miRNAs examined in the study, such as let-7, have been preserved by evolution because of their utility; humans and many other animals carry versions of them. "This is probably just the tip of the iceberg," says Fagegaltier. "There are likely many more miRNAs regulating sexual identity at the cellular and tissue level, but we still have a lot to learn about these differences in humans, and how they could contribute to developmental defects and disease."

Explore further: Scientists identify a gene that controls the timing of precisely ordered events during maturation

More information: "A Genome-Wide Survey of Sexually Dimorphic Expression of Drosophila miRNAs Identifies the Steroid Hormone-Induced miRNA let-7 as a Regulator of Sexual Identity" appeared online in Genetics on July 31, 2014.

Closely related organisms share most of their genes, but these similarities belie major differences in behavior, intelligence, and physical appearance. For example, we share nearly 99% of our genes with chimps, ...

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More than just X and Y: A new genetic basis for sex determination

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15 hours ago Jarin1 inhibits the enzyme JAR1 by displacing the natural substrate, Jasmonoyl-isoleucine (JA-Ile), from its binding site. Both substances overlap, so that JAR1 can no longer fulfil its tasks. The left panel shows an overview of the entire enzyme; the right panel a view into the active centre. Credit: Corey S. Westfall, Washington University, St. Louis

Researchers trying to get new information about the metabolism of plants can switch off individual genes and study the resulting changes. However, Erich Kombrink from the Max Planck Institute for Plant Breeding Research in Cologne and Markus Kaiser from the University of Duisburg-Essen adopt a different approach. They identify small molecules that block specific components of the metabolic process like brake pads and prevent the downstream reactions. In their search for these molecules, they use a biological selection process involving intact plants. This strategy has long been exploited in drug research. Its application in the plant sciences, however, is relatively new.

Kombrink, Kaiser and their colleagues have identified a molecule that interferes with the effect of jasmonic acid. This plant hormone influences flower formation, root growth, defence against herbivores and infections, wound healing, ageing of plants, and much more.

Although many questions about plant metabolism can be answered through targeted gene mutations, the method has its limits. This is also demonstrated in the case of jasmonic acid and its derivatives. So far, only one signalling chain has been discovered, but this cannot explain the wide-ranging effect of this plant hormone. Therefore, other hitherto undiscovered signalling paths and action mechanisms must exist. To find out more about them, Kombrink and Kaiser have adopted an approach that is similar to one used in medicine. Their strategy is based on the blocking of important metabolic pathways using low molecular weight compounds, which are easily assimilated by the plant. While in medical therapy such compounds are assimilated through the blood, in the plant they are introduced through the root.

The scientists embarked on their search with a screening of Arabidopsis thaliana and treating the plants with compounds in such a way that the desired selection could be identified by a conspicuous trait. Of the 1728 substances from a commercial compound library tested 16 emerged as inhibitors. This number was further reduced using more selective tests. In the end, only one substance turned out to be a specific inhibitor of the jasmonic acid signalling pathway and was given the name Jarin-1. "In terms of its basic structure, the substance is a plant alkaloid, whose two amino groups can carry different side chains," Kombrink explains. "However, its effect is associated with a particular side chain in one of the positions. Other side chains impair the activity of the substance. We also deliberately synthesised it once again to be certain that we had understood its chemical structure correctly."

The scientists also looked for the target of the newly discovered inhibitor. The known signalling chain starts with the conjugation of the jasmonic acid with the amino acid isoleucine by an enzyme called JAR1. The resulting pair leads to the expression following various detours of the genes necessary for the relevant effect of the jasmonic acid. Kombrink and Kaiser were able to show that JAR1 is the target of the newly discovered inhibitor. Due to the inhibition, the jasmonic acid conjugated with isoleucine does no longer accumulate in the cell. As a result genes are not expressed because the jasmonic acidisoleucine pair no longer activates the genes' starting point.

The Jarin-1 inhibitor identified by Kombrink and Kaiser not only works in Arabidopsis but also in Cardamine hirsuta or hairy bittercress. "So we are obviously dealing with a broadly applicable molecule," comments Kombrink. Under the effect of the inhibitor, the plants show the same features as they do following the targeted mutation of genes from the jasmonic acid signalling pathway.

The scientists also investigated the exact location where the molecule takes effect. They succeeded in demonstrating that it binds to the active centre of JAR1 and inhibits the natural substrate. "Our molecule is not a classical competitive inhibitor," says Kombrink. "But its effect can be explained, at least in parts, by displacement of the substrate from its binding site."

Small molecules are interesting new tools for plant research. Through their work, the researchers show how it is possible to search for them systematically and to identify their molecular mode of action.

Explore further: Signalling pathway links local and systemic plant immunity

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Researchers block plant hormone: Small molecule inhibits jasmonic acid, helps to explain its effects

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Kuala Lumpur, Malaysia (PRWEB) August 18, 2014

A Malaysian company has revolutionised wellness care through the screening of DNA to find ways to mitigate the risks for developing diseases. Results of the test can help health practitioners to develop more personalised wellness and fitness programmes for their patients.

Malaysian Genomics Resource Centre Berhad (MGRC) announced that conducting the Dtect Wellness genetic screening test on a persons DNA could identify genetic variations that affect an individuals overall wellness and fitness levels.

Based on the test results, wellness and medical practitioners can advise individuals on optimum dietary intake, lifestyle changes and suitable exercise.

Dtect Wellness test will be made available at all official Dtect partner wellness centres, in September 2014.

The launch of the new test is in conjunction with the companys 10th year of operations in Malaysia.

MGRCs Managing Director, Robert Hercus, said, Genetic applications are becoming an important part of preventive medicine. Dtect Wellness could assist medical practitioners to develop a more personalised health regime for their patients. In turn, patients may be suitably informed to take more proactive steps towards eating healthily and exercising effectively.

Beverly Wilshire Medical Centre Consultant Physician and Cardiologist, Dr Chin Sze Piaw, said, Beverly Wilshire Medical Centre is pleased to be working closely with MGRC to make genetic screening readily accessible to the public. MGRC has a proven track record of providing genetics-based services in Malaysia, as well as in South East Asia and Europe. We are confident that Dtect Wellness will become a vital component at wellness and health screening centres throughout the country.

Dtect Wellness is MGRCs flagship product in the Dtect range of genetic screening tests. It is designed to help individuals and families to better understand their genetic risks for conditions that affect their overall health.

About Malaysian Genomics Resource Centre Berhad Malaysian Genomics Resource Centre Berhad (MGRC) is a public company listed on the ACE Market of Bursa Malaysia. Established in 2004, MGRC has extensive experience in DNA-based analysis services for research and commercial projects. The company also provides genetic screening and molecular diagnostic services for the healthcare sector. More information on MGRC is available on http://www.mgrc.com.my.

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MGRC's New Genetic Screening Test to Dtect DNA for Wellness

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Mason, OH (PRWEB) August 18, 2014

Assurex Health, a leading personalized medicine company, announced that 100,000 mental health and chronic pain patients across North America have now been tested with GeneSight products that help clinicians select medications based on patients individual genetic profile.

This means that 100,000 people were helped on the road to mental wellness with GeneSight as an integral part of informing their treatment decisions, said Virginia C. Drosos, CEO of Assurex Health. We hope to bring the value of GeneSight to many more clinicians and patients who are working together to manage their mental health, chronic pain, and ADHD.

GeneSight helps health care providers make mental health and chronic pain treatment decisions based on a patients unique genetic makeup. Administered using a simple cheek swab, GeneSight is becoming a preferred step in helping clinicians treat patients with conditions such as depression, PTSD, bipolar disorder, chronic pain, and ADHD.

Many clinicians are making GeneSight the standard of care in their practices, said Joel Winner, M.D., Medical Director of Assurex Health and a practicing psychiatrist in Colorado. GeneSight is extremely beneficial in helping to identify genetically appropriate medications for patients. It gives us more precise information, so we can more quickly help patients get better.

Rapid Growth Expected to Continue

The number of patients tested using GeneSight has doubled since 2012, and is on pace to double again in 2014. Assurex Health expects up to one million patients could be tested by 2018.

Founded in 2006, Assurex Health has grown rapidly to service clinicians and patients throughout the U.S. and has recently expanded internationally through a partnership with Canadas Centre for Addiction and Mental Health (CAMH). Today, more than 8,500 clinicians in private practice, health systems, long-term care facilities and other care sites are registered to offer GeneSight.

Assurex Health recently secured $32 million in additional financing from GE Capital, Silicon Valley Bank, Sequoia Capital, Claremont Creek Ventures, Mayo Clinic, Cincinnati Childrens Hospital Medical Center, CincyTech and Allos Ventures, allowing it to enhance its focus on leading-edge science and delivering clinically proven results and product enhancements.

Assurex Health also recently introduced significantly enhanced versions of its GeneSight Psychotropic and GeneSight Analgesic products and added new commercial health insurance networks to increase patients coverage. In addition, the U.S. Department of Veterans Affairs in June approved use of GeneSight at VA medical centers, the largest health system in the United States, joining Medicare in reimbursing GeneSight.

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Mental Wellness Milestone: 100,000 Patients Tested with GeneSight to Support Medication Selection

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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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Utah research: Genetics help Tibetans thrive more than 2 miles in the sky

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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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UT Arlington Research Team's Work Could Lead To Earlier Diagnosis, Treatment Of Mental Diseases

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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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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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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.

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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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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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Be the Match Walk+Run

Bicentennial Park, 233 Civic Center Dr.

Contact: 1-800-507-5427, or click here

Times: 10 a.m. Saturday for the 5-kilometer run, with the event village opening at 8:30

Registration: $30 for 5K or adults in 1K; $15 for age 17 and younger in 1K, $10 Tot Trot; $25 virtual fundraiser

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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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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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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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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."

Story Source:

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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